Exam 3: Vascular disorders

Arterial disorders:
❖ Arteries become damaged or obstructed as a result of atherosclerotic plaque, thromboemboli,
chemical or mechanical trauma, infections of inflammatory processes, vasospastic disorders, and
congenital malformations
❖ A sudden arterial occlusion cause profound and irreversible tissue ischemia & tissue death (if
arteries involve, then it’s irreversible)
❖ When arterial occlusions develop gradually, less risk of sudden tissue death b/c collateral
circulation may develop (the rerouting of blood vessels, in which which new blood vessels join to
take over some of the circulation of blocked vessels), giving tissue the opportunity to adapt to
gradually decreased blood flow

Peripheral arterial disease

❖ Definition: any disease process that affects the arteries. Various PADs result in ischemia and
produce S/S in Box 18.1
- Arterial insufficiency of the extremities is a common cause of disability. The legs are
affected more than the upper extremities
- Clinical recognition of PAD is a slow process being in early adulthood & increases with age
- PAD is one manifestation of atherosclerosis, which affect arteries of the brain, heart,
kidneys, mesentery, and limbs should be suspected
- Over 1/3 have coronary disease, and 1/4 have carotid artery disease
- Pt w/PAD have an increased risk of mortality, myocardial infarction (MI), and cerebrovascular
disease

❖ Pathophysiology:
- The lumen narrows & blood flow decreases, ischemia occurs progressing to infarction in the
distal tissues
- In PAD, obstructive lesions are confined to segments of the arterial system extending from
aorta below the renal arteries to the popliteal artery. Distal occlusive disease is seen in pt
w/diabetes mellitus & elderly

❖ Forms of PAD:
- Arteriosclerosis (most common): A diffuse process whereby muscle fibers & endothelial lining of
the walls of small arteries and arterioles become thickened
- Atherosclerosis: a changes of the intimate consist of accumulation of lipids, calcium, blood
components, complex CHO, and fibrous tissue, referred to as atheroma or plaques. Causes
arterial stenosis, obstruction by thrombosis, aneurysm, ulceration, and vessel rupture
- Arterial bifurcations are more vulnerable to atherosclerosis than other areas of the arteries.
• These include the distal abdominal aorta: the common iliac arteries, the orifice of the
superficial femoral and profound femoris arteries, the superficial femoral artery in the
adductor canal.
• Gradual narrowing of the arterial lumen stimulates the development of collateral
circulation from pre-existing vessels

❖ Risk factors:
- Similar to those for developing coronary artery disease
- Modifiable risk factors (diet, smoking, tobacco use is most important in atherosclerotic lesion
development) and non-modifiable (race, age). Modification may slow the the disease process
- Nicotine decreases blood flow, increase HR and BP, and increase the risk for clot formation by
increasing platelet aggregation
- Hyperhomocysteinemia is an independent risk factor for atherosclerosis
• Homocysteine is a protein that promotes coagulation
• Elevated homocysteine lvl are associated w/genetic factors & a diet low in folic acid, vit
B6, and vit B12. Tx includes vit B6, B12, folate, lowers homocysteine level
• Elevated levels of C-reactive protein are strongly associated with the development of PAD
• HTN accelerates the rate at which atherosclerotic lesions form in high-pressure vessels and
is a major PAD risk factor
• Obesity, stress, & lack of exercise have been identified as contributing to the disease
process

Risk factors for PAD:

- Family history
- Age (14.5% of adults over 70 have PAD)
- Obesity
- Smoking
- Pre-existing health conditions:
• Coronary artery disease
• Cerebral artery disease
• Diabetes
• HTN
• Dyslipidemia
• Clotting disorders
• Hyperhomocysteinemia

❖ Clinical manifestation and assessment:

- Initially asymptomatic. Approximate 1%-5% of pt/PAD have critical limb ischemia (CLI), with
chronic ischemic pain at rest (rest pain), nonhealing, ulcers, or gangrene
- A small # of pt w/PAD have acute limb ischemia (ALI), a suffer decrease in limb perfusion,
caused by either thrombosis or embolism, that produces new or worsening symptoms that threaten
limb viability
- Other potential causes of acute arterial occlusions: atherosclerotic stenosis, aneurysm,
arterial dissection, arterial embolization, cardiac embolization, trauma, tumor compression,
graft thrombosis, drug abuse, low cardiac output, phlegmasia cerulean dolens, and compartment
syndrome
- Complain of pain in the fingers, feet or pain in the muscle groups with use (not the joints)
- Walking causes the pain in leg muscles, and upper extremity physical activity cause pain in the
arm muscles

Focused assessment of acute arterial occlusion:

Be alert for the following S/S, known as the Six Ps:
- Pain (severe, shooting, stabbing, burning sensation)
- Pallor (lighter color than the rest of the skin)
- Pulsenessless (no palpable pulse)
- Poikilothermia (cool temp to palpation)
- Paresthesia (numbness, tingling, hot/cold sensation)
- Paralysis (immobility [late sign], indicates severe tissue damage)

- Pain:
• Hallmark sx of PAD in the lower extremity is intermittent claudication (aching or cramping
in a muscle that occurs with same degree of exercise or activity) and is relieved w/rest
Caused by inability of arterial system to provide adequate blood flow to the tissues
in the face of increased demand for nutrients and O2 during exercise
• As tissues are forced to complete the energy cycle w/o adequate nutrients & oxygen, muscle
metabolites & lactic acid are produced;
Pain is experienced as metabolites aggravate nerve endings of surrounding tissue
Site of arterial disease can be determined by location of claudication (Pain occurs in
muscle groups distal to the diseased vessel)
• If the pt must sit to relieve pain, the pain may be caused by a nerve injury to the back or
non circulatory etiology
• Progression of arterial disease can be monitored by documenting ambulatory distance before
pain is felt
• Persistent pain in the anterior portion of the foot when pt is resting indicated a severe
degree of arterial insufficiency & a critical state of ischemia--known as rest pain
(discomfort often worse at night & may interfere w/ sleep)
• Rest pain frequently requires extremity to be lowered to dependent position to improve
perfusion to distal tissues; The dependency of the lower extremity may cause some dependent
edema in extremity--thus edema may be associated w/ PAD--Rest pain is associated w/ limb
threatening ischemia
• Upper extremity atherosclerotic stenosis may cause arm fatigue & pain w/ exercise (forearm
claudication) & inability to hold or grasp objects
Intermittent Claudication (IC)
- Cramp-like pain in a muscle
- Consistently reproduced w/the same degree of exercise of activity
- Relieved by stopping muscle use
- Caused by inability of the arterial system to provide blood for that keeps up with increased demand
- Site of arterial disease can be determined by the location of claudication
- Pain occurs in muscle groups distal to the diseased vessel
- 70-80% of pt do not have worsening symptoms
- 10% pf claudicants w/progress to critical limb ischemia
- Dependent position reduces pain

- Changes in skin appearance and temperature:

• Inadequate blood flow results in cool & pale extremities. Further reduction of blood flow
to tissue resulting in an even whiter or more blanched appearance to the skin
• When extremity is in a dependent position after elevation, it becomes reddish-blue color
called rubor (suggests severe peripheral arterial damage), in which vessels that can't
constrict remain dilated
• Cyanosis (bluish tint to skin) is manifested when the amount of oxygenated hemoglobin
contained in the blood is reduced
• Comparing the contralateral limb is the best way to discern color change
• Capillary refill time is frequently used as an assessment of peripheral perfusion (<2
second refill time)--Nurse considers this test not as a definitive marker for impaired
perfusion but rather as an adjective tool to consider when clustering other manifestations
of peripheral perfusion
• Additional changes resulting from a chronically reduced nutrient supply include: loss of
hair, brittle nails, dry/scaling skin, atrophy, & ulcerations.
• Skin and nail changes, ulcers, gangrene, & muscle atrophy may be evident in chronic
arterial disease but can't be relied on for dx of acute arterial insufficiency

- Pulses:
• Unequal pulses between extremities or the absence of a normally palpable pulse is a sign of
PAD. Palpation of pulses is subjective
• The present of foot pulse doesn’t exclude the possibility of PAD. DP and PT might not feel
it
• After exercise, the pulses may not be palpable. Known as “disappearing pulses”, and it is
caused by the increase need for blood flow in the working muscles, which the arteries
cannot provide
• Bruits may be auscultated w/stethoscope just distal to an arterial stenosis, indicating
turbulent blood flow that occurs with vessel stenosis

- Ankle-branchial index:
• The presence of PAD is defined as an ankle-brachial index (ABI) of less than 0.90. ABI is
calculated as the ration of the systolic BP in the ankle divided by the higher of the two
brachial systolic BP

- Sensory changes:
• Numbness, paresthesias, and motor deficits indicate tissue anoxia
• Motor deficits progress from vital to proximal, the nurse assesses initially for weakness
of the foot muscles. In contrast, paresthesia denotes ischemia that threatens limb survival

- Diagnostic tests
• Various noninvasive and invasive tests are performed to diagnose abnormalities affecting
the arteries
• When pulses cannot be palpated reliably, a handheld continuous wave (CW) Doppler ultrasound
device may be used to hear (insonate) signals in the vessel
• The Doppler emits a signal through the tissues, reflecting off the moving blood cells and
returned to the device
• Doppler studies are more useful when combined w/ankle-brachial index (ABI)
• The “gold standard” for diagnosis and evaluation of PAD is the invasive digital angiography

❖ Medical treatment:
- Goal: to aim at reducing the pt’s risk for life-threatening complications of atherosclerosis,
improving walking distance, & salvaging the limb, including the use of exercise, pharmacologic
 tx, risk factor modification (control of HTN, hypercholesterolemia, & diabetes, & cessation of
smoking), and invasive options
- Revascularization is recommended if there is a reasonable likelihood of symptomatic improvement
& there has been an inadequate response to pharmacologic or exercise therapy
- Invasive methods include surgery and percutaneous endoscopic procedures

- Management of intermittent claudication:

• Treatment goals for pts w/ intermittent claudication: relieve symptoms, improve exercise
performance, & improve functional abilities
• Generally, pt w/ intermittent claudication feel better when on an exercise program
• Initial treatment should be focused on a structured exercise program & pharmacotherapy
• Pt are advised to "walk into the pain" of claudication, pause until pain subsides, &
continue walking
• If program is combined w/ weight reduction & tobacco cessation, pt may improve activity
tolerance & experience pain relief w/o further intervention

- Pharmacologic therapy:
• Cilostazol is a phosphodiesterase III inhibitor that is a vasodilator & interferes w/
platelet aggregation; It is prescribed in combination w/ an exercise program to improve
walking distance. Guidelines recommend a 3-6 month course of cilostazol as 1st-line
pharmacotherapy treatment for pts w/ intermittent claudication
• Antiplatelet agents, such as aspirin or clopidogrel, help prevent formation of
thromboemboli, which can lead to MI & stroke.
Aspirin has been shown to reduce risk of MI, stroke, & death in pts w/ vascular
disease
Clopidogrel is indicated for prevention of cardiovascular ischemic events in pts w/
PAD but not for treatment of claudication

- Thrombolysis:
• A thrombotic stenosis or occlusion may be treated by thrombolysis
• After catheter insertion into the affected vessel, the thrombolytic agent is injected
directly into the thrombus; It will lyse the thrombus (clot)
• The pt is admitted to a special or critical care unit for continuous monitoring. Vital
signs are taken frequently, according to a protocol. The pt is closely monitored for any
signs of bleeding, as this is the most common side effect of thrombolytic therapy
• The nurse minimizes the # of punctures for IV lines & obtaining blood samples, avoids IM
injections, prevents tissue trauma, & applies pressure at least twice as long as usual
after any puncture performed
• Pts will have follow-up images to determine treatment effectiveness
• In order to monitor pt post intervention, it’s essential that a baseline assessment of the
extreme is documented so that the nurse can determine changes in perfusion of the extremity
post instrumentation

- Surgical management:
• Disabling claudication or risk for amputation is an indication for surgical or percutaneous
intervention
• The initial treatment goal for acute limb ischemia is to prevent worsening ischemia &
thrombus propagation, manage pain, & preserve tissue
• Anticoagulation is started immediately upon recognizing the acute ischemia.
Revascularization or arterial bypass is the 1st-line intervention used in acute limb
ischemia treatment
• Vascular surgical procedures are divided into 2 groups: inflow procedures (improve blood
supply from the aorta into the femoral artery) & outflow procedures (provide blood supply
to vessels below the femoral artery)
• When diffuse disease is present, an inflow procedure is performed 1st. The restoration of
arterial flow may be sufficient after this procedure, so that other procedures may not be
needed
• For some pts who are at high risk or in a life-threatening situation, a primary amputation
may be the best choice
• Bypass grafts are performed to reroute blood flow around the stenosis or occlusion; Grafts
below the knee require the use of native vein (autologous; the pt's own vein) to ensure
patency. However, synthetic grafts may be used for bypass procedures on larger vessels
above the knee
• Several synthetic materials are available for use as a peripheral bypass graft;
Cryopreserved saphenous veins & umbilical veins are also available, but usually don't last
as long as native veins or synthetic graft
 • Graft patency is determined by size of the graft, graft type, & location. Great care is
taken to prevent graft infection as the graft must be removed if infected
• Vein grafts may be reversed before creating the graft conduit to prevent the valves from
causing an occlusion, or they are left in place (in situ) & the valves are removed w/ a
special instrument (valvulotome)
• Doppler evaluation of the graft & the proximal vessels beyond the graft is usually
performed for postprocedure vascular pt. Pt may have arterial studies, ABI (ankle-brachial
index), & arterial wave form analysis performed in the vascular lab after arterial
reconstructive procedures & prior to discharge; Disappearance of a pulse or a Doppler
signal that was previously present may indicate an occluded graft

- Endovascular intervention:
• Several percutaneous interventional techniques are available to remove plaque & dilate
vessels
• Angioplasty (percutaneous transluminal balloon angioplasty (PTA)), may be performed w/ or
w/o a stent. Balloons are inserted into the vessels via a catheter & expanded at the
stenotic site within the vessel. The expanding balloon cracks the atherosclerotic plaque &
opens the vascular lumen. Stents may be inserted to support the vessel wall & maintain
patency. Performed in an outpatient setting
• Complications from PTA: hematoma, embolization, dissection of the vessel, bleeding, intimal
damage (dissection), & stent migration
• The advantage of angioplasty, stents, & stent-grafts compared to open surgical procedures
is the decreased length of hospital stay required for the treatment & less physical trauma
to the pt than open surgical procedures

Question
❖ A pt report experiencing pain in the left lower leg and foot when walking. This pain is relieved
with rest. The nurse should suspect that this pt has which of the following?
A. Coronary artery disease
B. Intermitten claudication
C. Arterial embolus
D. Raynaud’s disease

Nursing management
❖ Providing postoperative care:
- In postop period, nurse collaborates w/ the surgeon about the pt's appropriate activity lvl
based on the pt's condition
- Encourage pts to move the extremity & be active
- The primary objective in the postprocedure period is to maintain adequate circulation;
Anticoagulant therapy may be continued after surgery to prevent thrombosis of the graft
- Metabolic abnormalities, renal failure, & compartment syndrome (increasing pressure in a muscle
compartment causing impaired nerve & blood vessel function) are potential complications after
arterial occlusions or operations
- Nurse assesses for evidence of local complications (i.e. hemorrhage or thrombosis) by
performing neurovascular checks of the limb & systemic complications. Monitor vitals, intake &
output, physical assessment parameters (e.g. pulmonary, cardiac, PV, GI, mental status), & lab
data (check cholesterol level)
- Teach the pt not to cross their legs
- Any evidence of deterioration is reported to surgical team immediately (cool, dusky, weakened
pulses, delayed capillary refill, decreased sensory/motor function)

❖ Providing pain relief:

- Narcotics are need to manage rest pain until circulation can be restored
- Pt may need to take large doses of narcotics preop and may need more pain med than expected to
relieve symptoms

❖ Maintaining tissue integrity

- Poorly perfused tissues are susceptible to damage & infection. When lesions develop, healing
may be delayed or inhibited b/c of the poor blood supply to the area. Infected, nonhealing
ulcerations of extremities can be debilitating & may require prolonged & often expensive tx
- Pt are taught to avoid trauma; wear sturdy, well-fitting shoes/ slippers; & use neutral soaps &
body lotions
- Pt who have an open arterial or venous ulcer are given detailed wound care instructions
- Risk factor modification is the most effective intervention for preventing progression of
vascular disease.
 - Pt & their families are educated on environmental & behavioral risk factors associated w/
ischemia (Ex: excess heat may increase metabolic rate of the extremities & increase the need
for oxygen beyond that provided by the reduced arterial flow through the diseased artery.
- Cold temp is associated w/ vasoconstriction, decreasing perfusion to extremities. Nicotine from
tobacco products causes vasospasm & reduce circulation to extremities. Tobacco smoke impairs
transport & cellular use of O2 & increases blood viscosity)
- Pts w/ arterial insufficiency who use tobacco must be fully informed of the effects of nicotine
on circulation & encouraged to stop using tobacco. Secondhand smoke is also harmful to the
vascular system
- Emotional upsets cause vasoconstriction by stimulating the SNS, minimizing to some degree by
avoiding stressful situations or by following a stress-management program. Counseling services
or relaxation training may be indicated for people who can't cope effectively w/ situational
stressors
- Constrictive clothing & accessories are avoided, as are heating pads & hot water bottles; The
temp of bath water should also be evaluated, & the water temp in the home decreased to prevent
scalding. Tight socks, panty girdles, belts, & shoe laces impede arterial circulation to the
extremities & promote venous congestion & edema. Finally, crossing of the legs is avoided to
prevent vessel compression
- Elevation of lower extremities is associated w/ decreased flow, which lessens perfusion &
increases pain--dependent position improves flow & decreases pain
- Nursing alert: Lower extremity elevation is associated w/decreased arterial flow, lessens
perfusion to tissue and increase pain. A dependent position improves flow and decrease pain

Upper extremity arterial occlusive disease

❖ Arterial occasions form atherosclerosis occur less frequently in the upper extremities than in legs
❖ Not as common as lower extremity, a form of PAD

❖ Pathophysiology:
- Cause by vasospasm, trauma, or arterial constrictive disorders than by atherosclerosis
- Stenosis may occur at the origin of the subclavian artery proximal to the vertebral artery
- Arterial blood flows to the brain via the carotid & vertebral arteries. If there is diminished
flow to the arm from the subclavian artery due to the stenosis, there will be preferential
reverse flow down the vertebral artery to the arm when the arm is being used. This is called
subclavian steal syndrome as the arm is "stealing" blood from the brain

❖ Clinical manifestation and assessment:

- Complain of arm fatigue and pain when using the arm to paint, comb hair, driving
- Report dizziness, vertigo, ataxia, syncope, bilateral visual changes when use the arm
- Coolness and pallor of the affected extremity, decreased cap refill, decreased amplitude &
delay in radial artery pulse on the affected side, and a difference in arm BP of more than 20
mmHg

❖ Medical and nursing management:

- Surgical bypass or a percutaneous transluminal balloon angioplasty may be indicate
- If the stenosis involves the subclavian artery w/ siphoning of blood from the intracranial
circulation, a carotid-to-subclavian artery bypass or reimplantation of the subclavian to the
carotid artery may be performed

Raynaud disease and Raynaud phenomenon

❖ Refers to vasospasm occur w/cold or stress. Pt w/scleroderma or systemic lupus erythemotosus may
have the same S/S. Secondary Raynaud phenomenon

❖ Pathophysiology:
- Raynaud's disease is of unknown etiology; While its exact cause is unknown, it may be
associated w/ immunologic disorders
- Emotional factors or cold may trigger episodes
- Occurs in women b/w 16 & 40 yrs, & occurs more frequently in cold climates & during the winter
- Cause skin & muscle atrophy
- Prognosis varies; pts may slowly improve, become progressively worse, or show no change

❖ Clinical manifesto and assessment:

- Cyanotic due to vasospasm
- Vasodilation causes redness (rubor)
- Numbness, tingling and burning pain

❖ Medical and nursing management:

 - W/ appropriate pt teaching & lifestyle modifications, the disorder is generally benign & self-
limiting
- Pt is instructed to avoid the stimuli (e.g. cold, tobacco) that provokes vasoconstriction.
Encourage to dress warmly, wear gloves and mittens, protect the trunk, head, & feet with warm
clothing to prevent cold-induced reflex vasoconstriction. Tobacco use is contraindicated
- May be prescribed calcium channel blockers to relieve symptoms
- Sympathectomy (interrupting the sympathetic nerves) may help some pts

Aneurysm
❖ What is an aneurysm?
- An aneurysm is a localized out-pouching, sac, or dilation formed at a weak point in the artery
wall 
- Classified by its shape or form--The most common forms of aneurysms are saccular & fusiform
- Saccular aneurysms project from one side of the vessel only; If an entire arterial segment
becomes dilated, a fusiform aneurysm develop
- Very small aneurysms due to localized infection are called mycotic aneurysm
- Aortic aneurysms occur in the abdominal & thoracic aorta & are characterized by disruption &
loss of elastic fibers, resulting in degeneration of the medial vessel wall-- It is thought to
be an inflammatory process

❖ Common types: Abdominal aortic aneurysm, thoracic aortic aneurysm, peripheral aneurysm, dissecting
aneurysm

Abdominal aortic aneurysm: (most common one)

❖ The cause of abdominal aortic aneurysm (AAA), the most common type of degenerative aneurysm, has
been attributed to atherosclerotic changes in the aorta
❖ Linked to genetic, environmental, hemodynamic, & immunologic factors, w/atherosclerosis
contributing to the process
❖ Most AAA are asymptomatic & are found on routine exams or during a workup for another condition
❖ Aneurysms are serious b/c they can rupture, leading to hemorrhage & death-- If the AAA ruptures,
mortality rates as high as 80% are seen

❖ Pathophysiology:
- All aneurysms involve a damaged media layer of the vessel; This may be caused by congenital
weakness, trauma, or disease
- The degradation of the medial elastin fibers & collagen (which gives the vessel strength) leads
to weakening & dilation of the aorta & the development of aneurysm
- After an aneurysm develops, it tends to enlarge, growing at a rate of 0.4 cm per year on avg;
however, there is no predictable pattern

❖ Risk factor:
- Age (over 50 years old), male sex
- Tobacco use, family history, genetic
- Occlusive atherosclerotic disease and HTN
- High blood pressure, elderly

❖ Clinical manifestation and assessment:

- Complain that heart beat in the abdomen when lying down, or feel an abdominal mass or abdominal
throbbing
- Small cholesterol, platelet, or fibrin emboli may lodge in digital arteries, causing cyanosis,
and mottling of the toes
- Severe back or abdominal pain (persistent or intermittent). Abdominal pain is localized in the
middle or lower abdomen to the left of the midline
- Low back pain may be present b/c of pressure of the aneurysm on the lumbar nerves, indicating
the aneurysm is expanding rapidly and is about to rupture
- Indications of a rupturing AAA: constant, intense back pain, falling BP, decreasing hematocrit.
Rupture into the peritoneal cavity is rapidly fatal, surgical repair is the only change for
survival
- A retroperitoneal rupture of an aneurysm may result in hematomas in scrotum, perineum, flank,
or penis
- The most important diagnostic indication of an abdominal aortic aneurysm is a pulsatile mass in
the abdomen. These aneurysms can be palpated if the pt is not obese. A systolic bruit may be
heard over the mass
- Duplex ultrasonography or computed tomography (CT) is used to determine the size, length, &
location of the aneurysm
 ❖ Medical management:
- Pharmacologic therapy:
• Antihypertensive agents (i.e. diuretics, beta blockers, angiotensin-converting enzyme (ACE)
inhibitors, angiotensin II receptor antagonists, calcium-channel blockers, may be
prescribed to maintain the pt’s BP within acceptable limits

- Surgical management:
• Surgery is the tx of choice for AAAs more than 5.5 cm wide or those that are enlarging
• An alternative for treating an infrarenal (below the renal arteries) AAA is endovascular
grafting, which involves percutaneous transluminal placement & attachment of an aortic
graft prosthesis across the aneurysm. Performed under local or regional anesthesia
• Complications are similar to other endograft procedures; It is important to consider that
the overall surgical mortality rate associated w/ a ruptured aneurysm is 50%- 75%,
therefore early intervention is warranted

❖ manage blood pressure, monitor BP,

Venous disorders
❖ Venous blood flow is reduced by a thrombus or embolus obstructing a vein, by incompetent venous
valves, or by a reduction of the pumping action effectiveness of surrounding muscles
❖ Decreased venous blood flow causes increased venous pressure, increasing capillary hydrostatic
pressure, vacillating filtration of fluid out of the capillaries into the interstitial space, with
resultant development of tissue edema
❖ Edematous tissue doesn’t receive adequate nutrition from the blood and is more susceptible to
breakdown, injury, and infection. Thus, the nurse is aware that edematous tissue is fragile tissue.

Venous thrombosis (DVT)

❖ Virchow triad:
1. Stasis of blood: Caused by immobility (bed rest, long plane/car/train rides, obesity,
constrictive devices, paralysis, paresis, recent surgery, varicose veins, pregnancy)
2. Vessel wall injury: Caused by trauma (fractures, contusions), central venous catheterization,
vascular devices (PICC, central line, pacemaker wires), IV meds, cancer therapy (hormonal,
chemotherapy, radiotherapy)
3. Altered coagulation: Caused by estrogen-containing oral contraception or hormone replacement,
cancer (secretes procoagulants), smoking, dehydration, hypercoagulable states, late
pregnancy, and postpartum period)

❖ Pathophysiology:
- The terms venous thrombosis, deep vein thrombosis, thrombophlebitis, & phlebothrombosis do not
necessarily reflect identical disease processes, but they are grouped together for clinical
purposes
- Cause of venous thrombosis remains unclear. 3 factors, known as Virchow's triad are believed to
play a significant roe in the development of venous thrombosis
- Upper extremity venous thrombosis is not as common as lower extremity thrombosis. However, it
may occur in pts w/ IV catheters (IV lines or wires from pacemaker leads, chemotherapy ports,
dialysis catheters, or parenteral nutrition lines) or in pts w/ an underlying hyper coagulation
disorder. Effort thrombosis is caused by repetitive motion (as in competitive swimmers, tennis
players, & construction workers) that irritates the vessel wall, causing inflammation &
subsequent thrombosis
- Venous thrombi are aggregates of platelets attached to the vein wall that have a tail-like
appendage containing fibrin, WBCs, & many RBCs. The thrombus can propagate as successive layers
of thrombus form; A propagating venous thrombosis is dangerous b/c it is often the source of a
pulmonary embolism (PE). Thrombus fragmentation can occur spontaneously or in association w/ an
elevated venous pressure, as when a person stands suddenly or engages in muscular activity
after prolonged inactivity
- After an episode of acute DVT, recanalization of the lumen of the vessel occurs; However, the
venous valves remain open & are ineffective; Reverse venous flow contributes to chronic venous
insufficiency. Over time, postphlebitic syndrome occurs, manifested by skin & tissue changes

❖ Clinical manifestations and assessment:

- S/S are nonspecific. The exception is phlegmasia cerulea dolens (masive iliofemoral venous
thrombosis), in which the entire extremity becomes swollen, tense, painful, w/arterial ischemia
(bluish color) and potential loss of distal pulse
- Deep venous obstruction is associated w/ edema of extremity due to inhibition of venous
outflow. Swelling can be measured by obtaining circumference of affected extremity at specific
 lvl & comparing 1 extremity w/ the other at the same lvl;The affected extremity may feel warmer
that the unaffected extremity
- Tenderness is produced by inflammation of vein wall. Homans signs ( pain in the calf after the
foot is sharply dorsiflexed) is a sign of DVT. S/S of pulmonary embolism are 1st indication of
DVT
- Superficial vein thrombosis produces pain or tenderness, redness, & warmth in the involved
area. Many of them dissolve spontaneously. This condition may be treated at home w/ bed rest,
limb elevation, analgesics, & anti-inflammatory meds; Should be noted that while NSAIDs provide
analgesia, they may obscure clinical evidence of thrombus propagation
- Careful assessment is key in detecting early signs of lower extremity venous disorders-- Pts w/
a hx of varicose veins, hypercoagulation, neoplastic disease, CV disease, recent major surgery
or injury; those who are obese, immobile, or elderly; & women taking oral contraceptives are at
high risk
- Differences in leg circumference bilaterally from thigh to ankle; increases in surface temp of
leg, particularly in calf or ankle; & areas of tenderness or superficial thrombosis should be
noted; Asymmetry of extremities (calf swelling at least 3 cm larger than asymptomatic leg,
measured 10 cm below the tibial tuberosity), should alert nurse to a potential DVT; In
addition, nurse should assess for presence of a low-grade fever
- The D-dimer blood assay is a marker of coagulation activity; When a clot lyses, fibrin
degradation occurs & a D-dimer is positive; When positive, it is associated w/ clot breakdown,
such as the presence of DVT or PE, but it is also associated w/ a variety of nonthrombotic
disorders including recent surgery, hemorrhage, trauma, cancer, MI, pneumonia, & sepsis-- Thus,
D-dimers are frequently elevated due to some systemic illness; however, a negative D-dimer
decreases likelihood of a DVT or PE

❖ Prevention:
- Prevention measures should be instituted for pts at risk for DVT
- These might include physical interventions such as elastic compression stockings, intermittent
pneumatic compression devices, & body positioning & exercise
- Meds to prevent thrombosis include anticoagulant therapy, such as subQ unfractioned or low-
molecular-weight heparin

❖ Medical management:
- Pharmacologic therapy
• Heparin:
Anticoagulant therapy is effective prophylaxis, they don’t dissolve a thrombus that has
already formed

• Unfractionated heparin:
Administered subcuq to prevent development of DVT. Common practice is administer
heparin via an IV drip to prevent the extension of a thrombus & immediate anticoagulant
effect
Unfractionated heparin is administered via infusion pump tp carefully control the rate.
Dosage is based on the pt’s wt and possible bleeding tendencies are detected by a
pretreatment clotting profile
If renal insufficiency exists, lower doses of heparin are required. Periodic
coagulation test and hematocrit
• Low-molecular-weight heparin
• Direct thrombin inhibitor
❖ Nursing management

Varicose veins
❖ Risk factors
❖ Prevention
❖ Surgical treatments

Vascular ulcers
❖ Ulcer types
❖ Treatment
❖ Wound care

Lymphatic disorders
❖ Lymphangitis
❖ Lymphedema
 Gastrointestinal, hepatic, and biliary disorders
The GI system perform the fxn of ingestion, digestion, & elimination. Its major organs include
esophagus, stomach, small intestine, large intestine, pancreas, gallbladder, spleen, and liver (most
complex organ)

Basic information:
❖ Anatomic & physiologic overview of digestive system:
- GI tract extends from mouth to esophagus, stomach, small intestine, large intestine, rectum,
terminal structure, and anus
- The esophagus is located in the mediastinum, antiriot to the spine, and posterior to trachea &
heart. This hollow muscular tube, passes through the diaphragm at an opening called
diaphragmatic hiatus
- The stomach is situated in left upper portion of abdomen under left lobe of the diaphragm. It
stores food during eating, secrete digestive fluids, and propels digested food into the small
intestine
- The small intestine is longest segment of GI tract, its purpose is secretion and absorption,
the process by which nutrients enter bloodstream through intestinal walls. Consist of duodenum,
jejunum, and ileum
- The large intestine consist of ascending segment, transverse segment, descending segment,
sigmoid colon, rectum, anus
- The GI tract revives blood from arteries that originate along the entree length of thoracic and
abdominal aorta and veins that return blood from digestive organs and the spleen
- O2 and nutrients are supplied to the stomach by gastric artery & to the intestine by the
mesenteric arteries
- Structures lie behind parietal peritoneum are said to be retroperitoneal. SAD PUCKER stands for
suprarenal (adrenal) gland, aorta, duodenum, pancreas, ureters, colon, kidneys, esophagus,
rectum
- A mesentery is a double layer of peritoneum that encircles internal organs (i.e. the intestines
and contains blood vessels, nerves, and lymphatic vessel. An omentum is a fold of mesentery the
poses from the stomach to organs in the abdominal activity
- Both sympathetic and parasympathetic portions of autonomic nervous system innervate GI tract.
• Sympathetic nerves exert an inhibitory effect on GI tract, decreasing gastric secretion and
motility and causing the sphincters and blood vessels to constrict
• Parasympathetic nerve stimulation causes peristalsis & increase secretory activities
• The sphincters relax under the influence of parasympathetic stimulation except for the
sphincter of the upper esophagus and the external anal sphincter, which are under voluntary
control

❖ Digestive functions:
- All cells of body require nutrients. These nutrients are derived from diet and need the GI
system for digestion, absorption via blood or lymphatic channels, & elimination
- Primary fxn of GI tract are the following:
• The breakdown of food particles into the molecular form for digestion
• The absorption into bloodstream of small nutrient molecules produced by digestion
• The elimination of undigested unabsorbed foodstuffs and other waste products
- After food is ingested, it propelled through GI tract, coming into contact w/a wide variety of
secretions that aid in its digestion, absorption, or elimination

- Chewing and swallowing:

• The process of digestion begins w/the act of chewing, in which food is broken down into
small particles that can be swallowed and mixed w/digestive enzymes
• Swallowing begins as a voluntary act that is regulated by the swallowing center in the
medulla oblongata of the CNS.
• The act of swallowing requires the innervations of five CNs, (CNV, VII, IX, X, XII).
Diseases that disrupt the brain centers or CNs predispose the pt to aspiration
• Swallowing, propels the bolus of food into the upper esophagus, ends as a reflex action.
The smooth muscle in the wall of esophagus contracts in a rhythmic sequence from the upper
esophagus toward the stomach to propel the bolus of food along the tract
• During this process of esophageal peristalsis, the lower esophageal sphincter relaxes and
permits the bolus of food to enter the stomach. The lower esophageal sphincter closes
tightly, preventing reflux of stomach content into the esophagus

- Gastric function:
 • The stomach stores and mixes food with secretions, secrets a highly acidic fluid in
response to the presence or anticipated ingestion of food. This fluid, which can total
2.4L/day, can have a pH as low as 1 and derives it acidity from HCL secreted by glands of
the stomach
• The suction of the gastric secretion is twofold: to break down food into more absorbable
components and to aid in the destruction of most ingested bacteria
• Pepsin, an important enzyme for protein digestion, is the end product of the conversion of
pepsinogen from chief cell
• Intrinsic factor, secreted by gastric mucosa, combine with dietary vit B12 so that the
vitamin can be absorbed in the ileum. In the absence of intrinsic factor, vit B12 cannot be
absorbed and pernicious anemia results
• Peristaltic contractions in the stomach propel the stomach’s contents toward the pylorus.
B/c large food particles cannot pass through pyloric sphincter, they are churned back into
the body of the stomach.
• Peristalsis in the stomach and contractions of the pyloric sphincter allow the digested
food to enter the small intestine at a rate that permits efficient absorption of nutrients.
This partially digested food mixed with gastric secretion is called chyme

❖ GI system physiology
❖ Liver and biliary system

GI and liver:
❖ Assessments
❖ Common signs and symptoms
❖ Diagnostic and imaging tests

Temporomandibular joint disorders

❖ Signs and symptoms
❖ Medical management
❖ Nursing management

Oral and pharyngeal cancer

❖ Prevalence
❖ Risk factors
❖ Management
❖ Surgery- neck dissection

Esophageal disorders
❖ Achalasia
❖ Diverticulum
❖ Foreign bodies
❖ Hiatal hernia
❖ Perforation
❖ Barrett’s esophagus

Gastroesophageal reflux disease

❖ Causes
❖ Signs and symptoms
❖ Treatment

Esophageal cancer
❖ Risk factors
❖ Treatments
❖ Nursing priorities post surgery

Gastrointestinal intubation
❖ Indications
❖ Tube types
❖ Nursing management
❖ Administering tube feeds
❖ Parental nutrition

Question
❖ Which of the following methods is the most accurate indication of correct GI tube placement?
A. Instillation of air with simultaneous abdominal auscultation
B. Abdominal X-ray
C. Aspiration of gastric contents
D. Gentle traction on the tube
Chapter 23: Nursing management- Patients with gastric and duodenal disorders
Gastritis
❖ Definition: Inflammation of the gastric or stomach mucosa. May be acute (lasting several hrs to a
few days) or chronic (resulting from repeated exposure to irritating agents or recurring episodes
of acute gastritis)
❖ Stress cause the disorder
❖ Nursing independent lab test: occult test
❖ Black tarry stool

❖ Types:
- Acute gastritis:
• Caused by dietary indiscretion. Eating food that is irritating, too highly seasoned, or
contaminated w/ disease causing organisms. 
• Other causes of AG is overuse of aspirin and other NSAIDs, excessive alcohol intake, bile
reflux and radiation therapy. 
• A more severe form of AG is caused by the ingestion of strong acid or alkali. which may
cause the mucosa to become gangrenous or to perforate. Scarring can occur, resulting in
pyloric stenosis or obstruction. 
• May develop in acute illnesses, esp. when the pt has had major traumatic injuries, burns,
severe infection, liver, kidney, or respiratory failure, or major surgery

- Chronic gastritis:
• Chronic gastritis and prolonged inflammation of the stomach may be caused either by benign
or malignant ulcers of the stomach or by bacteria Helicobacter pylori
• Sometimes associated with autoimmune diseases (i.e. pernicious anemia; dietary factors such
as caffeine; the use of meds such as NSAIDs, bisphophonate, risedronate, or ibandronate;
alcohol; smoking; or chronic reflux of pancreatic secretions and bile into the stomach

❖ Pathophysiology:
- The gastric mucous membrane becomes edematous and hyperemic (congested w/ fluid and blood) and
undergoes superficial erosion.
- It secretes scanty amount of gastric juice containing very little acid but much
mucus. Superficial ulceration may occur and can lead to hemorrhage.

❖ Signs and symptoms:

- Acute gastritis: may have a rapid onset of s/s, such as abd discomfort, headache, lassitude,
and N/V, anorexia and hiccuping.
- Chronic gastritis: may complain of anorexia, heartburn after eating, belching, burping, a sour
taste in the mouth or N/V. Pt w/chronic gastritis from vit B12 caused by the production of
antibodies that interfere with the binding of vit B12 to intrinsic factor
- Gastritis is sometimes associated w/ achlorhydria or hypochlorhydria (absence or low levels of
HCl) or w/ hyperchlorhydria (high levels of HCl).
- Diagnosis can be determined by an upper GI x-ray series or endoscopy and histologic exam of a
tissue specimen obtained by biopsy.

❖ Medical and nursing management (treatment):

- Gastric mucosa is capable of repairing itself after about of gastritis (about 1 day) but
diminished appetite for 2-3 days.
- Instruct pt to refrain from alcohol and food until symptoms subside. 
- If ingestion of strong acids or alkalis, emergency tx consists of diluting and neutralizing the
offending agent. 
- Therapy is supportive and may include nasogastric intubation, analgesic agents and sedatives,
antacids and IV fluids. 
- Chronic gastritis is managed by modifying the pts diet, promoting rest, reducing stress,
recommending avoiding alcohol and NSAIDs, and initiating pharmacotherapy to tx H. pylori.
- Diet modification: limit alcohol, smoking, caffeine; fatty or spicy food limit; adequate rest;
reduce stress
- Medication: antibiotic, pepcid, axid, PPI (pantoprazole)

Peptic ulcer disease

❖ Definition: Referred to gastric, duodenal, or esophageal ulcer, depending on its location.
- Peptic ulcer is an excavation (hollowed out area) that forms in the mucosal wall of the
stomach. , in the pylorus, in the duodenum or in the esophagus. 
- Erosion of a circumscribed area of mucous membrane is the cause.
 - Esophageal ulcers occur as a result of the backward flow of HCl from the stomach into the
esophagus.

❖ Pathophysiology:
- Peptic ulcer occur in the gastroduodenal mucosa b/c this tissue cannot withstand the digestive
action of gastric acid and pepsin. Caused by the increased conc. or activity of acid-pepsin or
by decrease resistance of mucosa
- Pt w/duodenal ulcer disease secrete more acid than normal, whereas pt with gastric ulcer tend
to secrete normal or decreased levels of acid. Damage to the gastroduodenal mucosa allows for
decreased resistance to bacteria and infection form H.pylori bacteria may occur
- The use of NSAIDs inhibits the secretion of mucus that protects mucosa. 
- Zollinger-Ellison syndrome (ZES) is suspected when a pt has several peptic ulcers or an ulcer
that is resistant to standard medical therapy
• ZES is identified by the hypersecretion of gastric juice, duodenal ulcers, and gastrinomas
in the pancreas
• Diarrhea and steotorrhea (unabsorbed fat in the stool) may be evident
• May have coexisting parathyroid adenomas (benign tumor of glandular origin) or hyperplasia,
may exhibits signs of hypercalcemia. Most common symptom is epigastric pain
- Stress-related mucosal disease (SRMD): the phenomenon of injury to the lining of the stomach
and the duodenum during the conditions of physiologic stress
- Ulceration is preceded by a shock state, involving hypovolemia & hypoperfusion; leading to
decreased gastric mucosal blood flow and gastric ischemia

❖ Causes:
-
❖ Stress-related mucosal disease (SRMD):
- The phenomenon of injury to the lining of the stomach and the duodenum during conditions of
physiologic stress
- Stress erosion, stress ulcer, stress gastritis, erosion gastritis, & hemorrhagic gastritis:
acute mucosal ulceration of the duodenal or gastric area that occurs after physiologically
stressful events (i.e. burn, shock, severe sepsis,
❖ Signs and symptoms
❖ Medical and nursing management

Morbid obesity
❖ Defining characteristics
❖ Conservative management
❖ Surgery
❖ Complications r/t surgery

Gastric cancer
❖ Prevalence
❖ Prognosis
❖ Risk factors
❖ Signs & symptoms
❖ Treatment

Question
❖ A patient has just been diagnosed with gastric cancer and the nurse is taking a history on this
patient. What would be a priority question to ask?
A. What is your smoking and alcohol history?
B. What is your work history?
C. What is your level of fatigue?
D. What is your family history of smoking and alcohol use?

Gastric surgery
❖ Perioperative assessments
❖ Nursing interventions

Duodenal tumors
❖ Incidence
❖ Treatment
Chapter 24: Nursing management- Patients with intestinal and rectal disorders
Intestinal and rectal disorders
❖ Constipation:
- Abnormal frequency or irregularity of defecation, abnormal hardening of stools that makes their
passage difficult and sometimes painful, a decrease in actual stool volume, or retention of
stool in the rectum for a prolonged period
- More common in people 60 yrs and older. 
- Most common complaint is the need to strain in order to pass stool (hard stool)
- Chronic laxative use may contribute to this problem and is a major health concern in the U.S

- Pathophysiology:
• Interference with one of three major functions of the colon:
mucosal transport (mucosal secretions facilitate the movement of colon contents)
myoelectric activity (mixing of the rectal mass and propulsive actions)
process of defecation
• The urge to defecate is stimulated normally by rectal distention, which initiates a series
of four actions: (interference w/any these processes can lead to constipation)
stimulation of the inhibitory rectoanal reflex
relaxation of the internal sphincter muscle
relaxation of the external sphincter muscle and muscles in the pelvic region
increased intra-abdominal pressure
• Atony or decreased muscle tone occurs with aging, leading to constipation b/c the stool is
retained for longer periods

- Risk factors:
• certain medications (i.e. opioids, tranquilizers, anticholinergic, antidepressants,
antihypertensive, etc.)
• rectal or anal disorders (i.e. hemorrhoids, fissures)
• obstruction (i.e bowel tumors)
• metabolic, neurologic, neuromuscular conditions (i.e. Hirschsprung disease, Parkison
disease, multiple sclerosis)
• lead poisoning
• endocrine disorders (i.e.diabetes mellitus, hypothyroidism)
• can occur w/ any acute disease process in the abdomen (appendicitis or cholecystitis)
• abdominal surgery (i.e. appendicitis or cholecystitis)
• prolonged bedrest, decrease food intake, reduced mobility, weak abdominal and pelvic
muscles and multiple chronic illness requiring meds
• depression, weakness
• IBS and diverticular disease are associated with constipation

- Clinical manifestations and assessment:

• fewer than 3 bowel movements per week
• abdominal distention
• pain and pressure
• decreased appetite
• headache
• fatigue
• indigestion
• straining at stool
• small lumpy dry hard stools
• The nurse elicit info about the onset and duration of constipation, current and past
elimination patterns, the pt’s expectation of normal bowel elimination, and lifestyle info
during health history interview. Medical & surgical hx, current meds, and laxative and
enema use are important, as is info about the sensation of rectal pressure or fullness, abd
pain, excessive straining at defecation and flatulence

- Medical and nursing management:

• Tx is aimed at the underlying cause of constipation and includes education, bowel habit
training, increased fiber and fluid intake and judicious use of laxatives. 
• Discontinue laxative abuse
• Routine exercise to strengthen abd muscles is encouraged
• Daily dietary intake of 6 to 12 tsp of unprocessed bran is recommended
• If laxative use is necessary, one of the following may be prescribed: bulk-forming agensts,
saline and osmotic agents, lubricants, stimulants, for fecal softeners
 • Enemas and rectal suppositories are generally not recommended for treating constipation,
should reserved for the tx of impaction
• Patient education should include establishing a bowel routine, provide dietary info, and
reduce pt anxiety
• Goals for the pt include restoring or maintaining a regular pattern of elimination by
responding to the urge to defecate, ensure adequate intake of fluid and hog-fiber foods,
learning methods to avoid constipation, relieve anxiety about bowel elimination patterns
and avoiding complications

- Complications:
• HTN
• fecal impaction
• hemorrhoids (dilated portions of anal veins)
• fissures (tissue folds)
• Megacolon (abnormal enlargement of the colon)
• increased arterial pressure can occur with defecation
• Straining at stool, which results in Valsalva Maneuver (i.e. forcibly exhaling with the
glottis closed) which has a striking effect on arterial blood pressure.
• CO decreased and a transient drop in arterial pressure
• Rebound phenomenon
• Fecal impaction occurs when accumulated mass of dry feces cannot be expelled. The mass may
be palpable on digital examination, may produce pressure on the colonic mucosa that results
in ulcer formation, and causes seepage of liquid stools
• Megacolon is caused by a fecal mass that obstructs the passage of colon contents. Sx
include: constipation liquid fecal incontinence, and abd distention. Can lead to
perforation of the bowel

❖ Diarrhea:
- increased frequency of bowel moments of more than 3 per day, an increased amount of stool (>200
g/day) or abnormally liquid stool or abnormal liquid stool
- associated with increased urgency, perianal discomfort, and incontinence
- lasting less than 2 weeks is considered acute (most often associated w/ infection and self-
limiting)
- lasting more than 4 weeks is considered chronic which persists for a longer period and may
return sporadically.
- Any conditions cause increase inessential secretions, decreased mucosal absorption, or altered
motility can produce diarrhea
- IBS, inflammatory bowel disease, and lactose intolerance are frequently the underlying disease
processes that cause diarrhea

- Pathophysiology:
• Secretory diarrhea: high volume diarrhea and is caused by increased production and
secretion of water and electrolytes by the intestinal mucosa into the intestinal lume
• Osmotic diarrhea: occurs when water is pulled into the intestines by the osmotic pressure
of unabsorbed particles, slowing the reabsorption of water.
• Mixed diarrhea: caused by increased peristalsis (usually from inflammatory bowel disease)
and a combination of increased secretion and decreased absorption in the bowel.

- Risk factors:
• certain meds (i.e. thyroid hormone replacements, stool softeners and laxatives, antibiotic,
chemotherapy, etc.)
• certain tube feeding formulas
• metabolic and endocrine disorders (i.e. diabetes, Addison disease, thyrotoxicosis)
• viral and bacterial infectious processes
• nutritional and malabsorptive disorders and sphincter defect, intestinal obstruction,
paralysis ileum, AIDS

- Clinical manifestation and assessment:

• abdominal cramps
• distention
• intestinal rumbling (borborygmus)
• anorexia
• thirst
• painful spasmodic contractions of the anus and ineffective straining (tenesmus)
• watery stools with small bowel
 • semisolid stools are associated more often w/ disorders of the large bowel. 
• nocturnal diarrhea may be a manifestation of diabetic neuropathy
• The following diagnostic tests: CBC, serum chemistries, urinalysis, routine stool
examination, stool examination for infectious or parasitic organisms, bacterial toxins,
blood, fat, and electrolytes
• Endoscopy or barium enema may assist in identifying the cause
• **elderly pts can become dehydrated quickly and develop low potassium levels.

- Medical and nursing assessment:

• primary management is directed at controlling symptoms, preventing complications and
eliminating or treating the underlying disease. 
• medications, antibiotic = and anti-inflammatory agents may be used to reduce the severity
of the diarrhea and treat the underlying disease.
• the nurse’s role include assess and monitor the characteristics and pattern of diarrhea. A
health history should address the pt’s medication therapy, medical & surgical hx, and
dietary patterns & intakes
• reports of recent exposure to acute illness or recent travel to another geographic area are
important as tx can chance depending on the pt’s illness and travel hx
• vital signs are assessed for fever and fluid volume deficit
• inspection of the mucous membrane and skin is important to determine hydration status.
Stool samples are obtained for testing
• encourage bedrest and intake of liquids and foods low in bulk until acute attack subsides. 
• when pt can eat ; bland diet of semisolid and solid foods.
• avoid caffeine, carbonated beverages, and very hot and very cold foods due to stimulation
of intestinal motility
• restrict milk product, fat, whole-grain product, fresh fruits, and vegetable
• antidiarrheal med (i.e. lomotil or imodium) may be administered as prescribed to reduce the
frequency and amt of stools
• IV fluid therapy may be necessary for rapid rehydration in some pt (elderly and pt with
pre-existing GI conditions, IBD)
• Monitor serum electrolyte levels closely as imbalances (i.e. hypokalemia, K+ less than 3.5
mEq/L) and acute metabolic acidosis due to a direct loss of HCO3 (less than 22 mEq/L) can
occur
• The nurse reports evidence of arrhythmias, muscular weakness, fatigue or flaccid paralysis,
and hyporeflexia (associated with a K+ less than 2.5 mEq/L)

❖ Fecal incontinence
- involuntary passage of stool from the rectum. 
- “double incontinence” or difficulties with both urine and stool incontinence
- factors that influences fecal continence include the ability of the rectum to sense and
accommodate stool, the amt and consistency of stool, the integrity of the anal sphincters and
musculature, and rectal motility
- nurse should initiate a bowel training program that involves setting a schedule establish bowel
regularity. Goal is to help pt achieve fecal continence.

- Pathophysiology:
• Continence is maintained by tonic contraction of the muscles around the rectum
• During defection, nerves relax the muscles, causing a straightening of the rectoanal angel
• Distention of the rectum causes relaxation of the sphincter
• Fecal incontinence is a failure of this process and can occur for a variety of reasons

- Risk factors:
• Result from trauma (i.e. after surgical procedures involving the rectum), neurologic
disorder (i.e stroke, MS, diabetic neuropathy, dementia), inflammation, infection,
chemotherapy, radiation tx, fecal impaction, pelvic floor relaxation, laxative abuse, meds,
or older age (i.e. weakness or loss of anal or rectal muscle tone)

- Clinical manifestations and assessments:

• Minor soiling, occasional urgency and loss of control, or complete incontinence
• Poor control of flatus, diarrhea, constipation
• The nurse obtains a thorough health hx
• A visual and digital examination of the rectal area is completed and check for
abnormalities that may be contribution to the incontinence
• A rectal examination and other endoscopic examination are performed to rule out tumors,
inflammation or fissures
 • X-ray studies, barium enemas, CT, anorectal manometry, and transit studied identify
alterations in intestinal mucosa and muscle tone or in detection other structural or
functional problems

- Medical and nursing management:

• frequently fecal incontinence is a sx of a fecal impaction
• biofeedback therapy can be of assistance if the problem is decreased sensory awareness or
sphincter control
• Bowel training programs can be effective
• Surgical procedures (i.e. surgical reconstruction, spinster repair, fecal diversion)
• The nurse initiate a bowel training program involves setting a schedule to establish bowel
regularity

- Complications:
• Problem with perineal skin integrity (maintain skin integrity is a priority)
• The nurse encourages and teaches meticulous skin hygiene, turning the pt every 2 hrs and
apply barrier creams or sprays to protect the skin

❖ Irritable bowel syndrome:

- most common GI condition
- Pt w/IBS have a higher likelihood of other functional GI disorders than those in the general
population

- Pathophysiology:
• results from a functional disorder of intestinal motility
• may be r/t neuroendocrine dysregulation, infection or irritation, or a vascular or
metabolic disturbance.
• peristaltic waves are affected at specific segments of the intestine and in the intensity
with which they propel the fecal matter forward.

- Risk factors:
• stress can contribute to it
• More common in women
• heredity
• a diet high in fat and stimulating or irritating food
• alcohol consumption, smoking
• psychological stress, depression, anxiety
• As many as 90% of ppl diagnosed with IBS present with sx of major depression

- Clinical manifestations and assessment:

• primary sx is an alteration in bowel patterns— constipation, diarrhea, or a combination of
both
• Pain and abdominal distention accompany changes in bowel pattern
• A definite diagnosis of IBS requires tests that confirm the absence of structural or other
disorders
• Stool studies, X-ray studies, proctoscopy may be performed to rule out other colon diseases
• Barium enema and colonoscopy reveal spasm, distention, or mucus accumulation in the
intestine
• Manometry and electromyography are used to study intraluminal pressure changes generated by
spasticity

- Medical and nursing management:

• goal of tx are relieving ab pain, controlling the diarrhea/constipation and reducing
stress. 
• high fiber diet is prescribed to help control the diarrhea and constipation.
• Exercise can reduce anxiety and increase intestinal motility. 
• antidepressants can assist in treating underlying anxiety and depression. 
• fluid should not be taken with meals (causes distention)
• alcohol use and cigarettes should be avoided

❖ Malabsorption:
- inability of the digestive system to absorb one or more of the major vitamins (A, B12),
minerals (Fe, Ca), and nutrients (carbs, fats, proteins)
- interruptions in the complex digestive process may occur anywhere in the digestive system and
cause decreased absorption.
 - Pathophysiology:
• The conditions that cause malabsorption can be grouped into the following categories:
Mucosal (transport) disorders
Infectious diseases
Luminal disorders
Post operative malabsorption
Disorders that cause malabsorption of specific nutrient

- Risk factors:
• Any process that interferes with the body’s ability to absorb nutrient
• Abdominal disease or deformities, surgery, radiation therapy and certain meds that inhibit
bacterial growth within the intestine (antibiotic)
• Bodily fluid losses (i.e. polyuria, emesis, wound drainage, or diarrhea can decrease
absorption)
• Use of meds (i.e. mineral oil or laxatives can decrease

- Clinical manifestation and assessment:

• diarrhea, frequent, loose, bulky, foul-smelling stools that have increased fat content and
are grayish in color
• Abdominal distention, pain, increase flatus, weakness, wt loss, and a decreased sense of
well-being
• malnutrition, wt loss, other signs of vitamin and mineral deficiency
• weak and emaciated b/c of starvation and dehydration
• failure to absorb the fat-soluble vitamin A, D, and K causes a corresponding avitaminosis
(chronic of longterm vitamin deficiency)
• Diagnostic test: stool studies, lactose tolerance test, D-xylose absorption tests, and
Schilling test
• hydrogen breath test is performed to evaluate CHO malabsorption is suspected
• Endoscopy with biopsy of the mucosa is the best diagnostic tool. Biopsy of SI is performed
to assay enzyme activity or to identify infection or destruction of mucosa
• Ultrasound studies, CT scan, and X-ray findings reveal pancreatic or intestinal tumors that
may be the cause
• CBC is used to detect anemia. Pancreatic function test can assist in the diagnosis of
specific disorders

- Medical and nursing management:

• Intervention is aimed at avoid dietary substance that aggravate malabsorption and at
supplementing nutrients that have been lost
• Common supplements are water-soluble vitamin (i.e. B12, folic acid), fat-soluble vitamin
(i.e. A, D, and K) and mineral (Ca, Fe)
• Antidiarrheal agents may be used to decrease intestinal spasms
• Parental fluid may be treat dehydration
• The nurse educate the pt regarding diet and the use of nutrition supplements. It’s
important to monitor pt with diarrhea for fluid & electrolyte imbalance
• The nurse conduct ongoing assessment R/T nutritional deficits have abated

- Complicaitons:
• HTN, hypokalemia, insomnia, euphoria
• prolonged prothrombin time (PT) and internal normalized ration (INR) if the pt is taking
warfarin

❖ Appendicitis:
-small finger like appendage that is attached to the cecum just below the ileocecal valve. 
-appendix fills w/ food and empties regularly into the cecum.
-b/c it empties inefficiently and its lumen is small, the appendix is prone to obstruction and is
particularly vulnerable to infection (appendicitis)
-most common reason for ER abdominal surgery

-Pathophysiology:
• Appendix becomes inflamed and edematous as a result of becoming kinked or occluded by a
fecalith, tumor, or foreign body
• The inflammatory process increases intraluminal pressure, initiating a severe, generalized
or periumbilical pain that becomes localized to the right lower quadrant of the abdomen
within a few hrs
• Eventually, the inflamed appendix fills with pus
 -Risk factors:
• more prevalent in the young
• appear in winter months
• family hx of appendicitis may increase a child’s risk for the illness (esp males and having
cystic fibrosis)

-Clinical manifestation and assessment:

• periumbilical pain progresses to right lower quadrant pain; usually accompanied w/ low
grade fever and N & V
• loss of appetite is common. 
• local tenderness at McBurney's point when pressure is applied
• rebound tenderness may be present 
• Rovsing's sign (may be elected by palpating LLQ, causing pain to be felt in RLQ)
• Constipation can also occur w/ appendicitis. If laxatives are administered it may result in
perforation of the inflamed appendix. 
• A laxative or cathartic should NEVER be given when a person has fever, nausea or pain
• CBC has elevated WBC count (w/ elevation of neutrophils)

-Medical and nursing management:

• Appendectomy is performed as soon as possible to decrease the risk of perforation once
diagnosed w/ appendicitis. 
• Pre op nursing intervention; Iv infusion to replace fluid loss and promote adequate renal
function and abs therapy to prevent infection. 
• If perforation occurs, an abscess may form; initially tx with abs and may drain the abscess
as well. 
• post surgery; place pt in high fowlers position to reduce the tension on the incision and
ab organs helping to reduce pain. 
• morphine sulfate to relieve pain. 
• food is provided as desired and tolerated once normal bowel sounds are present. 
• pt must make appointment to have the surgeon remove the sutures b/w the 5-7 day after
surgery
• Normal activity can usually be resumed within 2-4 wks.

-Complications:
• major complication of appendicitis is perforation of the appendix, which can lead to
peritonitis, abscess formation or portal pylephlebitis (septic thrombosis of the portal
vein caused by vegetative emboli that arise from septic intestines).
• perforation; usually occurs 24 hours after the onset of pain. 
• s/s include; fever (100F or higher), a toxic appearance, and continued abdominal pain or
tenderness.

❖ Diverticular disease:
- sac like herniation of the lining of the bowel that extends through a defect in the muscle
layer. 
- may occur anywhere in the small intestine or colon 
- most commonly in the distal sigmoid colon.

- Pathophysiology:
• form when the mucosa and submucosal layers of the colon herniate thought the muscular wall
b/c of high intralumial pressure, low volume in the colon, and decreased muscle strength in
the colon wall. 
• bowel contents can accumulate in the diverticulum and decompose, causing inflammation and
infection
• Diverticulum can become obstructed and inflamed if the obstruction continues
• Inflammation and subsequent infection of the diverticulum can sued the development of
abscesses, eventually perforate, leading to peritonitis and erosion of the arterial blood
vessels, resulting in bleeding
• Occur as an acute attack or may persist as continuing, smoldering infection
• low intake of dietary fiber is considered a predisposing factor

- Risk factors:
• a congenital predisposition is suspected when the disorder occurs in those younger than 40
years of age

- Clinical manifestation and assessment:

• chronic constipation often precedes the development of diverticulosis
 • s/s mild; bowel irregularity w/ intervals of diarrhea, N, anorexia and ab distention.
• pt reports an acute onset of mild to severe pain in the LLQ, accompanied by fever, N & V,
chills, and leukocytosis. 
• typically diagnosed by colonoscopy

- Gerontologic consideration:
• increase with age b/c of degeneration and structural changes in the circular muscles layers
of the colon and b/c of cellular hypertrophy
• Elderly may not have abd pain until infection occurs
• Delay reporting gsx b/c they fear surgery or are afraid that they may have cancer

- Medical and nursing management:

• can be treated on an outpatient basis with diet and med
• w/ onset of s/s, rest analgesics and antispasmodics are recommended. 
• initial clear liquid diet until inflammation subsides. 
• then high fiber, low-fat diet is recommended
• abx are prescribed for 7-10 days
• hospitalization is often indicated for elderly, immunocompromised or those taking
corticosteroids. 
• NSAIDs are associated w/ increased risk of perforation and should be avoided. Opioids are
prescribed for pain
• stabilization of the pt by drainage of the abscess and resolution of the inflammation is
complete after approx. 6 wks

- Complications:
• peritonitis
• abscess formation 
• bleeding

❖ Peritonitis:
❖
❖ Inflammatory bowel disease (IBD)
❖ Crohn disease
❖ Ulcerative colitis

Medical and nursing management of IBD

❖ Priorities
❖ Interventions
❖ Ielostomy

Colorectal cancer
❖ Incidence
❖ Symptoms
❖ Medical management
❖ Nursing care

Intestinal obstruction
❖ Small bowel
❖ Large bowel

Other rectal disorders

❖ Anal fistulas and fissures
❖ Hemorrhoids
❖ Sexually transmitted anorectal diseases
❖ Pilonidal cysts
Chapter 25: Nursing management- Patients with hepatic and biliary disorders
Hepatic dysfunction
❖ Jaundice:
- Yellowing of the skin & sclerae of eyes are caused by impairment of the liver’s ability to
metabolize & secrete bilirubin (Level of bilirubin exceeded 3 mg/dL indicated jaundice)
- The differential diagnosis of jaundice can result form the following causes:
• Hepatocellular jaundice: caused by viral hepatitis, hepatotoxins (i.e drugs, alcohol),
metabolic disorders, ischemia, autoimmune hepatitis, or pregnancy
• Obstructive jaundice: caused by obstruction of the bile ducts, gallstones, inflammation of
bile ducts caused by primary sclerosing cholangitis, biliary strictures, maglignancies of
the biliary system, pancreatic cancer, liver cancer, and pancreatitis
• Hemolytic jaundice: caused by increased production of bilirubin due to hemolysis,
hematologic disorders, resorption of a hematoma, or multiple transfusions
• Hereditary hyperbilirubinemia: caused by the inherited disorders of bilirubin metabolism,
including various syndromes, some of which require transplantation

❖ Portal hypertension:
- Increased resistance to blood flow through liver and increased blood flow due to vasodilation
in splanchnic circulation.
- Leads to ascites and gastroesophageal varices.

❖ Vitamin deficiencies
❖ Ascites:
- Fluid accumulates in the peritoneal cavity. Increased blood flow in the veins draining the
portal system results in dilation and the development of varicose veins

- Pathophysiology:
• Portal HTN & the resulting increase in capillary pressure and obstruction of venous blood
flow through the damaged liver are contributing factors.
• The failure of the liver to metabolize aldosterone increases Na+ and H2O retention by the
kidney
• Na+ and H2O, increased intravascular fluid volume, increase lymphatic flow, and decreased
synthesis of albumin by the damaged liver all contribute to the movement of fluid from the
vascular system into the peritoneal space
• The prices becomes self-perpetuating as loss of fluid into the peritoneal space cause Na+
and H2O retention by the kidney in an effort to maintain the vascular fluid volume
• As a result of liver damage, large amounts of albumin-rich fluid, 15 L or more, may
accumulate in the peritoneal cavity as ascites

- Clinical manifestations and assessment:

• Abdominal girth, weight gain, and swelling of the lower extremities (pedal edema)
• Dyspnea present as the result of abdominal distention or pleural effusions
• Abdominal hernias due to increased intra-abdominal pressure may be visible as well as
visible collateral veins and striate (stretch marks)
• Early satiety, anorexia, and general weakness
• The detection of ascites by physical examination can be assessed by percussion for shifting
dullness. Bulging flanks may reveal the presence of ascites
• Accurate physical assessment of ascites through examination may be decreased if ascetic
fluid is less than 1,500 mL or if the patient is obese
• Ultrasonography of the liver and abdomen will definitely confirm the presence of ascites is
performed routinely on its presenting with ascites upon hospital admission to detect the
presence of spontaneous bacterial peritonitis. This complication of cirrhosis has a high
mortality rate

- Medical and nursing management:

• Dietary modification:
Dietary restriction of salt intake is the mainstay of tx of ascites to achieve a (-)
Na+ balance to reduce fluid retention
The recommended daily Na+ intake of pt w/ascites should be 2,000 mg or less
Pt on sodium-restricted diets should receive nutritional education and guidance on
foods that contains high sodium content and avoid the used of added salt in meals and
food preparation

• Diuretics:
 The addition of diuretics with sodium restriction will result in decreased ascites in
90% of pt
Combination of drug therapy using spironolactone, an aldosterone-blocking agent, and
furosemide (Lasix), a loop diuretic agent is the most effective regimen to control
ascites and pedal edema
Pt should be monitored for daily weight changes (not to exceed 0.5 kg/day gain or loss
in pt w/o peripheral edema))
Frequent failure to achieve weight reduction and decrease in ascites with the use of
therapeutic doses of diuretic is due to insufficient salt restriction
Possible complications of diuretic therapy: dehydration, volume depletion, electrolyte
abnormalities (i.e hypokalemia, hyperkalemia, hyponatremia, kidney impairment, and
hepatic encephalopathy)
Dietary salt restriction to less than 2,000 mg daily should be reinforced

• Paracentesis:
The removal of fluid from the peritoneal cavity through a puncture or a small surgical
incision through the abdominal wall under sterile conditions
Therapeutic paracentesis provides only temporary removal of fluid, ascites rapidly
recurs, necessitating repeated fluid removal

• Transjugular intrahepatic portosystemic shunt (TIPS):

A method of treating ascites in which a cannula is threaded into the portal vein by the
transjugular route
To reduce portal HTN, an expandable stent is inserted to serve as an intrahepatic shunt
btwn the portal circulation and the hepatic vein
It’s extremely effective in decreasing Na+ retention, improving the renal response to
diuretic therapy, and preventing recurrence of fluid accumulation
TIPS is an effective tx for pt with refractory ascites, it doesn’t increase survival
benefit and it increases hepatic encephalopathy

- Complications:
• Infection develops in the ascitic fluid, from E.Coli (a gram negative bacteria)
• Diagnostic paracentesis should be performed in all pts with cirrhosis and ascetics admitted
to the hospital and in any inpatient w/cirrhosis showing signs of infection or w/
abnormalities in liver or kidney fxn
• The tx of SBP includes: the use of IV antibiotic or oral tx if tolerated. Long-term
prophylaxis with oral antibiotic therapy is recommended to prevent future infection in pt
who have had a diagnosis of SBP

❖ Esophageal varices:
- Present in 50% of pt with cirrhosis and the most life-threatening complication in pt with
chronic liver disease

- Pathophysiology:
• Esophageal varices are dilated, tortuous veins that are found in the submucosa of the lower
esophagus but may develop higher in the esophagus or extend into the stomach
• Increased obstruction of the portal vein, venous blood form the intestinal tract and spleen
seeks an outlet through collateral circulation. The effect is increased pressure ( in the
vessels in the submucosal layer of the lower esophagus and upper part of the stomach)
• Gastroesphageal bleeding is due to high
- Clinical manifestation and assessment:
❖ Hepatic encephalopathy and coma

Viral hepatitis
❖ Hepatitis A
❖ Hepatitis B
❖ Hepatitis C
❖ Other hepatic disorders

Cirrhosis
❖ Nursing assessment
❖ Symptoms
❖ Nursing interventions

Hepatocellular carcinoma
❖ Signs & symptoms
 ❖ Treatments
- Surgery
- Liver transplantation

Gallbladder disorders
❖ Cholelithiasis
❖ Cholecystitis

Pancreatic disorders
❖ Acute pancreatitis:
-
❖ Chronic pancreatitis:
-
❖ Pancreatic cancer