Med Surg Study Guide

Med-Surg.

Final
Study Guide
Med Surg Final

Altered LOC
Head Injuries
Cerebral Vascular Disease
Seizure Disorders
Brain Tumors
Brain Surgery
Diabetes Mellitus
Oxygen Therapy
Pneumonia
Tuberculosis ?
Asthma/COPD (Bronchitis, Emphysema)
Fractures
Hip Fractures
Amputations
Osteoarthritis
Orthopedic Surgery
Cancer
Women’s Health
Osteoporosis
STD’s
PUD
Gastritis
Intestinal Obstruction
Diverticulosis
Diverticulitis
CAD
MI
Angina Pectoris
EKG
Hypertension
PVD
CHF
Systemic Lupus Erythematosus (Not Included)
Rheumatoid Arthritis (Not Included)
Precautions – Contact, Airborn, Droplet (Not included)



Med-Surg Neurological System
Head Injuries
Pathophysiology
Primary injury
Initial damage to the brain from a traumatic event
Contusion – bruising of the brain surface, an injury that doesn’t disrupt the integrity of the skin, caused by a blow
to the body and characterized by swelling, discoloration, and pain.
Laceration – a torn, jagged wound
Torn blood vessels – Aneurism leading to hemorrhage
Acceleration & Deceleration – an increase in the speed or velocity of an object or reaction – Closed blunt brain
injury occurs when the head accelerates and then rapidly decelerates or collides with another object and brain
tissue is damaged but there is no opening through the skull or dura.
Foreign body penetration – Depressed skull fracture with bone fragments embedded in the brain, penetrating
head wounds require surgical debridement to remove foreign bodies and devitalized brain tissue and to control
hemorrhage. IV antibiotic treatment is instituted immediately, particularly for dural lacerations, and blood
component therapy is administered if indicated.

Secondary injury
Hrs and days after the initial injury
Brain swelling (edema), ischemia, and chemical changes associated with direct trauma to the brain
Ongoing bleeding

Increased ICP
It can cause lateral displacement of the brain against the rigid structures of the skull.
Restriction of blood flow to the brain tissue decreasing O2 delivery and waste removal.
Cells within the brain become anoxic and cannot metabolize properly, producing ischemia, infarction, irreversible
brain damage, brain death.

Classifications
Scalp Injury: (Minor head injury)
ABRASION (brush wound)
CONTUSION (bruising of the brain surface, an injury that doesn’t disrupt the integrity of the skin, caused by a
blow to the body and characterized by swelling, discoloration, and pain.
LACERATION (avulsion or tearing away of the scalp)
HEMATOMA UNDER THE SCALP TISSUE –(Subgaleal hematoma - collection of blood)
Skull Fractures: (Break in the continuity of the skull by forceful trauma)
Open (laceration or tear in the dura, ie. Bullet)
Closed (intact dura)
Simple (linear) fracture is a break in the continuity of the bone.
Comminuted refers to a splintered or multiple fracture line
Depressed fracture refers to bone fragments are embedded in the brain tissue
Basilar refers to a fracture at the base of skull resulting in CSF loss at ears, nose, eyes

S&S
Persistent & localized pain: fracture
Fractures of the base of the skull:
Hemorrhage from the nose, pharynx, or ears.
Blood under the conjunctiva
Battle sign (Ecchymosis over the mastoid)
CSF drainage from the ears & nose ( otorrhea, rhinorrhea)
Bloody CSF suggest brain laceration or contusion

Diagnostic tools & Assessment
Ct scan – Computed Tomography uses high-speed xray scanning to detect less apparent abnormalities. It is fast,
accurate, and safe diagnostic procedure that shows the presence, nature, location, and extent of acute lesions.
Cerebral edema, contusion, hematomas, subrachnoid & intraventricular hemorrhage, (infarction) hydrocephalus,
abd.
MRI – Magnetic Resonance Imagery is used to evaluate patients with head injury when a more accurate picture
of anatomic nature of the injury is warranted and when the Pt is stable enough to undergo this longer diagnostic
procedure.
Cerebral angiography – identifies supratentorial, extracerebral, and intracerebral hematomas and cerebral
contusions. Lateral and anteroposterior views of the skull are obtained.

Management Scalp injury
Basilar Skull Fractures
↑ HOB 30 degree to reduce ICP and promote spontaneous closure of the leak.
Instruct patient to avoid blowing the nose & sneezing.
Depressed Skull Fractures
ABT’s (antibiotics) therapy
Scalp is shaved and cleanse with copious amount of saline to remove the debris.
Surgical repair (non-depressed skull Fx usually do not required surgical TX)

Brain Injury (injury that is severe enough to interfere with normal functioning)
Closed (blunt) injury
Head rapidly accelerates and decelerates or collides with another object.
Brain tissue damage with no opening through the skull and dura.
Open injury
Object penetrates the skull and damages the soft brain tissue.
Penetrating injury
Concussion
Temporally loss of neurologic function (from dizziness to complete loss of consciousness) after a head
trauma with no apparent structural damage
Last from seconds to minutes
Frontal lobe: bizarre irrational behavior
Temporal lobe: amnesia and/or disorientation
Contusion
More severe than concussion
Bleeding
Loss of consciousness for more than few minutes
S&S depend on the extend of the cerebral edema
Residual vertigo and headaches are common
Diffuse axonal injury
Widespread damage to the axons in the cerebral hemispheres, corpus callosum, and brain stem.
Severe injury leads to coma with decorticate and decerebrate posturing

Intracranial Hemorrhage
Intracranial hemorrhage
Collection of blood that develops within the cranial vault
Most serious brain injury epidural, subdural, or intracerebral hematoma
P. 1914
Epidural hematoma:
Blood collects between the dura and the skull
Classic sign: “Lucid interval”
Emergency with poss. obvious neurologic deficit and Resp. arrest within min.
TX: burr holes to decreased ICP immediately, craniotomy, both with drain
Subdural hematoma
Collection of blood between the dura and the brain
Cause: Trauma, coagulopathies, ruptured aneurysm but most common is venous in origin and is caused by a
rupture of small vessels that bridge the subdural space.
Acute: S&S within 24-48 hrs. AMS (altered mental status), pupillary signs, hemiparesis.
Sub-acute: S&S within 48hrs-2wks. S&S similar to Acute Subdural Hematoma
Chronic: repetitive minor head injuries. S&S appear wks-months. On-and-off severe headaches, mental
deterioration, seizures, and personality changes
TX: burr holes, craniotomy
Intracerebral hemorrhage
Bleeding into the brain tissue
Causes: HTN, ruptured vein/aneurysm, vascular anomalies, tumor, leukemia, hemophilia, aplastic anemia,
thrombocytopenia, and anticoagulant therapy.
S&S: Headache and neurologic deficits
TX: craniotomy, cranietomy (? Surgery depends on location and containment of blood)
Management includes supportive care, control of ICP, and careful administration of fluids, electrolytes, and
antihypertensives



Brain Injury Management
Every pt with head injury is presumed to have a cervical spine injury until proven otherwise.
Cervical collar and cervical X-Rays
Neurological assessment
CT scan & MRI
PET Scan – Positron emission tomography is a method of scanning that examines brain function rather than
structure
Prevention of ↑ ICP
Prevention of further neurological deterioration – Treatments to prevent secondary injury include stabilization of
cardiovascular and respiratory function to maintain adequate cerebral perfusion, control of hemorrhage and
hypovolemia, and maintenance of optimal blood gas values

Brain Injury NSG
Assessment
Glasgow Coma Scale – a tool for assessing a patient’s response to stimuli. Scores range from 3 (deep coma) to
15 (normal) (<8 indicates severe head injury)
Eye opening response – Spontaneous 4, To Voice 3, To Pain 2, None 1
Best Verbal Response – oriented 5, Confused 4, Inappropriate words 3, Incomprehensible sounds 2,
none 1
Best Motor Response – Obeys command 6, localizes pain 5, Withdraws 4, Flexion 3, Extension 2, none 1
LOC
Vital signs
Neurological assessments (**Pupil response)
Maintaining the airway
Monitor fluid and electrolyte balance
Promote adequate nutrition
Preventing injury
Maintain skin integrity
Med-Surg Neurological System
Altered level of consciousness

The patient is:
Not oriented
Does not follow commands
Needs persistent stimuli to achieve a state of alertness
(LOC sensitive indicator of neurological function).

Coma
A clinical state of unconsciousness in which the patient is unaware of self or the environment for prolonged periods.
A clinical state of un-arouseable unresponsiveness in which there are no purposeful responses to internal or
external stimuli.

Akinetic Mutism
A state of unresponsiveness to the environment in which the patient makes no movement or sound but
sometimes open the eyes. Eye movement is measured for responsiveness

Altered LOC
Pathophysiology
Symptom of multiple pathologies: Neurologic, toxicologic, and/or metabolic.
Neurologic: Head injury or stroke
Toxicologic: Drug overdose, ETOH intoxication
Metabolic: Hepatic and/or renal failure, and DKA (Diabetic Ketoacidosis – diabetic coma, an acute lifethreatening
complication of uncontrolled DM. S&S urinary loss of water, K, Ammonium, and sodium results in hypovolemia,
electrolyte imbalance, extremely high blood glucose levels, and breakdown of free fatty acids, causing acidosis,
often with coma.)
Disruption in the anatomic structure is cause by head trauma, edema, pressure from tumors, increased/decreased
blood or CSF circulation.

Altered LOC
S&S
Decreased state of alertness and consciousness
Behavioral changes (restlessness & anxiety) are initial changes which are subtle
Sluggish pupillary response (as the Pt becomes comatose, the pupils become fixed)
Change in verbal and motor response
If Pt is comatose but with pupillary light reflexes preserved, a toxic or metabolic disorder is suspected.
If Pt is comatose and has localized signs such as abnormal papillary and motor responses, it is assumed that
neurologic disease is present until proven otherwise

Diagnostic tools
Lab tests:
•Glucose – Test whether Pt is hyperglycemic or hypoglycemic (glucose blood levels which help to indicate liver
function (metabolism of glucogon) and indicate the need for insulin because if Plasma levels are to high that
could indicate pancreas function problems, as well as insulin receptor functionality and glucose metabolism at
the cellular level.
•Electrolytes – critical for cellular functions, provide inorganic chemicals for a variety of cellular functions (e.g.,
nerve impulse transmission, muscular contraction, water balance). Concentrations of cation’s. Na, K, Ca, Mg is
higher in the plasma than in the interstitial fluid.
•Na – The most abundant cation (90% of the electrolyte fluid) and the chief base of the blood. Primary function
in the body is maintain osmotic pressure and acid-base balance chemically and to transmit nerve impulses.
Determinations of plasma sodium levels detect changes in water balance rather than sodium balance. Sodium
levels are used to determine electrolytes, acid-base balance, water balance, water intoxication, and
dehydration.
•K – Potassium is the principal cation of intracellular fluid and the primary buffer within the cell itself. 90% of K
is concentrated within the cell; only small amounts are contained in bone and blood. Damaged cells release K
into the blood. 80% to 90% of cells K is excreted in the urine by the glomeruli of the kidney’s; the remainder is
excreted in sweat and stool. Even when no K is taken into the body 40 to 50 mEq is still excreted daily in the
urine. The Kidneys do not conserve K, and when an adequate amount of K is not ingested, a severe deficiency
will occur. K plays an important role in nerve conduction, muscle function, acid-base balance, and osmotic
pressure. Along with Ca and Mg, K controls the rate and force of contraction of the heart and thus cardiac
output. Evidence of a K deficit can be noted on an ECG by the presence of a U wave.
•Ca – The bulk of the bodies calcium (99%) is stored in the skeleton and teeth which act as huge reservoirs for
maintaining blood levels of calcium. About 50% of the blood Ca is ionized; the rest is protein bound. Only
ionized Ca can be used by the body in such vital processes as muscular contraction, cardiac function,
transmission of nerve impulses, and blood clotting. The amount of protein in the blood also affects calcium
levels because 50% is protein bound. Thus, a decrease is serum albumin will result in a decrease in total
serum Ca.
•Mg – Mg in the body is concentrated (40-60%) in the bone, 20% muscle, 30% within the cell itself, and 1% in
the serum, and is required for use of ADP as a source of energy. It is necessary for the action of numerous
enzyme systems such as carbohydrate metabolism, protein synthesis, nucleic acid synthesis, and contraction
of muscular tissue. Mg also regulates neuromuscular irritability and the clotting mechanism. Mg deficiency will
result in the drift of calcium out of the bones, possible resulting in abnormal calcification in the aorta and the
kidney. When there is decreased kidney function, greater amounts of magnesium are retained, resulting in
increased blood serum levels. Magnesium measurement is used to evaluate renal function, electrolyte status,
and evaluate magnesium metabolism.
•Cl – Chloride, a blood electrolyte, is the major anion that exists predominantly in the extracellular spaces as
part of sodium chloride or hydrochloric acid. Cl maintains cellular integrity through its influence on osmotic
pressure and acid-base and water balance. In an emergency, chloride is the least important electrolyte to
measure. However, it is especially important in the correction of hypokalemic alkalosis.
•Ammonia – NH
3,
an end product of protein metabolism, is formed by bacteria acting on intestinal proteins together
with glutamine hydrolysis in the kidneys. The liver normally removes most of this ammonia via the portal vein
circulation and converts the ammonia to urea. Because any appreciable level of ammonia in the blood affects the
body’s acid-base balance and brain function, its removal from the body is essential. The liver accomplishes this by
synthesizing urea so that it can be excreted by the kidneys.
•BUN – Blood Urea Nitrogen test – which measures the nitrogen portion of urea, is used as an index of glomerular
function in the production and excretion of urea. Rapid protein catabolism and impairment of kidney function will
result in an elevated BUN level. The rate at which the BUN level rises is influenced by the degree of tissue
necrosis, protein catabolism, and the rate at which the kidneys excrete the urea nitrogen. A markedly increased
BUN is conclusive evidence of sever impaired glomerular function. In chronic renal disease, the BUN level
correlates better with symptoms of uremia than does the serum creatinine.
•Serum osmolarity -
•PT – Prothrombin Time normal range 11.0 to 13.0 seconds. Prothrombin is a protein produced by the liver for
clotting of the blood. Prothrombin production depends on adequate vitamin K intake and absorption. During the
clotting process, prothrombin is converted to thrombin. The prothrombin content of the blood is reduced in patients
with liver disease. PT directly measures a potential defect in stage II of the clotting mechanism (extrinsic
coagulation system) through analysis of the clotting ability of five plasma coagulation factors (prothrombin,
fibrinogen, factor V, factor VII, and factor X). The PT is used also to evaluate disfibrinogenemia, evaluate the
heparin effect and coumarin effect, liver failure, and vitamin K deficiency.
•PTT – Partial Thromboplastin Time normal range 21-35 seconds, one stage clotting test, screens for coagulation
disorders. Specifically, it can detect deficiencies of the intrinsic thromboplastin system and also reveals defects in
the extrinsic coagulation mechanism pathway. Prolonged PTT occurs in congenital deficiencies, Heparin therapy,
Warfarin (Coumadin) therapy, Vitamin K deficiency, liver disease, DIC (disseminated intravascular coagulation)
fibrin breakdown products. Shortened PTT occurs in: extensive cancer, except when the liver is involved,
Immediately after acute hemorrhage, very early stages of DIC.
•Serum ketones – Level of concentration of ketones. Ketoacidosis vs Ketoalcolosis
•ETOH level – Ethanol is absorbed rapidly from the GI tract, with peak blood levels usually occurring within 40 to 70
minutes of ingestion on an empty stomach.Quantitation of alcohol level may be performed for medical or legal
purposes, to diagnose alcohol intoxication, and to determine appropriate therapy. Alcohol level must be tested as a
possible cause of unknown coma because alcohol intoxication mimics diabetic coma, cerebral trauma, and drug
overdose. This test is also used to screen for alcoholism and to monitor ethanol treatment for methanol
intoxication.
•Toxicology – the scientific study of poisons, their detection, their effects, and methods of treatment for conditions
they produce. Urine drug screen. Common Urine Drug Tests include Alcohol, Amphetamines, Analgesics,
Barbiturates, Benzodiazepines, Cocaine “crack”, Cyanide, LSD, Major tranquilizers, Marijuana, Opiates, PCP,
Sedatives Stimulants, Sympathomimetics.
•ABG’s – Arterial Blood Gases – measurement are obtained to assess adequacy of oxygenation and ventilation, to
evaluate acid-base status by measuring the respiratory and nonrespiratory components, and to monitor
effectiveness of therapy. They are also used to monitor critically ill patients, to establish baseline values in the
perioperative and postoperative periods, to detect and treat electrolyte imbalances, to titrate appropriate oxygen
flow rates, to qualify a patient for use of oxygen at home, and in conjuction with pulmonary function testing.
Glasgow coma scale – is a tool for assessing a patient’s response to stimuli. Scores range from 3 (deep coma) to
15 (normal).
Eye opening response – Spontaneous 4, To Voice 3, To Pain 2, None 1
Best Verbal Response – oriented 5, Confused 4, Inappropriate words 3, Incomprehensible sounds 2,
none 1
Best Motor Response – Obeys command 6, localizes pain 5, Withdraws 4, Flexion 3, Extension 2, none 1
Ct scan – Computed Tomography uses high-speed xray scanning to detect less apparent abnormalities. It is fast,
accurate, and safe diagnostic procedure that shows the presence, nature, location, and extent of acute lesions.
Cerebral edema, contusion, hematomas, subrachnoid & intraventricular hemorrhage, (infarction) hydrocephalus,
abd. Can Identify bleeding without contrast.
MRI – Magnetic Resonance Imagery is used to evaluate patients with head injury when a more accurate picture
of anatomic nature of the injury is warranted and when the Pt is stable enough to undergo this longer diagnostic
procedure.
EEG – Electroencephalography, an instrument used for receiving an recording the electric potential produced by
the brain cells. Electroencephalogram, a graphic chart on which is traced the electric potential produced by the
brain cells, as detected by electrodes placed on the scalp. The resulting brain waves are called alpha, beta, delta,
and theta rhythms, according to the frequencies they produce. Variations in brain wave activity are correlated with
neurologic conditions, psychologic states, and level of consciousness.

Altered LOC
Assessment
Mental status – the degree of competence shown by a person in intellectual, emotional, psychologic, and
personality functioning as measured by psychologic testing with reference to a statistical norm. Alertness is
measured by the patients ability to open the eyes spontaneously or in response to a vocal or noxious stimulus. Pt’s
with severe neurologic dysfunction cannot do this.
Cranial nerves – 12 pairs of nerves emerging from the cranial cavity through various openings in the skull.
Beginning with the most anterior, they are designated by Roman numerals and named:

Cranial Nerve I Olfactory Smell
Cranial Nerve II Optic Visual acuity and visual fields
Cranial Nerve III Oculomotor Muscles that move the eye and lid, papillary constriction, lens
accomodation
Cranial Nerve VI Trochlear Muscles that move the eye
Cranial Nerve V Trigeminal Facial sensation, corneal reflex, mastication
Cranial Nerve VI Abducens Muscles that move the eye
Cranial Nerve VII Facial Facial expression and muscle movement, salivation, and tearing,
taste, sensation in the ear
Cranial Nerve VIII Vestibulocochlear Hearing and equilibrium
Cranial Nerve IX Glossopharyngeal Taste, sensation in pharynx and tongue, pharyngeal muscles,
swallowing
Cranial Nerve X Vagal Muscles of pharynx, larynx, and soft palate; sensation in external ear,
pharynx, larynx, thoracic and abdominal viscera; parasympathetic
innervation of thoracic and abdominal organs
Cranial Nerve XI Accessory Sternocleidomastoid and trapezius muscles
Cranial Nerve XII Hypoglossal Movement of the tongue

Cerebellar function (balance & coordination)
Reflexes – Deep tendon reflexes & pathologic reflexes e.g., Babinski’s sign
Sensory and motor function – applying a painful stimulus (firm but gentle pressure to the nailbed or by squeezing
the muscle. If the patient attempts to push away or withdraw, the response is recorded as purposeful or
appropriate (“patient withdraws with painful stimuli)

Altered LOC
Complications
•Respiratory failure
Pneumonia – hospital aquired
Pressure ulcers – from lack of mobility and being in one position for too long
Aspiration -
Venous stasis – Deep vein thrombosis
Musculoskeletal deterioration – loss of muscle tone an mass resulting from inactivity
Disturbed GI function – Constipation, peristalsis

Medical Management
Maintain a patent airway (mechanical ventilation if needed)
Maintain adequate perfusion to the brain and the body (B/P & Heart Rate)
IV access
Nutritional intake

NSG Assessment
Alertness (pt’s ability to open eyes spontaneously or with stimulation)
Determine patient orientation to person, place, and time (AAOx3)
Verbal response (clear vs. slurred speech, aphasia & incoherent speech)
Motor response: Spontaneous, response to stimulus (light touch vs. deep pain), and posturing
decerebrate – involving extension and outward rotation of upper extremities and plantar flexion of the feet
decorticate – involving adduction and flexion of the upper extremities, internal rotation of the lower extremties,
and plantar flexion of the feet

Posture
Decorticate: (towards the body)
Severe brain injury
Flexion of upper extremities and extension of lower extremities
Internal rotation of lower extremities

Decerebrate: (away from the body)
•Extension of upper extremities
•Outward rotation of upper extremities
Continuous assessment (q15 min-q1hr)
V/S,
Respiratory Status,
Pupils, (PERRLA)
Reflexes
Neurological exam
Indicates deeper and more severe dysfunction than does decorticate posturing; implies brain pathology; poor
prognostic sign

Altered LOC
Nursing Interventions
Maintain a patent airway:
Administer O2 as ordered
↑ HOB 30 degree
Frequent suctioning and mouth care (for deep suction get order from physician after initial suction)
Turn patient from side to side
Chest physiotherapy and postural drainage as ordered
Lungs auscultation

NSG: Maintain a patent airway
Suctioning: the pt lacks pharyngeal reflexes
Mouth care
↑HOB 30 degree: Prevents aspiration
Chest physiotherapy & postural drainage (promotes removal of secretions)
Chest auscultation (to ID adventitious breath sounds)

NSG: Mouth care
Assess for dryness (dehydration), inflammation and crusting (infection) – Keep membranes moist
Provide mouth care (remove crust, excess saliva, maintain moisture & dental integrity)
Apply moisturizing sol. to the lips.

NSG: Preserve corneal integrity
Clean with NS with sterile gauze to prevent dryness
Use of artificial tears Q2hrs, as ordered (saline ampules)
Eye patches to prevent corneal damage and blindness

NSG: Thermoregulation
Causes of fever:
• Infection
• Drug reaction
• Damage to the hypothalamus (if neurological then the fever will never go down! Mortality rate is high,
maybe 100%)
• (low grade) dehydration

Use minimum amount of bedding to increase surface cooling.
Minimum amount of bedding
Antipyretics as prescribed most common acetaminophen (no Tylenol if liver problem, renal no motrin)
Give a cool vs. tap H2O sponge bath
Use of hypothermia blanket
Elderly don’t regulate the body temperature as well

NSG: Provide sensory stimulation
Talk and touch the pt while performing nursing care.
Encourage the family to communicate with the pt.
Orient the patient to time and place Q shift.
Coma: Use of T.V. and radio
Arousing from coma: Minimize stimulation, quiet environment and limit visitors to avoid agitation and anxiety
(good sign)

Fluids & nutritional needs
Assess mucous membrane and skin turgor for hydration status
Accurate I&O
Report any abnormal lab results: BUN, Creatinin, Albumin level (aids in movement of fluids / protein which shows
the nutritional status of patient), RBC, Hemoglobin & Hematocrit (H&H)
IV access for hydration and Parenteral feeding
NGT placement

Maintain skin & joint integrity
Order low-air-loss mattress (protocol)
Follow a regular schedule of turning & repositioning Q2hrs. (prone for 15 minutes a day)
Avoid dragging the pt up in bed (use drop/pull sheet) – dragging creates a shearing force and friction on the skin
surface
PROM (encourage family to participate) Passive Range of Motion – gets the family involved and also helps
prevent contractures
Prevent contractures and foot drop – PROM exercises and the use of splints or foam boots aids in the prevention
of foot drop and eliminates the pressure of bedding on the toes. The use of traochanter rolls to support the hip
joints keeps the legs in proper alignment. The arms ar in abduction, the fingers lightly flexed, and the hands in
slight supination. The heels of the feet are assessed for pressure areas. Specialty beds, such as fluidized or low-
air-loss beds, may be used to decrease pressure on bony prominences.

Benefits of turning
Kinesthetic stimulation (sensation of movement)
Propioception stimulation (awareness of position)(I’m on my right side, I’m on my left side)
Vestibular stimulation (equilibrium)

NSG: Promote Bladder function (Bladder & Bowel or B&B)
Palpate pelvic area for bladder distention – the bladder is palpated or scanned at intervals to determine whether
urinary retention is present, because a full bladder may be an overlooked cause of overflow incontinence.
If urine retention: insert indwelling catheter, as ordered
Accurate I&O
If Catheter is in place, monitor for S&S of infection e.g., fever and cloudy urine, the area around the urethral
orifice is inspected for drainage.
Bladder training protocol (when you have a foley the patient has no sense of full bladder and lose bladder tone,
train the bladder by clamping the foley for 30 minutes at a time so the patient gets full bladder sensation)
The incontinent patient is monitored frequently for skin irritation and skin breakdown. Appropriate skin care is
implemented to prevent these complications

NSG: Promote bowel function
Auscultate ABD (abdomen) for bowel sounds
Palpate ABD for distention, tenderness &/or mass
Institute a regular pattern (promote walking for peristalsis, normal daily schedule)
Provide privacy
Presence of diarrhea - infection (antibiotics kill the normal flora leading to infection), ABT’s (antibiotics), and
hyperosmolar fluids (osmotic pressure – the pressure exerted on a differentially permeable membrane by a solution
containing one or more solutes that cannot penetrate the membrane, which is permeable only by the solvent
surrounding it.
Prevent Fecal impaction – increase fiber intake to prevent
Prevent Constipation: (due to lack of activity & dietary fiber) Fiber, stool softener, and enemas ,as ordered

NSG: Provide safety
Side rails up (x2 or X4)
Padded side rails
Call light within easy reach
Bed in the lowest position
Keep belongings within easy reach
Keep room clutter free
Provide privacy
Explain every procedure to the pt

References:
Bare. B. & Smeltzer. S. (2004). Altered level of consciousness. Textbook of Medical-Surgical Nursing. 1850-
1856
Med-Surg Neurological System
Cerebrovascular Disease
Two things to remember:
Ischemic – no blood supply to brain due to blockage therefore the tissue dies / able to reperfuse the area using
anticoagulants
Hemorrhagic – bleeding into the brain (too much blood) / increased intercranial pressure due to edema / takes
longer for recuperartion

CVA
Leading cause of serious, long term disabilities in USA
Divided into 2 major categories:
Ischemic
Hemorrhagic

Ischemic stroke
Vascular occlusion and significant hypo-perfusion occur (due to thrombosis)
85% of CVA cases
Sudden loss of function resulting from disruption of the blood supply to a part of the brain.
8% result in death within 30 days

Types of ischemic attacks
Large artery Thrombotic stroke-caused by atherosclerosis plaques of large vessels of the brain. Thrombus
formation and occlusion at the site of the atherosclerosis result in ischemia and infarction (a localized area of
necrosis in a tissue resulting from anoxia) (deprivation of blood supply)
Small artery Thrombotic stroke – most common type of ischemic stroke. Affects one or more vessels, also called
lacunar strokes because infarcted (a localized area of necrosis in a tissue resulting from anoxia) brain tissue
disintegrates creating a cavity
Cardiogenic emboli - R/T cardiac dysrhythmias, usually atrial fibrillation, embolic strokes can also be associated
with valvular heart disease and thrombi in the left ventricle.
Cryptogenic - No known cause
Other causes – strokes from other causes such as illicit drug use, coagulopathies, migraine, and spontaneous
dissection of the carotid or vertebral arteries
Watch for “this is the worst headache of my life!” this could definitely be ruptured anurism

CVA: Hemorrhagic
Account for 15% to 20% of cerebrovascular disorders and are primarily caused by intracranial or subarachnoid
hemorrhage
Extravasation of blood into the brain, ventricles, or subrachnoid space.
Intracranial or subrachnoid hemorrhage.
More severe with longer recovery.
Causes:
Primary intracerebral hemorrhage from a spontaneous rupture of small vessels accounts for 80% of
hemorrhagic strokes chiefly by uncontrolled hypertension.
Subarachnoid hemorrhage results from a ruptured intracranial aneurysm (a weakening in the arterial wall) in
about half the cases.
Intracerebral hemorrhage in the elderly is cerebral amyloid angiopathy, which involves damage cause by the
deposit of beta-amyloid protein in the small and medium-sized blood vessels of the brain.
Secondary intracerebral hemorrhage is associated with arteriovenous malformations (AVM’s), intracranial
aneurysms, intracranial neoplasms, or certain medications.
AVM (arteriovenous malformation, birth defect)
Anticoagulants (toxicity)
Amphetamines, cocaine, crack (vasoconstriction and rupture)

CVA: Pathophysiology
Ischemic
Blood flow obstruction - due to thrombosis resulting in deprivation of blood supply
Ischemic cascade – Begins when cerebral blood flow decreases to less than 25 mL per 100 g per minute. At this
point, neurons are no longer able to maintain aerobic respiration. The mitochondria must then switch to anaerobic
respiration, which generates large amounts of lactic acid, causing a change in the pH level. This switch to the less
efficient anaerobic respiration also renders the neuron incapable of producing sufficient quantities of ATP to fuel the
depolarization processes. The membrane pumps that maintain electrolyte balances begin to fail, and the cells
cease to function. Each step in the ischemic cascade represents an opportunity for intervention to limit the extent
of secondary brain damage caused by a stroke.
Penumbra region - (saveable region) Early in the ischemic cascade, an area of low cerebral blood flow referred to
as the penumbra region, exists around the area of infarction. The penumbra region is eschemic brain tissue that
may be salvaged with timely intervention. The ischemic cascade threatens cells in the penumbra because
membrane depolarization of the cell wall leads to an increase in intracellular calcium and the release of glutamate.
The influx of calcium and the release of glutamate, if continued, activate a number of damaging pathways that
result in the destruction of the cell membrane, the release of more calcium and glutamate, vasoconstriction, and the
generation of free radicals. These processes enlarge the area of infarction into the penumbra, extending the
stroke.
TIA (transient ischemic attack) – same as stroke but only lasts 10 -30 minutes

CVA: Pathophysiology
Hemorrhagic
Symptoms are produced when a primary hemorrhage, aneurysm, or AVM presses on nearby cranial nerves or
brain tissue or, more dramatically, when an aneurysm or AVM ruptures, causing subarachnoid hemorrhage
(hemorrhage into the cranial subarachnoid space)
Normal brain metabolism is disrupted by the brain’s:
Being exposed to blood
Increased ICP by sudden bleeding into the brain (entry of blood into the subarachnoid space, which
compresses and injures brain tissue)
Secondary ischemia of brain tissue is caused by reduced perfusion and vasospasms that frequently
accompany subarachnoid hemorrhage

CVA: Risk factors
Non-modifiable (there is nothing you can do about it)
Age >65 years
Male > women
Blacks higher incidence (less medical care as well)
Modifiable (preventable)
HTN (80%)
Diabetes
High cholesterol
Atherosclerosis
Obesity
Smoking
(P. 1892 chart 62-2)

CVA: Risk factors
Phenylpropanolamine:
Chemical substance found in appetite suppressant drugs and in cold & cough agents related to the incidence of
hemorrhagic strokes.

CVA: Diagnostic tools
Plain CT scan of the brain (ischemic vs. hemorrhagic) (without contrast) any Pt with suspected stroke should
undergo a CT scan to determine the type of stroke, the size and location of the hematoma, and the presence or
absence of ventricular blood and hydrocephalus (blood in the subarachnoid space or ventricles impedes the
circulation of CSF. This test and the cerebral angiography provide information about the affected arteries, veins,
adjoining vessels, and vascular branches.
12 lead EKG: cardiac arrhythmias (study of the electrical conduction of the heart)
Carotid U/S: stenosis (an abnormal condition characterized by the constriction or narrowing of an opening or
passageway in a body structure) & atherosclerosis (a common disorder characterized by yellowish plaques of
cholesterol, other lipids, and cellular debris in the inner layers of the walls of arteries.
MRI – Magnetic Resonance Imagery is used to evaluate patients with head injury when a more accurate picture of
anatomic nature of the injury is warranted and when the Pt is stable enough to undergo this longer diagnostic
procedure.
MRA – the use of special MR imaging pulses to visualize the vascular sysem and identify regions of non-flowing
blood. It may be performed with or without contrast.
Cerebral angiography – identifies supratentorial, extracerebral, and intracerebral hematomas and cerebral
contusions. Lateral and anteroposterior views of the skull are obtained.
Carotid angiography – identify abnormalities or blockages pertaining to the arteries that supply the head and neck
Toxicology screen – When diagnosing a hemorrhagic stroke in a patient younger than 40 years of age, some
clinicians obtain a toxicology screen for illicit drug use.
Lumbar puncture – is performed if there is no evidence of increased ICP, the CT is negative, and subarachnoid
hemorrhage must be confirmed. Note: Lumbar puncture in the presence of increased ICP could result in brain
stem herniation or rebleeding.

Diagnostic tools
Initial nursing assessment
Respiratory status and airway patency
Cardiovascular status
ID gross Neurologic deficits:
Altered LOC
Sluggish papillary reaction
Motor and sensory dysfunction
Cranial nerve deficits (extraocular eye movements, facial droop, presence of ptosis)
Speech difficulties and visual disturbance
Headache and nuchal rigidity or other neurologic deficits

CVA: Complications
Respiratory failure
Pneumonia
Pressure ulcers
Aspiration
Venous stasis
Musculoskeletal deterioration
Disturbed GI function

CVA: Complications
Hemorrhagic
Acute hydrocephalus: accumulation of fluid in the brain
Cerebral hypoxia: lack of oxygen to the brain
Vasospasm: spasm in a blood vessel (narrowing of the lumen of the involved cranial blood vessel)

Hemorrhagic complications Management
Cerebral hypoxia:
1. Administer supplemental O2
2. Maintain H&H at acceptable levels
3. Hydration to ↓ blood viscosity and improve cerebral blood flow
4. Seizure Tx, prophylaxis

Vasospasm:
1. R/T ↑ amount of blood in the subarachnoid cisterns and cerebral fissures
2. Causes ↑ vascular resistance, brain ischemia, and infraction.
3. Caused by influx of calcium into the cells.
4. Administration of Ca channel blockers IV, and fluid expanders

Acute hydrocephalus:
1. Management of ↑ ICP with Mannitol
2. CSF drainage by lumbar puncture or ventricular catheter drainage

Systemic hypertension
1. Antihypertensive meds (avoid sudden drop pf BP to prevent brain tissue ischemia)
2. Administration of stool softeners to avoid straining

Craniotomy – any surgical opening into the skull, performed to relieve intracranial pressure, to control bleeding, or
to remove a tumor

CVA: S&S Hemorrhagic
“Worst headache of my life”
Arteriovenous Malformations (AVM) is caused by an abnormality in embryonal development that leads to a tangle
of arteries and veins in the brain that lacks a capillary bed. The absence of a capillary bed leads to dilation of the
arteries and veins and eventual rupture. AVM is a common cause of hemorrhagic stroke in young people
Rupture of an aneurysm or AVM often produces a loss of consciousness for a variable period of time
Nuchal rigidity (pain and rigidity in the back of the neck) and back pain due to meningeal irritability.
Visual disturbances (visual loss, diplopia [double vision caused by defective function of the extraocular muscles or
a disorder of the nerves that innervate the muscles], ptosis [one or both eyelids droops because of an acquired
weakness of the levator]

CVA: Ischemic & Hemorrhage S&S
Neurologic deficits depends on the affected region of the brain
Chief complaint:
Numbness &/or weakness of face, arm, or leg, especially on one side of the body
Confusion or change in mental status
Changes of LOC, dizziness, headache
Aphasia -trouble speaking or understanding speech
Visual disturbances
Ambulatory difficulties – difficulty walking, dizziness, or loss of balance or coordination

CVA: Ischemic S&S
Motor loss
Lesion of the upper motor neurons results in lost of voluntary control over motor movements.
1
st
flaccid paralysis and loss/decreased deep tendon reflexes
Hemiplegia - paralysis of one side of body caused by a lesion (stroke) of the opposite side of the brain (most
common dysfunction)
Hemiparesis - weakness of one side of the body
Spasticity - Abnormal increase in muscle tone, 48hrs after when deep tendon reflexes re-appear
Ataxia - An impaired ability to coordinate movement, an unsteady gait.
Apraxia - inability to perform a previously learned action, as may be seen when a patient makes verbal
substitutions for desired syllables or words.

CVA: S&S
Communication loss
Stroke is the most common cause of aphasia
Dysarthria – difficulty in speaking, caused by paralysis of the muscles responsible for producing speech
Dysphasia - impaired speech
Aphasia - loss of speech (expressive, receptive, global)
Apraxia - inability to perform a previously learned action, as may be seen when a patient makes verbal
substitutions for desired syllables or words.

CVA:S&S Ischemic & Hemorrhage Stroke
Perceptual disturbance:
Perception is the ability to interpret sensation
Homonymous Hemianopsia - loss of ½ the visual field (visual perceptual dysfunction) which may occur from
stroke and may be temporary or permanent. The affected side of vision corresponds to the paralyzed side of the
body.
Sensory loss:
The sensory loss from stroke may take the form of slight impairment of touch, or it may be severe, with loss of
proprioception as well as difficulty in interpreting visual, tactile, and auditory stimuli.
Propioception - ability to perceive the position and motion of body parts.
Difficult interpretation of visual, tactile, and auditory stimuli
Agnosias – are deficits in the ability to recognize previously familiar objects perceived by one or more of the
senses
Paresthesia – any subjective sensation, experienced as numbness, tingling, or a “pins and needles” feeling.

CVA: S&S Ischemic & Hemorrhage Stroke
Cognitive impairment
Frontal lobe: (impaired intellectual function, memory & learning)
Memory loss
Decreased attention span
Impaired ability to concentrate
Altered judgment

CVA:S&S Ischemic & Hemorrhage Stroke
Psychological effect:
Emotional lability (mood swings)
Hostility
Frustration
Resentment
Lack of cooperation
Depression

TIA: Medical management
Carotid Endarterectomy
Peripheral vascular procedure.
Removal of atherosclerotic plaque or thrombus from the carotid artery (surgical excision of stheromatous
segments of the endothelium and tunica media of the carotid artery, leaving a smooth tissue lining and facilitating
blood flow through the vessel. Surgery is done to prevent stroke)

Brain Aneurysm

Stroke Animation

CVA: Medical management
ischemic
Thrombolytic therapy
Dx. Made within 3 hrs of onset of symptoms.
Stimulates fibrinolysis of the atherosclerotic plaque.
Dissolves blood clot that blocks blood flow to the affected area of the brain.
TPA (Tissue Plasminogen activator) ( no anticoagulants for 24hrs), follow protocol for contraindications.

CVA: Medical management
ischemic
Anticoagulant therapy
Heparin and low-molecular weight heparin (Lovenox, Agrastat, etc)

CVA: Medical management
Continuous homodynamic monitoring
Maintain BP within set parameter to avoid further bleeding or ischemic damage.
Neurologic assessment
Patent airway and respiratory support with supplemental O2 administration.

CVA: NSG care and goals
Discharge planning and rehab begins the admission day.
Improve mobility
Avoid should dislocation and pain
Relief sensory deprivation
Improve self care
Continence of Bowel & Bladder
Maintain skin integrity
Absence of complications
Restore family function

CVA: Nursing management
Acute phase may last for 1-3 days.
Assessment:
LOC, (baseline and monitor for changes)
Sensory-Motor (baseline and monitor for changes)
Respiratory status
Homodynamic status (report any abnormal ↑↓ BP levels)
Presence of bleeding
Recent surgeries (within the last 6mo)
Recent head trauma/ falls TPA
Presence of S&S of GI bleed (Melena)

CVA: NSG interventions
Turn and reposition Q2hrs
(15-30 min ad-lib, prone position aids prevention of knee, hip, shoulder contractures, aids in the removal of
bronchial secretions)
OOB, ASAP
Assist with ambulation
PROM 4-5xday to maintain joint mobility
Prevention of shoulder pain
Enhance self care

CVA: NSG interventions
Dysphagia
Monitor pt for cough, food dribbling or pooling at one side of the mouth, food retained for long periods, and nasal
regurgitation.(also Tears)
Consult with speech pathologist
Instruct pt to tuck the chin toward the chest as he swallows
Thickened fluids (avoid thin liquids)
Complications: Aspiration, dehydration, and malnutrition.

CVA: NSG interventions
Aphasia
Broca’s area: Comprehension and formulation of language
Right sided paralysis- speech disorders vs. the left sided one.
Supportive role
P. 1900 chart 62-5

CVA: NSG interventions
Implementing aneurysm precautions:
Provide quiet, non-stressful environment
Restrict visitors
Elevate HOB (semi fowler's position)
Dim lighting of the room
Avoid coffee and tea – caffeine will cause increased blood pressure which could burst an existing aneurism.
Caffeine stimulates the CNS.
Prevent any exertion by assisting the patient with bathing, and dressing including toileting and the Valsalva
maneuver.
No enemas, however stool softeners are allowed
No TV, Radio, or reading

CVA: NSG interventions
Monitor for S&S of vasospasm:
Assess for HA (headache), decreased level of responsiveness
Altered LOC responsiveness (confusion, lethargy, disorientation)
A new focal neurological deficit (aphasia, hemiparesis, hemiplegia)

Implement seizure precautions:
Avoid injury and maintain tissue perfusion (airway patency)
Medication therapy - phenytoin (Dilantin)

CVA: NSG interventions
Maintain skin integrity
B&B training
Assist family with emotional support and referring to community resources.

CVA: NSG Interventions
Team work
Med-Surg Neurological System
Seizure Disorders
Seizures
•Episodes of abnormal motor, sensory, autonomic, or psychic activity (or a combination of these) resulting from
sudden excessive discharge from cerebral neurons.
•Epilepsy: chronic unprovoked recurrent seizures
•Aura: Peculiar sensation preceding the onset of a generalized seizure that may take the form of gustatory, visual,
or auditory experience. “Funny feeling”
•Prodromal – pertaining to early symptoms that may mark the onset of a disease. Early manifestation that occurs
hrs to days before a seizure.

Seizures: Classifications
Seizures: Etiology
•Seizure: A symptom of an underlying disorder
•Epilepsy: Cause is unknown for most of them. Can be Primary (idiopathic) or secondary (when the cause is
known and the epilepsy is a symptom of another underlying condition, such as a brain tumor)
•Occurs in areas with lesions (stroke)

Seizures: Etiology
•Metabolic and toxic conditions (renal failure, hyponatremia, hypocalcemia, hypoclycemia, pesticides)
•Congenital malformations
•Genetic predisposition
•Perinatal injury
•Postnatal trauma
•Brain tumor, infection
•Vascular disease (hypoxemia)
•Drug or/and alcohol abuse
•Alcohol withdrawal
•Fever (childhood)
•Allergies
•Head trauma

Seizures: Triggering Factors
•Stress
•Sleep deprivation
•Menses
•Drug and alcohol ingestion or withdrawal
•Change of seizure meds
•Missed meds

Seizures: diagnostic tests
•Metabolic panel
•Drug toxicology
•MRI – is used to detect structural lesions such as focal abnormalities, cerebrovascular abnormalities, and
cerebral degenerative changes.
•SPECT (Brain CT, Single Proton Emission Computed Tomography)
•EEG (electroencephalogram) – helps to classify the type of seizure

Seizures: NSG Interventions
•Seizure precaution:
•Keep bed to the lowest position
•2 to 3 side rails padded & up
•Call light within easy reach
•Clutter free environment
•Protect the patients head
•Post-seizure:
•Place pt on the side lying position to facilitate drainage of oral secretions (prevent aspirations).
•Maintain a patent airway
•The patient, on awakening, should be reoriented to the environment
•If the patient becomes agitated after a seizure, use calm persuasion and gentle restraint
•The patient may want to sleep for a while after the seizure so that’s ok.

Seizures: NSG Interventions (Epilepsy in woman)
•Bone loss R/T long term use of anti-seizure Meds
•Assess for low bone mass and osteoporosis
•Risk for long bone fractures

Seizures: NSG Teaching
•Advise about state driving regulations
•Advice about swimming alone or operating dangerous equipment
•Patient should not to discontinue meds abruptly
•Wear medic alert bracelet
•R/T birth defects – The risk for congenital fetal anomaly is two to three times higher in mothers with epilepsy. The
effects of maternal seizures, antiseizure medications, and genetic predisposition are all mechanisms that contribute
to possible malformation.
•Valproic acid alters the effectiveness of birth control pills. The effectiveness of contraceptives is decreased by
antiseizure medications.

Seizures: Status Epilepticus (acute prolonged seizure activity)
•A series of generalized seizures that occur without full recovery of consciousness between attacks and lasting
over 30 minutes
•Medical Emergency
•Cumulative effects – Vigorous muscular contractions impose a heavy metabolic demand and can interfere with
respirations. Some respiratory arrest at the height of each seizure produces venous congestion and hypoxia of the
brain. Repeated episodes of cerebral anoxia and edema may lead to irreversible and fetal brain damage.
•Precipitating factors – withdrawal of antiseizure medication, fever, and concurrent infection

Seizures: Status Epilepticus
TX: the goals of treatment are to stop the seizures as quickly as possible, to ensure adequate cerebral
oxygenation, and to maintain the patient in a seizure-free state.
•Valium – (intravenous diazepam)
•Ativan – (lorazapam)
•Cerebyx - (fosphenytoin) , Dilantin
O2 supplemental therapyMed-Surg Neurological System
Med-Surg Neurological System
Brain tumors
Description
•Primary brain tumors:
•Abnormal cells growth from tissue within the cranium
•Normally grows as spherical mass, but it also can grow diffusely and infiltrate tissue.
•Named by origin (gliomas, meningiomas, acoustic neuroma, etc.)
•May be malignant or benign

•Secondary brain tumors:
•Metastasize from the lung, breast, kidney, or GI tract.

Etiology
•Unknown
•Gliomas: 46% of all CNS tumors (Glial tissue)
•Grades 1-4. 3&4 more invasive, faster growing and with poor prognosis.
•Meningiomas: rarely malignant, cure with complete excision.
incidence
•Gliomas: Most common in men
•Meningiomas & pituitary adenomas: most common in women
•Meningiomas increased with age
•Primary cerebral lymphomas R/T AIDS.

Diagnostic tools
•CT scan
•MRI
•Angiography
•Hormone profile
•Neurological exam (focal cranial nerve or motor deficits)

S&S
•Headaches
•Dull and aching
•Increase intensity over wks
•2
nd
to hydrocephalus or pressure over sensitive structures
•New onset of seizures in adulthood
•Hx of nausea & vomiting with headaches
•Neurological S&S depending on the affected area of the brain.

Management
•Neurosurgical referral for excision
•Oncology referral
•Radiation & chemotherapy
•Dexamethasone for cerebral edema
•Anticonvulsant therapy

NSG
•Self care deficit R/T impairment of motor/sensory functions.
•Keep the patient as independent as possible
•Assist patient with self care
•Referral for home care
•Develop an individualized exercise program.

NSG
•Imbalance nutrition less than body requirement R/T cachexia
•Reposition patient for comfort during meals
•Provide attractive trays and food plates to enhance appetite
•Provide enough fluids
•Increased opportunities for socialization during meals
•Referral to dietitian

NSG
•Anxiety R/T fear of dying
•Spend time with patient to allow him/her to express fears and concerns
•Referral to spiritual advisors, social workers, and mental health professional.
•Referral to support groups and hospice care as needed


Med-Surg Neurological System
Brain surgery
Pre-op care
Diagnostic studies include Ct scan, MRI, and cerebral angiography, etc.
Meds:
anti-seizure (Dilantin most common)
Corticosteroids (Decadron most common)
Hyper osmotic agent: Mannitol (to prevent & TX ↑ICP
Diuretic (Lasix)

Pre-op Nursing Care
Obtain a baseline
(LOC, neuro-deficits, V/S)
Obtain consent
Prepare medical record with MD orders, labs, radiology results, consent, & nurses’ admission notes
Keep pt NPO, as ordered

Types of brain surgeries
Craniotomy: Opening of the skull. Bony flap can be repositioned after surgery.
Transsphenoidal: Approach through the mouth and nasal sinuses to the pituitary gland.
Burr holes Circular openings made in the skull
Cranietomy: Excision of a portion of the skull
Cranioplasty: Repair of a cranial deflect using a plastic or metal plate.

Post-op management
Reduce cerebral edema (Mannitol and Decadron)
Relieve pain (Acetaminophen, codeine, and Morphine sulfate)
Prevention and treatment of seizures (Dilantin, and diazepam)
Monitor ICP (Monitor draining system)

Complications:
Increase ICP
Infections
Seizures
Neurological deterioration (nerve damage)
Bleeding
Fluid and electrolyte disturbances

Post-op management
Monitor ventricular drainage system (JP’s)
Vital signs (Maintain temp >99.6)
Anti-seizure meds prescribed such as Dilantin and valium
Meds to reduce cerebral edema such as mannitol and Decadron

Post-op management
NSG
Assess Resp. function: (small degree of hypoxia increases cerebral ischemia)
Resp. rate and pattern
ABG’s
Assess for hyperthermia (2
nd
to hypothalamus damage0
Neurologic assessment (a change in LOC or response to stimuli is the 1
st
sign of increased ICP)
Assess for seizure activity (record and report)

NSG: Post-op management
Maintain cerebral tissue perfusion
Assess Vital signs and neurological status every 15 min
Avoid extreme head rotation (raises ICP)
Monitor Resp. Rate, depth, and rhythm
Provide O2 as ordered
Place pt. In fowler’s position (according to surgeon’s choice)
Change patient’s position every 2 hrs
Provide skin care frequently

NSG: Post-op management
Regulating Temperature
Monitor temp (V/S)
Fever
Remove blankets, apply ice bags to axilla and groin areas
Use hypothermia blanket
Give prescribed meds to reduce fever
Hypothermia
Re-warming should occur slowly to prevent shivering (increases O2 demand)

NSG: Post-op management
Improve gas exchange
Assess for signs of Pulmonary infections
↑ temp, ↑pulse, changes in Resp.
Auscultate lungs ( decreased breath sounds/adventitious sounds)
Re-position the pt every 2 hrs (mobilization of pulmonary secretions and prevent stasis)
Teach pt to deep breathing & coughing, and the use of incentive spirometry
Suction of oropharynx and trachea
O2 humidifier

NSG: Post-op management
Preventing infection
Monitor incision site for redness, tenderness, bulging, separation, and foul odor.
Use of aseptic technique when handling dressing
Monitor for S&S of infections

NSG: Post-op management
Seizure activity
Keep bed to its lower position
Side rails up (padded)
Call light within easy reach
Keep room clutter free
O2 available with suction tubing
Never force the patient into a position
Never attempt to insert anything into the pt’s mouth
Document eventMed-Surg Lecture Notes

Med-Surg Neurological System
Diabetes Mellitus
Objectives: MDC, Nursing Curriculum, P 110.
Outline:
Diabetes Mellitus:
Etiology – characterized by increased levels of glucose in the blood (hyperglycemia) resulting from defects in
insulin secretion, insulin action, or both. The cells stop responding to insulin or the pancreas may stop producing
insulin entirely. This hyperglycemia can result in acute metabolic complications such as DKA and hyperglycemic
hyperosmolar nonketotic syndrome (HHNS).
Pathophysiology(type1 & type2)
Insulin – a hormone secreted by the beta cells of the islets of langerhans of the pancreas, (that is necessary for
metabolism of carbohydrates, proteins, and fats, controlling the level of glucose in the blood.
Classifications of Diabetes -
Risk factors
Incidence
S&S
Diagnostic findings
Complications
Management
Education
Nutrition
Exercise
Pharmacology
DKA
HHNKS
Foot care
Nursing diagnosis

Diabetes Mellitus
Definition:
Metabolic disease
Hyperglycemia
Defects in insulin secretion, insulin action, or both.

Insulin
Controls the level of glucose in the blood by regulating the production and storage of glucose.
Inhibits glycogenolysis (breakdown of stored gulcose)
Inhibits gluconeogenesis (production of new glucose from aminoacids)

Classification of Diabetes
Type 1 Diabetes
Type 2 Diabetes
Gestational Diabetes Mellitus
Diabetes Mellitus related to other conditions
Impaired glucose tolerance test (140-200 mg/dL)
Impaired fasting glucose test (110-126 mg/dL)

Risk Factors for Diabetes
Family history of diabetes
Low high-density lipoprotein (HDL) cholesterol
High triglycerides
High blood pressure
History of gestational diabetes
High-risk racial or ethnic background (African American, American Indian, Asian American, Pacific Islander, or
Hispanic American/Latino).

Diabetes
20.8 million Americans have diabetes, although 6.2 million of those are undiagnosed.
Each day, approximately 2,200 people are diagnosed with diabetes.
Type 2 diabetes accounts for up to 95 percent of all diabetes cases, affecting 8 percent of the population age 20
and older.
The prevalence of type 2 diabetes has tripled in the last 30 years, much of it due to an upsurge in obesity.
Diabetes afflicts 120 million people worldwide, and the World Health Organization estimates that number to
skyrocket to 300 million by 2025.

Mortality

Diabetes is the 5th leading cause of death in America.
Overall, the risk of death for people with diabetes is about 2 times that for people without diabetes.

Type 1 Diabetes
Acute onset, usually before 30
5-10 % of cases
Destruction of beta cell
Genetic predisposition, infections (virus), and autoimmune response
Production of little or no insulin
Insulin injections requirement

Type 1 Diabetes
Pathophysiology
Decreased or no production of insulin
Unchecked glucose production by the liver
Glucogenolysis & gluconeogenesis
Increased renal threshold for glucose (180-200 mg/dL). Glucosuria
Osmotic diuresis (loss of fluid and electrolytes with glucosuria)
Increased production of ketones (fat breakdown)

Type 2 Diabetes
Most common in obese people over 30
May go undetected for many years
Can be prevented or delayed with weight reduction and exercise
90-95% of cases
Controlled with oral agents, insulin, or a combination of both

Type 2 Diabetes
Pathophysiology
Insulin resistance
•Less effective insulin to stimulate glucose uptake by the tissue
•Less effective insulin to regulate glucose release from the liver
Impaired insulin secretion
•Beta cells cannot keep up with the production of ineffective insulin, glucose levels rises

Gestational Diabetes
Any degree of glucose intolerance with its onset during pregnancy
Secretion of placental hormones causes insulin resistance
Occurs in up to 14% of pregnancies
After delivery blood sugar returns to normal, but with a risk of type 2 diabetes later in life.

Diabetes
S&S
Three P’s
Polyuria, polydipsia, and polyphagia
Fatigue and weakness
Sudden vision changes
Tingling and numbness in the hands/feet
Dry skin
Skin lesions that take long to heal
Recurrent infections

Diagnostic findings
Criteria to Dx Diabetes
Fasting plasma glucose > 126 mg/dL
Random plasma glucose > 200mg/dL on more than one occasion
Symptoms of diabetes

Diagnostic tests
Hemoglobin A1C – 4 – 6 average glucose levels over lifetime of rbc’s 120 days
(Glycosylated hemoglobin)
Long term measure of glucose control
Glucose attaching to the hemoglobin for the life of the RBC (5-7 % good control)
Urinalysis for protein, glucose, and ketones
BUN, Creat, urinalysis
Serum cholesterol and lipid profile
EKG and chest X-Ray for pulmonary and coronary pathology

Complications
Type 1 Diabetes
DKA
Type 2 Diabetes
HHNS – a metabolic disorder of type 2 diabetes resulting from a relative insulin deficiency initiated by an
intercurrent illness that raises the demand for insulin; associated with polyuria and severe dehydration.

Complications
(target organ damage)
Retinopathy (eyes)
Peripheral neuropathy
Nephropathy and renal failure
Cardiovascular disease with lipid abnormalities
Erectile dysfunction
Infections
Foot and skin ulcerations

Prevention of Diabetes complications
Preventable kidney failure: 50%
(with better control of blood pressure and blood glucose levels)

Blindness: up to 90% (with proper screening and care)

Amputation: up to 85%
(with implementation of foot care programs that include regular examinations and patient education)

Death due to heart disease or stroke: up to 30%
(with improved control of blood pressure, blood
glucose and lipid levels)

Heart disease and stroke: up to 50%
(with improved control of blood pressure and
cholesterol and lipid levels)

Nerve disease: 40%
(with a 1% reduction in hemoglobin A1c test)

Management
Nutritional
Exercise
Monitoring
Pharmacologic therapy
Education

Nutritional management
Primary treatment for type 2 is weight reduction
Priority for a young patient with type1 is to meet the caloric requirements to enhance growth and development
Nutrition
3 meals with 3 snacks per day
Avoid simple sugars, and refined CHO
Caloric intake as follow: 30% protein, 20%fats, 50% CHO
Cholesterol 300 mg/day
Fiber 25 g/1000 calories
Food Pyramid

Diabetes
Dietary intake for small-frame woman
Choose these servings from each food groups to have 1,200 to 1,600 calories a day:
6 starches
2 milk and yogurt
3 vegetables 2 meat or meat substitute
2 fruit up to 3 fats
Diabetes: Exercise
Lower blood sugar levels by:
↑ glucose uptake by muscles
Improves insulin utilization
Snack before or might suffer a hypoglycemic event
Snack should be low carb and sugar free

Controls lipids levels by:
↑high density lipoprotein
↓total cholesterol & triglycerides levels
Diabetes: Exercise
Teaching
Eat a snack before and after exercising to prevent hypoglycemia
Closely monitor blood sugar levels
Use proper foot wear
Inspect feet daily after exercise
Avoid exercise during periods of uncontrolled sugar levels
Diabetes
Education
Eat about the same amount of food each day.
Eat your meals and snacks at about the same times each day.
Do not skip meals or snacks.
Take your medicines at the same times each day.
Exercise at about the same times each day.

Diabetes
ABC’s
A1C
Blood pressure monitoring
Cholesterol
The target LDL cholesterol for most people with diabetes is less than 100
Diabetes
Pharmacologic therapy
Insulin
Oral anti-diabetic agents
Diabetes Management
Oral antidiabetic agents (Cannot use during pregnancy) (p. 1170) (only insulin)
Sulfonylureas
Biguanides
Alpha glucosides inhibitors
Thiazolidinediones
Meglitinides

Oral anti-diabetic agents
Sulfonylureas (stimulates pancreas to release insulin) improves insulin action
Biguanides (facilitates insulin action on peripheral receptor sites)
Alpha-glucosidase inhibitors (delays absorption of glucose in the GI system)
Thiazolidinediones (enhance insulin action, for pts with insulin therapy)
Meglitinides (stimulates insulin release, has fast action with short duration)

Diabetes Insulin therapy:
Human insulin has a shorter duration of action that animal derived insulin.
Humalog and Novolog produce a more rapid effect than Regular insulin. (onset 10-15min) (p. 1164)
Insulin dose is based on the serum glucose level
Give it Subcutaneous only. If given IM then it takes longer to react.

Insulin
time-course Agent Onset Peak Duration
Complications of Insulin Therapy
Local allergic reaction
Systemic allergic reaction (rare)
Insulin lipodystrophy (loss of subcutaneous fat)
Insulin resistance
Morning hyperglycemia (dawn phenomenon & somogyi effect)
Inhale insulin
Approved January 27
th
, 2006 by the FDA.
Treatment of type 1 and type 2 diabetes
It is the first new insulin delivery option since the discovery of insulin in the 1920s
EXUBERA
Powder form of medication inhale through the mouth.
Has a peak level from 30-90 minutes.
SE:
hypoglycemia
Cough
SOB
sore throat
dry mouth
EXUBERA (new inhalant insulin)
Contraindications:
Smoking, recently stop smoking (within the last 6 months).
Patients with asthma, bronchitis, or emphysema.
Baseline tests for lung function are recommended after the first 6 months of treatment and every year thereafter,
even if there are no pulmonary symptoms.
Peak of 30 to 90 minutes
DKA
Caused by NO insulin production (or small amounts)
Hyperglycemia
Dehydration with electrolyte loss
Acidosis
Diabetes
DKA
Markedly inadequate amounts of insulin. (without insulin there is no glucose uptake by the cells therefore the liver
produces more glucose)
Excessive production of ketones bodies (p. 1180)
Ø insulin= lipolysis= free fatty acids + glycerol
Fatty acids convert to ketones

DKA
No insulin → ↓glucose uptake
↑release of fatty acids
↓
Gluconeogenesis & Ketogenesis
(Extremely elevated blood sugar levels)
↓
Metabolic acidosis
DKA
S&S
Hyperglycemia = Polyuria & dehydration
Deficits of Na, PO4, Mg levels
Marked hypokalemia (serum level may appear normal due to hypovolemia and shift from the cell due to metabolic
acidosis)
Kussmaul Resp. (to compensate the metabolic acidosis)
CNS depression
Nausea, polyurea, thirst
ketonuria

DKA Treatment
Continuous administration of insulin IV
Fluids and electrolytes replacement

HHNKS (Hyperglycemic hyperosmolar Nonketotic Syndrome)
Insulin resistance (poor quality)↓
Hyperglycemia & hyperosmolarity
Altered level consciousness
Minimal/absent ketosis
Electrolyte imbalance (↑Na)
Dehydration

HHNKS
S&S
Profound dehydration
Hypotension & tachycardia
AMS (from sensory deficits to seizures)
Mortality rate is 10-40 %
Diabetes: Patient Education
Recognition of S&S
Self-glucose monitoring
Nutritional counseling follow the American Diabetes Association (ADA) guidelines
Avoid alcohol and smoking (inhibits the release or breakdown of glucose or sugar from the liver)
Exercise, reduces insulin resistance
Use of proper fitting shoes at all times
Medi-alert ID bracelet or necklace
Annual influenza vaccine (every year and pneumococcal vaccine every 5 years
Diabetes
Geriatric considerations:
Elderly pts may not identify S&S of hypo/hyperglycemia
If renal insufficiency: oral hypoglycemic agents take longer to be excreted.
Deficiency nutritional intake R/T decreased appetite, poor dentition, and/or financial limitations. (p.1179)
Foot Care (p.1194) General guidelines: (Assess your feet regularly)
(use of mirror to inspect the bottom of the feet)
•Careful daily assessment of the feet
•Assess for redness, blisters, fissures, calluses, ulcerations, skin temp changes, and new deformities
•Assess interior surface of the shoes
•Assessment of feet during every health care visit.
•Once a year podiatrist evaluation
•Neuropathy: Monofilament study.
•Proper cleaning, drying, and foot lubrication. Avoid excess moisture between toes.
•Wearing closed-toe shoes that feet well.
•Trimming toenails straight across, mainly by a podiatrist.
•Avoid:Walking barefoot, open-toed shoes, soaking the feet, shaving calluses, and using heating pads.
•Blood glucose control.
Nursing Diagnosis
Imbalanced nutrition
Risk for impaired skin integrity
Deficient knowledge about diabetes and self care
Risk for infection

RESPIRATORY DISORDERS

Class notes:
• The % of the atmosphere is 21%
• atelectisis: lung collapse; there is not expansion of the lungs they collapse
• COPD has problem with air traveling
• When the hemoglobin decrease pt has problem with respirations and carrying of oxygen
• Treatment of carbon monoxide toxicity is administration of 100% of O2
• People living at high altitudes have increased hemoglobin and when coming to the city they get short of
breath, respirations problem.
• Increased metabolic rate you get tachycardia
• Person with fever administer O2 because O2 increase with increased metabolic rate
• Hyperventilate when anxious. CO2 is blown out and become alkaline. Respiratory alkalosis.
• Hypoventilation happens with overdose or sedation
• Cyanosis: bluish color on the thorax, lips
• The most reliable test is ABGs (to test for oxygen)
• Higher than 2 Liters administer humidifier
• CPT: tapping over the chest
• 50% of pneumonia is caused by viruses
• treat pneumonia with antibiotics before doing a sputum collection but it create a resistance. First you need
to get sputum then treat it.
• 23% are prevented with a simple vaccine
• immobility: staying of the secretions at the lungs
• viral: low grade fever
• CO2 is a waste product
• Lungs are responsible for gas exchange
• Dyspnea: difficulty breathing
• Cough: assess the sputum (amount, odor, color, consistency)
• If the pt has a non productive cough do not administer spectorants
• Wheezing: the air is trying to pass through the inflammated alveoli
• Clubbing of the finger: COPD, years of hypoxia
• Hemoptysis: coughing blood
• Pt with hemoptysis needs to put in isolation.
• Contact: wounds, CDEF
• Airbone: TB
• Droplet: bacterial pneumonia, MRSA
• 6 ft from the pt bed you are not expose to the virus
• hemoptysis patient need to be in negative pressure room
• cyanosis: central bluish color, not just the finger nail beds
• treatment of pulmonary edema: administer diuretics (lasix)
• 250 ml in the lungs to put you in CHF
• pulmonary edema: profuse, frothy pink sputum
• infection: foul smelling sputum
• liquify the sputum to remove it
• wash the mouth with water before getting a sputum sample.
• Teach the patient to dispose sputum correctly
• Vancomysin used to treat MRSA
• Walking pneumonia very common in nurses
• Consolidation: black lungs
• COPD is irreversible. Happens through the years. Takes time to get to this point.
• Asthma is reversible because you are able to treat it but is always there
• Chronic bronchitis is like asthma
• Polycythemia: because there is impaired gas exchange and pt needs to produce more RBCs
• Steroids: to reduce inflammation (prednisome, solumetrol)
• Low flow oxygen in pts with COPD because they have an increased CO2 levels and more than 2 liters of
O2 would make the pt stop breathing
• Emphysema: end of the lugs being exposed to contaminators
• Lungs remain inflated, don’t recoil back and interfere with gas exchange. Has barrel chest. A lot of air tap in
the lungs. Looks black
• No levels of oxygen. Increased CO2 in the lungs
• High levels of CO2 lungs not able to recoil back. The gas exchange is impaired. There is more blood flow
to the lungs to bring O2 but CO2 goes to the arterial blood and the CO2 levels remain high in the blood.
There is more pressure.
• Pt learns to breath in low levels of O2 and high levels of CO2
• You should administer low levels of O2 because if you give high levels of O2 pt stops breathing
• Kidneys try to compensate from acidosis retaining HCO3. has to be good kidneys. Body try to compensate
by reataining HCO3.
• Emphysema mainly in patient in their 60s
• A lot of impaired activity tolerance
• Pt with short of breath loose weight
• Pt at the end of the stage barrel chest
• Low level of oxygen but high hemoglobin
• Risk factor #1 is smoking cigarettes.
• Emphysema get a lot of antibiotics profilactive because of the accumulation of secretions
• Antibiotics: put them at risk for superinfections
• Carboxyhemoglobin: is the combination of carbon monoxide with hemoglobing and is hard to break the
bonds 25 time more harder
• Emphysema is an end stage condition. A lot of complications
• Rescue medications: albuterol
• Corticosteriods: reduce inflammation
• Flu shot every year; munoccocal vaccine every year
• Bulluctony: one piece vs a big piece
• Administer low level of oxygen
• Nurses need to teach patients and encourage to stop smoking

OXYGEN THERAPY
• Oxygen: the cardiac and respiratory systems supply the body with oxygen demands
• Oxygenation: 3 steps in the process of oxygenation
• Ventilation: is the process of moving air into and out of the lungs. A major muscle is the diaphragm,
innervated by the phrenic nerve with exits the spinal cord at the 4
th
cervical vertebra. Any process that
changes the bronchial diameter or width affects airway resistance and alters the rate of airflow for a given
pressure gradient during respiration. Factors that determine the lungs compliance are the surface tension
of the alveoli, and the connective tissue of the lungs. Compliance is determined by examining the volume
pressure relationship in the lungs and the thorax. Increased compliance occurs if the lungs have lost their
elasticity and the thorax is over distended. Low compliance if the lungs are stiff.
• Inspiration: the diaphragm and external intercostals muscles contract to create a negative pressure that
increases the size of the thorax. It is an active process, stimulated by chemical receptors in the aorta
• Expiration: it is a passive process that depends on the elastic recoil properties of the lungs. Clients with
COPD lose elastic recoil of the lungs and the thorax.
• Perfusion: Respiratory gases are exchange in the alveoli and the capillaries of the body tissues. (Blood
flow to the lungs and tissue). Most oxygen is transported by hemoglobin in the form of oxyhemoglobin. The
pulmonary circulation is considered a low pressure system because the systolic blood pressure in the
pulmonary artery is 20 to 30 mm Hg and the diastolic pressure is 5 to 15 mm Hg. Perfusion also is
influenced by alveolar pressure. Pulmonary artery pressure, gravity, and alveolar pressure determine the
patterns of perfusion.
• Diffusion: it occurs at the alveolocapillary membrane where molecules move from areas of higher
concentration to an area of lower concentration. Increased thickness of the membrane impedes diffusion
because gases take longer to transfer across seen in pulmonary edema, infiltrates, and effusions,
emphysema, pneumothorax, and lobectomy. Is the process by which oxygen and carbon dioxide are
exchanged at the air blood interface.
Oxygen Therapy - Factors affecting oxygenation
• Anemia: decrease O2 carrying capacity of blood.
• Toxic inhalants: reduces the amount of available hemoglobin to transport oxygen. Carbon monoxide is the
most common toxic inhalants; this bond is 200 times greater than the one with oxygen.
• Airway obstruction
• High altitude: atmospheric O2 concentration is lower
• Fever: increase metabolic rate and tissue O2 demand
• Decreased chest wall motion: prevents lowering of the diaphragm

Oxygen Therapy - Alteration in respiratory function
• Hyperventilation: excess ventilation more than required to eliminate the normal venous carbon dioxide
commonly seen in anxiety, infections, drugs, or acid base imbalances.
• Fever: increases the metabolic rate and the production of CO2
• Salicylate poisoning causes excessive stimulation of the respiratory center
• Amphetamines increase ventilation
• Acid base imbalance: the body tries to compensate for metabolic acidosis by producing a respiratory
alkalosis
• COPD: inappropriate administration of excessive oxygen results in hypoventilation because this type of
client has adjusted to high levels of carbon dioxide and their stimulus to breath is a low oxygen level. If
excessive O2 is given the O2 requirement is satisfied and the stimulus to breath is negated.
• Hypoventilation: ventilation is inadequate to meet the body’s demand or to eliminate sufficient carbon
dioxide commonly seen in atelectasis (collapse of the alveoli).
Sign and symptoms of hypoventilation:
mental status change
dysrrhythmias
cardiac arrest
convulsion
unconsciousness
death
• Hypoxia: low O2 concentration at the cellular level. Causes: low hemoglobin level, high altitudes, cyanine
poisoning, pneumonia, shock and impaired circulation as in multiple ribs fractures. Can occur from either
severe pulmonary disease or from extrapulmonary disease affecting gas exchange at the cellular level. The
need for oxygen is assessed by ABGs analysis and pulse oximetry as well as by clinical evaluation.
Sign and symptoms:
Apprehension
Restlessness
inability to concentrate
decrease level of consciousness
dizziness
behavioral changes
The patient appears fatigue and agitated
Tachycardia with tachypnea is also present.
• Cyanosis: a late sign of hypoxia although is a not reliable measure of oxygen status. Peripheral cyanosis
is often a result of vasoconstriction. Is a bluish coloring of the skin, is a very late indicator of hypoxia. The
presence or absence of cyanosis is determined by the amount of unoxygenated hemoglobin in the blood. A
patient with anemia rarely manifest cyanosis, and a patient with polycythemia may appear cyanotic may
appear cyanotic.
Oxygen Therapy - Implementation:
• The airway is patent when the trachea, bronchi, and large airways are free from obstructions. Airway
maintenance requires adequate hydration to prevent thick, tenacious secretions. Proper coughing removes
secretions and keep the airway open.
Implementation - Humidifier: adds H2O to the gas. It helps loosen and mobilize pulmonary
secretions. Needed when O2 therapy >4 liters. Nebulizer: adds moisture or medication to the
inspired air. It improves clearance of pulmonary secretions.
Implementation - CPT (chest physiotherapy): is a group of therapies use in combination to
mobilize pulmonary secretions. It includes postural drainage, chest percussion, and vibration.
Percussion and vibration is needed for those clients who produce more than 30 ml of sputum per
day.
Oxygen Therapy - Oxygen supply
• Three types of O2: compressed, liquid, and concentrators.
• O2 concentration in the air with breath is about 21%.
• OXYGEN SUPPLY
Device Flow rate O2 concentration
Nasal canula 1 L-6L 24%-44%
Face mask 5L-8L 40-60%
Venti mask 2-14 L 28-55%
Non-rebreather --------- 100%
• When the atmosphere is 21% and you give 1 liter you increase concentration.
• Respiratory system
o Medulla oblongata and the pons control inspiration and expiration
o O2 is required for oxidation of CHO, fats, and proteins
o Oxidation produces CO2
o Respiratory system is responsible O2 and CO2 transport (gas exchange)
• Respiratory system signs and symptoms
o Dyspnea: difficult or labored breathing, breathlessness, shortness of breath. Is a symptom
common to many pulmonary and cardiac disorders particularly when there is decreased lung
compliance or increased airway ressitance. Sudden dyspnea in a healthy person may indicate
pneumothorax, acute respiratory obstruction. In immobilized patients sudden dyspnea may denote
pulmonary embolism. Orthopnea (inability to breathe easily except in an upright position) may be
found in patients with heart disease and occasionally in patients with COPD. Placing the patient at
rest with the head elevated and administering oxygen sometimes achieve relief of the symptom.
o Cough: although cough is a reflex that protects the lungs form the accumulation of secretions or
the inhalation of foreign bodies, it can also be a symptom of a number of disorders of the
pulmonary system or it can be suppressed in other disorders. It results from the irritation of the
mucous membranes anywhere in the respiratory tract. The stimulus that produces a cough may
arise form an infectious process or from an air bone irritant such as smoke, smog, dust, or a gas. A
dry, irritative cough is characteristic of an upper respiratory tract infection or viral origin. Coughing
at nighttime may herald the onset of left-sided heart failure or bronchial asthma. A cough in the
morning with sputum production may indicate bronchitis. A persistent cough may affect a patient’s
quality of life and may produce embarrassment, exhaustion, inability to sleep, and pain. Cough
suppressants must be used with caution, because they may relieve the cough but do no address
the cause of the cough.
o Sputum production: a patient who coughs long enough almost invariably produces sputum.
Violent coughing causes bronchial spasm, obstruction, and further irritation of the bronchi and may
result in syncope (fainting).
Bacterial infection: a profuse amount of purulent sputum thick and yellow, green, or rust-
colored.
Viral bronchitis: thin, mucoid sputum
Chronic bronchitis: gradual increase of sputum over time
Cancer: pink-tinged mucoid sputum
Pulmonary edema: profuse, frothy, pink material, often welling up into the throat
Infection: foul-smelling sputum and bad breath point to the presence of a lung abscess,
bronchiectasis and infection caused by fusospirochetal or other anaerobic organisms.
• Relief measures: if the sputum is too thick for the patient to expectorate, is
necessary to increase water content through adequate hydration and inhalation of
aerosolized solutions. Smoking is contraindicated because it interferes with ciliary
action, increases bronchial secretions causes inflammation. The nurse encourages
adequate oral hygiene and wise selection of food. Also, encourage the patient and
family to remove sputum cups, emesis basins and soiled tissues properly
o Chest pain: chest pain associated with pulmonary conditions may be sharp, stabbing, and
intermittent. Chest pain may occur with pneumonia, pulmonary embolism and pleurisy. The nurse
assesses the quality, intensity, and radiation of pain and identifies and explores precipitating
factors and their relationship to the patient’s position. Analgesic medications may be effective in
relieving chest pain.
o Wheezing: is often major finding in a patient with bronchocostriction or airway narrowing. Oral or
inhalant bronchodilator medications reverse wheezing in most instances
o Clubbing of the fingers: is a sing of lung disease that is found in patients with chronic hypoxic
conditions, chronic lung infections, or malignancies of the lung.
o Hemoptysis: expectoration of blood form the respiratory tract is a symptom of both pulmonary and
cardiac disorders. Diagnostic evaluation to determine the cause includes several studies: chest x-
ray, chest angiography, and bronchoscopy.
o Cyanosis: a bluish coloring of the skin is a very late indication of hypoxia. The presence or
absence of cyanosis is determined by the amount of unoxygenated hemoglobin in the blood. In the
presence of a pulmonary condition, observing the color of the tongue and lips assesses central
cyanosis. Peripheral cyanosis results from decreased blood flow to a certain area of body, as in
vasoconstriction of the nail beds or earlobes from exposure to cold.
PNEUMONIA
• Inflammation of the lung parenchyma caused by an infection
• Pneumonitis: inflammatory process in the lung tissue that may predispose or place pt at risk for microbial
invasion.
• 7
th
leading cause of death in the United States, and in those over 65 years of age the 5
th
leading cause.
• Caused by various microorganisms including bacteria, mycobacteria, chamydiae, mycoplasma, fungi,
parasites, and viruses.
Pneumonia classification:
• Community acquired pneumonia: (CAP) onset prior to hospitalization or within the first 48 hours of
hospitalization. The causative agents for CAP are S. pneumoniae, H. influenzae, Lengionella,
Pseudomonas aeruginosa.
o Pneumonia caused by s. pneumoniae is the most common CAP in people younger than 60
years of age. Most prevalent in winter and spring. Lives in the upper respiratory tract. It may occur
as a lobar or bronchopneumonic form in patients of any age and may follow a recent
o mycoplasma pneumonia occurs most in children and young adults and is spread by person to
person.
o H. influenzae: affects elderly people and those with COPD, alcoholism, diabetes mellitus. Chest x-
ray may reveal multibolar, patchy bronchopneumoniae or areas of consolidation (tissue that
solidifies as a result of collapsed alveoli or pneumonia).
• Hospital acquired pneumonia: (HAP): onset 48 hours after admission. Also know as nosocomial
pneumonia. Occurs when at least one of the three conditions exits: host defenses are impaired, and
inoculum of organisms reaches the lower respiratory tract and overwhelms the host’s defenses. The
common organism responsible for HAP include the pathogens E. coli, h. influenzae, serratia marcescens,
p. aeruginosa, MRSA, s. pneumoniae.
o Pseudomonal pneumonia: occurs in patients who are debilitated, those with altered mental
status, and prolonged intubation
o MRSA: highly virulent. Patients with MRSA are isolated in a private room, and contact precautions
are used.
o Pneumonias from E. coli, proteus, serratia are characterized by destruction of lung structure
and alveolar walls, consolidation and bacteremia.
• Pneumonia in the immunocompromised host: occurs with use of corticosteroids or othter
immunosuppressive agents, chemotherapy, nutritional depletion, use of broad spectrum antimicrobial
agents, AIDS, genetic immune disorders. Patients with compromised immune system commonly develop
pneumonia from organisms of low virulence. Can be caused by host seen in CAP, HAP (s. pneumoniae, s.
aureus, h. influenza, p. aeruginosa, m. tuberculosis.) has a subtle onset, with progressive dyspnea, fever,
and nonproductive cough. The organism that causes CPC is pneumocystitis carinii.
• Aspiration pneumonia: refers to pulmonary consequences resulting form entry of endogenous or
exogenous substances into the lower airway. Common pathogens are S. pneumoniae, h. influenzae, s.
aureus. Other substances can be aspirated such as gastric contents, exogenous chemical contents. This
type of aspiration or ingestion may impair lungs defenses, cuase inflammatory changes and lead to
bacterial growth and resulting of pneumonia.
• Broncho pneumonia: pneumonia that is distributed in a patchy fashion, having originated in one or more
localized areas whitin the bronchi and extending to the adjacent surrounding lung parenchyma.
• Lobar pneumonia: substantial portion of one or more lobes. An entire lobe is consolidated.
• Pneumonia Risk factors:
o Heart failure: risk for pneumoccocal disease because of chronic illness
o Diabetes: risk for pneumoccocal disease because of chronic illness
o Alcoholism: alcohol suppresses the body’s reflexes, may be associated with aspiration, and
decreases white cell mobilization and ciliary motion.
o COPD: condition that produces mucus or bronchial obstruction and interfere with normal lung
drainage.
o AIDS: compromised defenses against infections
• Pneumonia Sign and symptoms
o Sudden onset of shaking chills
o Rapidly raising fever (101-105 degree)
o Pleuritic chest pain (aggravated by deep breathing and cough)
o Tachypnea (25-45 b/min)
o SOB (shotness of breath)
o Tachycardia and bounding pulse
o Pt may exhibit orthopnea (shortness of breath when reclining)
o Appetite is poor
o Sputum is purulent
• Walking pneumonia signs and symptoms
o Headache
o Low grade fever
o Pleuritic pain
o Myalgia
o Pharyngitis
o Mucopurulent sputum
o Consolidation CXR
o COPD (purulent sputum may be the only sign)
• Pneumonia Diagnostic tools
o The diagnosis of pneumonia is made by history, physical exam, chest x-ray, blood culture CBC
(increased WBC), sputum examination
o The sputum example is obtained by having pt rinsing the mouth with water, breath deeply, cough
deeply, and expectorate the raised sputum. Also, it may be obtained from a bronchoscopy.
• Pneumonia Management
o Antibiotics for bacterial infectiosn
o Supportive treatment for viral infections
o Respiration support measures
O2 administration
Endotracheal intubation
Mechanical ventilation
o Prompt administration (within 4 to 8 hours) of antibiotics in patients in whom CAP is strongly
suspected or confirmed is the key treatment meauser.
o For patients with MRSA vaconmysisn is used.
o The recommended duration of treatment for pneumoccocal pneumonia is 72 hours after the patient
become afebrile. Patient with most other forms of pneumonia caused by bacterial pathogens are
treated for 1 to 2 weeks after they become afebrile. Those with atypical pneumonia are usually
treated for 10 to 21 days.
• Pneumonia Nursing interventions:
o Improve airway patency: remove secretions is important. The nurse encourage hydration.
Humidification may be used to loosen secretions and improve ventilation. The nurse encourages
the patient to perform an effective, directed cough. Chest physiotherapy is important. Change
position and after that encourage patient to breathe deeply and cough.
o Promote fluid intake: encourage fluid intake of at least 2 liter per day, unless contraindicated
o Maintain adequate nutritional intake: fluids such as Gatorade may help provide fluid, calories, and
electrolytes. In addition, IV fluids and nutrients may be administered if necessary
o Promote rest
• Pneumonia Nursing diagnosis
o Ineffective airway clearance related sputum production
o Activity intolerance
o Risk for deficient fluid volume related fever and dyspnea
o Imbalance nutrition: less than body requires
o Knowledge deficit related treatment regimen
EMPHYSEMA
• Impaired gas oxygen and carbon dioxide exchange results from destruction of the walls of overdistended
alveoli.
• An abnormal distention of the air spaces beyond the terminal bronchioles with destruction of the walls of
the alveoli.
• It is the end stage of a process that has progressed slowly for many years.
• The alveolar surface area in direct cotact with the pulmonary capillaries continually decreases causing
impaired oxygen diffusion, which leads to hypoxemia.
• In the later stages of the disease CO2 elimination is impaired resulting in an increased CO2 in arterial
blood ( hypercapnia) and causing respiratory acidosis.
• Right sided heart failure ( cor pulmonale) is one of the complications of emphysema.
• Hypercapnea:
o CO2 elimination is impaired
o Increased CO2 tension in the arterial blood
o Respiratory acidosis
o Increased pulmonary blood flow
o Right ventricle is forced to maintain a higher BP in the pulmonary arteries
o Right sided failure (cor pulmonale) most common complication
o Types of emphysema
Palobular and centrilobular signs and symptoms
• Hyperinflated chest (barrel chest)
• Weight loss
• Polycythemia
• Central cyanosis
• Emphysema - Risk factors
o 80% exposure to tobacco smoke
o Occupational exposure
o Air pollution
o Genetic abnormalities
Cigarette smoking
• It depress the activity of the scavenger cells
• Affects the ciliary’s cleansing mechanism
• Free passage of inhaled irritants, bacteria, and other foreign matter
• Obstruction of air flow, and air becomes trapped behind the obstruction
• Irritates the globet cells and mucous glands
• Increase accumulation of mucous
• Formation of carboxyhemoglobin equal less O2 carry capacity
• Emphysema - Sign and symptoms
o Cough
o Sputum
o Dyspnea on exertion
o Weight loss due to dyspnea and the use of energy and accessory muscles for respiration
o Barrel chest
o Ribs fixation in the inspiratory position
o Shoulders to heave upward
o Anxiety
o Fatigue
• Emphysema - Diagnostic findings
o Pulmonary function studies
Perfusion
Diffusion
Ventilation
o ABGs
o Spirometry
o CXR
o Electrolyte studies
• Emphysema - Complications
o Respiratory insufficiency
o Respiratory failure
o Pneumonias
o Atelectasis
o Pneumothorax
o Cor pulmonale
• Emphysema - Management
o Smoking cessation is the most important and effective treatment
o Medications (improve breathing)
Bronchodilators (albuterol): relieve bronchospams and reduce airway obstruction by
allowing increased oxygen distribution throughout the lungs and improving alveolar
ventilation.
Diuretics: decrease the fluids retained on the lungs
Corticosteroids: decrease inflammation of the alveolis
o Influenza (flu) vaccines every year
o Pneumovax (pneumonia vaccine) every 5 years
o Lung reduction surgery
o Bullectomy
o Lung transplant
o Oxygen therapy
Hypoxemia: stimulates breathing, high flow of O2 will suppress the respiration drive
High O2 administration equal increased CO2 retention
• Emphysema - Nursing implementations
o Promoting smoking cessation: the nurse must discuss smoking cessation strategies with the
patient. The nurse should educate the patient regarding the hazards of smoking and cessation
strategies and provide resources regarding smoking cessation, counseling and formalized
programs available in the community
o Improve gas exchange and airway clearance: monitor patient for dyspnea and hypoxemia. The
nurse instructs the patient in directed or controlled coughing. Chest physiotherapy with postural
drainage, intermittent positive pressure breathing, increased fluid intake.
o Improve activity tolerance: education is focused on rehabs therapies to promote independence in
executing activities of daily living.
o Promote self -care: emphasize the importance of setting goals, avoiding temperature extremes,
and modifying lifestyle.
o Monitor complications: the nurse must assess for various complications of COPD such as
atelectasis, infections. Cognitive changes, increased dyspnea, tachypnea, tachycardia, hypoxemia.
The nurse monitors pulse oximetry values to assess the patient’s need for oxygen and administer
supplemental oxygen.
COPD
• Chronic obstructive pulmonary disease: airflow limitation, and irreversible condition.
o Includes chronic bronchitis, emphysema, and asthma (reversible inflammation)
o Currently COPD is the fourth leading cause of mortality and the 12
th
leading cause of diability in the
USA.
o 5
th
leading cause of death among men and 4
th
for women, 3
rd
cause of home care services
o Incidence increases with age
• Chronic bronchitis
o Disease of the airway, is defined as the presence of cough and sputum production for at least 3
months in each of two consecutive years.
o How chronic bronchitis occurs:
Higher incidence in the winter months
Inspired irritants
Increased mucous production
Impaired ciliary function
Thick and tenacious mucous perfect medium for bacteria to growth
Increase susceptibility to infections
Inflammation and thickness of bronchial wall
Airway obstruction, air trapping, dyspnea
Hypventilation (increased CO2) and hypoxemia
o Chronic Bronchitis Risk factors:
Active and passing smoking
Genetics
Occupational exposure
Air pollution
o Chronic Bronchitis Sign and symptoms
Productive cough (smoker cough)
Activity intolerance
SOB, wheezing
Hypoxemia
Polycythemia
Cyanosis
Pulmonary hypertension
o Chronic Bronchitis Management:
Bronchodilators
Expectorants
Chest physiotherapy
Antibiotics
Steroids (late)
Low-flow oxygen
o Chronic Bronchitis Nursing implementation (teaching)
Nutrition: counseling about meal planning and supplementation is part of the rehabiliation
process. Continual monitoring of weight and interventions as necessary are important part
of the care of patients with COPD.
Respiratory hygiene
Recognition of early signs of infection
Techniques to relieve dyspnea (pursued lips breathing): pursued lip breathing helps slow
expiration, prevent collapse of small airways, and control the rate and depth of respiration.
It also promotes relaxation, which allows patients to gain control of dyspnea and reduce
feeling of panic
ASTHMA
• Asthma is chronic inflammation disease of the airways that causes airway hyperresponsivenss, mucosal
edema, and mucus production. This inflammation ultimately leads to recurrent episodes of asthma
symptoms: cough, chest tightness, wheezing, and dyspnea.
• Asthma differs from other obstructive lung diseases in that it is largely reversible, either
spontaneously or with treatment.
• Asthma (how it happens)
o Airway hyper response
o Mucosal edema: recurrent episodes (cough, chest tigness, wheezing)
o Reduction of airway diameter and bronchospasm
o Mucous production
o Bronchi obstruction
• ASTHMA Classification based on severity
o Step 1: mild intermittent (symptoms no more than two weeks)
o Step 2: mild persistent (symptoms more than two weeks, but less than once/day)
o Step 3: moderate persistent ( daily symptoms)
o Step 4: severe persistent (continual symptoms)
• ASTHMA Triggers
o Airway irritants (air pollutants, cold, heat, weather changes, strong odors or perfume, smoke)
o Exercise
o Medications
o Post nasal drip
o Viral respiratory tract infections
o Gastroesophageal reflux
• ASTHMA Sign and symptoms
o Attacks: night or early morning ( circadian variations that influence airway receptor thresholds)
o Cough, dyspnea, wheezing ( the most common symptoms of asthma)
o Chest tightness
o Prolonged expiration ( expiration requires effort and becomes prolonged)
o Diaphoresis, tachycardia, widened pulse
o Hypoxemia
o Central cyanosis
• ASTHMA Diagnostic tools
o Family, environmental, and occupational history
o Increased serum levels of immunoglobulin E (allergy)
o Increased eosinophils
o Spirometry
• Decreased expiratory flow rate
• Decreased forced expiratory volume
• Increase total lung capacity
o ABGs
Hypoxemia
Early respiratory alkalosis or late respiratory acidosis
• ASTHMA Complications
o Status asthmaticus
o Respiratory failure
o Pneumonia
o Atelectasis
• ASTHMA Management medications
o Short acting meds
Beta adrenergic agonist
o Long acting medications
Corticosteroids ( most potent and effective anti inflammatory medications )
Beta adrenergic agonist (control asthma symptoms at night)
Leukotriene modifiers ( are potent bronchoconstrictors that also dilate blood vessels and
alter permeability
• ASTHMA Nursing interventions
o Monitor severity of symptoms
o Breath sounds
o Pulse oxymetry
o Vital signs
o Administer fluids
o Teach the pt to rinse mouth after inhaled corticosteroids use
o Advise smoking cessation and to avoid allergens
• ASTHMA Nursing diagnosis
o Ineffective airway clerance
o Knowledge deficit related to disease process
o noncompliance

Muscoloskeletal chapters (66-69)

Class notes

• A fracture is a break in the continuity of the bone. It happens when there is trauma to
the bone.
• Risk factors: bone cancer, osteoporosis
• Osteoporosis: brittle bones
• Osteomalacia: soften of the bones (lack of calcium, vitamin D)
• Osteomyelitis: infections of the bone
• Diagnostic tools: x-ray, CT scan, bone scan, MRI
• Bone scan: athletes use it the most
• Complete fracture: complete cut in the bone. Require surgery most of the time. Aligning
of the bones.
• Incomplete: greenstick (irregular) it doesn’t go directly to the bone. The bones still attach.
• Communited fracture: a lot of bone pieces
• Avascular necrosis: dying of the bone. You need bone transplant
• Open fracture: the piece of bone comes out through the skin.
• Open fracture wounds:
o Grade 1: clean wound and less than 1 cm
o Grade 2: clean wound but larger. Not too much trauma to the skin
o Grade 3: highly contaminated, dirty, big, really bad
• Stress fracture: you can hardly see it on an x-ray. Common in athletes (runners, aerobic
instructors). It is a fine fracture. Most common in lower extremities
• Sign and symptoms
o #1 pain
o Loss of function
o Deformity
• Pain at fractures is constant. Immobilize first the extremeties and then administer
analgesics
• Loss of function: bone affected because of the pain
• Deformity; malformation secondary to fracture
• Shortening: common in hip fracture
• Hip fracture: classic sign is shortening of the extremity that is fracture
• Crepitus: feeling of bone rubbing.
• Echymosis, hematoma in the affected area
• Prevention:
o Vitamin D, calcium
o Delay and decreased severity of osteoporosis
o Activity
o Smoking
o Alcohol intake
• Goal: reduction, immobilize extremities, to regain normal strength and function through
rehab
• Priority:
o Immobilize the affected area
o Moving: hold above the fracture and below the fracture
o Open fracture: cover the bone with sterile dressing to prevent further
contamination with normal saline to keep moist. Then proceed with
immobilization.
o Do not reduce fraction. It is done by the doctor
• Reduction: realignment of the fracture bone. Surgery as soon as possible to prevent
further damage
• Pt having orthopedic surgery loose a lot of blood
• Place the pt in traction. The weight should be hanging so it can pull the skin.
• Close reduction: manipulate from the outside
• Open reduction: surgery
• Most fractures heal in 4-6 weeks (simple fractures)
• The swelling and strength takes another 4-6 weeks.
• Simple fractures heal in 8-12 weeks
• Complications
o Compartment syndrome
o Fat embolism
o Gas gangrene (1-14 days after fracture)
o Thromboembolus
o Delayed complications (most common in elderly)
• Compartment syndrome: takes 6 hr in order to cause severe damage (permanent
damage) to lower extremities. Cast is very tight and there is swelling. That pressure
compress the veins and arteries. There is some nerve damage, no blood supply. this can
lead to permanent damage and avascular necrosis happens.
• It is very important to assess the cast
• The result from compartment syndrome is irreversible muscle ischemia within 6
hours.
• Compartment syndrome assessment
o Assess pain (pain is not relief with anything) localized everywhere.
o Assess for numbness and tingling
o Assess for ability to flex and move fingers
o Assess skin temp, color, and pulsations
• The difference between fracture pain and compartment syndrome pain is that
compartment syndrome pain is unrelieved.
• The first thing you do is elevate the extremities to relief pressure and pain in
compartment syndrome
• Do not document that the patient has dorsalis pedis pulse when there is a cast covering
the foot.
• Application of cold packs and removal of dressing you need to call physicians
• To test for tightness of the cast put your finger in and you should be able to put some
• The nurse needs to assess the cast edges for erythema and irritation
• Instruct pt not to put anything inside the cast
• Handle cast by grabbing it from the bottom. Do not grab it from the top. You may cause
indentation on the cast
• Skin traction: weight should be hanging to pull the skin.
• Phantom pain: pt tells you they have pain in an amputated limb.
• You need to believe the pt pain and administer pain medications
• Osteomyelitis: infection of the bone. Treatment with IV antibiotics
• ORIF: open reduction internal fixator
• 45-70% with orthopedic surgeries develop DVT. You need to administer anticoagulant
postoperative to the pt
• 20% orthopedic postoperative to the pt develop pulmonary embolism and 3% result in
death
• Prevention of joint dislocation prosthesis (until 4 months)
o do not cross the legs
o shouldn’t sit in more than 60 degrees
o use high seat and high toilet seats
o prevent bending 90 degree
o place pillow between legs
• Dislocation: pt tells, “I felt something pop up”.
• You need to take pt to bed, call the physician. Provide pain medication, keep pt as flat as
possible
• AMPUTATION

o Is the removal of a body part, usually an extremity. Amputation of a lower
extremity is often necessary because progressive peripheral vascular disease.
Amputation is used to relieve symptoms, to improve function, and most
importantly to save or improve the patient’s quality of life.
o Perform at the most distal point that will heal successfully. The site of
amputation is determined by two factors: circulation in the part and functional
uselfuness.
AEA (above elbow amputation)
BEA (below elbow amputation
AKA (above knee amputation)
BKA (below knee amputation)
o Contributing factors
Fulminating gas gangrene
Trauma
Congenital deformities
Chronic osteomyelitis
Malignant tumors
o Advantages
Relieve symptoms
Improve function
Save pt’s life (sepsis)
o Complications
Hemorrhage: because major blood vessels have been severed, massive
bleeding may occur.
Infection: is a risk with all surgical procedures. It increases with
contaminated wounds after traumatic amputation.
Skin breakdown: skin irritation caused by the prosthesis.
Phantom limb pain: is caused by severing of peripheral nerves
J oint contracture: caused by positioning and a protective flexion
withdrawal pattern associated with pain and muscle imbalance
o Influencing factors:
Muscle and skin perfusion are evaluated with Doppler flow meter,
segmental BP readings, and PaO2 levels. The circulatory status of the
extremity is evaluated through physical examination and diagnostic
studies.
Preservation of knee and elbow joint for post-op prosthesis use
Staged amputation: (1
st
guillotine amputation is done to remove the
infected tissue and systemic ABTs (antibiotics) therapy is started) few
days after 2
nd
stage an amputation with skin closure is done.
o Management:
The objective of treatment is to achieve healing of the amputation
wound, the result of being a non-tender residual limb with healthy skin
for prosthesis use.
Gentle handling of the residual limb, control of residual limb edema
through rigid enhances healing or soft compression dressings, and use
of aseptic technique in wound care to avoid infection.
Systemic antibiotics (ABTs)
o Nursing implementation
Assessment (post-op): evaluate the neurovascular and functional status
of the extremity through history and physical assessment. Assess
circulatory status and function of the unaffected extremity. Evaluate the
patient nutritional status. Assess the psychological status. Assess
circulatory status of residual limb and unaffected one. Assess function of
residual limb and unaffected one. Signs and symptoms of infection
(enlarge lymph nodes, fever, drainage, increased WBC, erythema,
wound dehiscence). Assess for concurrent health conditions such as
dehydration, anemia, cardiac insufficiency, chronic respiratory problems
and diabetes mellitus. Assess grief response.
Pain management: evaluation of the patient’s pain and responses to
interventions is an important part of the nurse’s role in pain
management. Surgical pain can be controlled with analgesics.
Minimize altered sensory perception: when a patient describes phantom
pains or sensations the nurse acknowledges these feelings and helps
the patient modify these perceptions. Distraction techniques and activity
are helpful. In addition, beta-blockers may relieve dull, burning
discomfort; antiseizure medications control stabbing and cramping pain;
and tricyclic antidepressants are used to improve mood and coping
ability. Phantom pain described as usual sensation before the
amputation. Numbness, tingling, cramps, pain, presence of the
amputated extremity, legitimate feelings. The cause is unknown.
Promotion of wound healing: whenever dressing is changed, aseptic
techniques is required to prevent wound infection and possible
osteomyelitis. The nurse instructs the patient and family in wrapping the
residual limb with elastic dressings. Monitor signs and symptoms of
infection. Proper handling of limb
Increase level of activity: postoperative ROM exercises are started early
because contracture deformities develop rapidly. Strength and
endurance are assessed and activities are increased gradually to
prevent fatigue.
Promotion of self-care: the patient is encouraged to be an active
participant in self -care. The nurse encourages the patient to do self-
care activities. The nurse and the therapist work with the patient to
achieve maximum independence. Encourage pt to actively participate in
self-care. Independence in toileting, dressing, bathing.
o Prevention of contractures
Encourage patient to turn from side-to-side and to assume prone
position: prevents flexion contractures of the hips
ROM of knee: important for prosthesis fitting
Use of over-head trapeze to strengthen the biceps
• FRACTURES
o A fracture is a break in the continuity of bone and is defined according to its type
and extent.
o Fractures occur when the bone is subjected to stress greater that it can absorb.
o Direct blows, crushing forces, sudden twisting motions, and extreme muscle
contractions cause fractures.
o Risk factors:
Tumor
Osteoporosis
Osteomyelitis
Osteomalacia
Can cause the bone to break regardless of trauma
o Diagnostic tools
X-ray of the affected area
CT scan to evaluate the degree of displacement, and for compression
fractures
Bone scan, useful to identify occult stress fractures
MRI to detect lesions that affect the bone
o Types of fractures
Complete fracture: involves a break across the entire cross-section of
the bone and is frequently displaced (removal from its normal position)
Incomplete fracture (eg. Greenstick fracture): involves a break through
only part of the cross-section of the bone.
Comminuted fracture: is one that produces several bone fragments
Closed fracture (simple fracture): is one that does not cause a break in
the skin.
Open fracture (compound, or complex, fracture): is one in which the skin
or mucous membrane wound extends to the fracture bone.
o Open fractures are graded according to the following criteria:
Grade I is a clean wound less than 1 cm long
Grade II is a larger wound without extensive soft tissue damage
Grade III is highly contaminated, has extensive soft tissue damage, and
is the most severe.
o Stress fracture
Fine fracture line that results from indirect trauma to the bone.
Not easily seen in x-rays
Most commonly seen in athletes: runners who participate in repetitive
activities (jumping).
Most common sites: calcaneous, patella, metatarsal, etc.
o Fracture signs and symptoms
Pain: the pain is continuous and increases in severity until the bone
fragments are immobilized.
Loss of function: after the fracture the extremity cannot function properly
because normal function of the muscles depends on the integrity of the
bones to which they are attached. Pain contributes to the loss of
function.
Deformity: displacement, angulation, or rotation of the fragments in a
fracture of the arm or the leg causes a deformity that is detectable when
the limb is compared with he uninjured extremity.
Shortening: in fractures of long bones, there is actual shortening of the
extremity because of the contraction of the muscle that are attached
distal and proximal to the site of the fracture.
Crepitus: when the extremity is examined with the hands, a grating
sensation is felt. Caused by the rubbing of the bone fragments against
each other.
Local swelling and discoloration: localized edema and discoloration of
the skin (ecchymosis) occurs after fracture.
o Prevention and screening
Weight bearing and physical activity – makes the bone stronger and
reduces calcium loss
Adequate dietary intake of calcium
Avoid smoking
Avoid excessive alcohol intake
o Management:
Goal: reduction, immobilization, and regaining normal strength and
function through rehab
Emergency care:
• Immediately after injury, whenever a fracture is suspected, it is
important to immobilize the body part (priority #1) before the
patient is moved. If an injured patient must be removed from a
vehicle before splints can be applied, the extremity is supported
distal and proximal to the fracture site to prevent rotation as well
as angular motion.
• With an open fracture, the wound is covered with a sterile
dressing to prevent contamination of deeper tissue. No attempt
is made to reduce the fracture, even if one of the bone
fragments is protruding through the wound.
Reduction:
• Reduction of a fracture refers to restoration of the fracture
fragments to anatomic alignment and rotation. The physician
reduces a fracture as soon as possible to prevent loss of
elasticity from the tissues through infiltration by edema or
hemorrhage. In most cases reduction becomes more difficult as
the injury begins healing. Before fracture reduction and
immobilization, the patient is prepared for the procedure,
permission is obtained, and an analgesic is administered.
o Close reduction: is accomplished by bringing the bone
fragments into apposition through manipulation and
manual traction. The immobilizing device maintains the
reduction and stabilizes the extremity for bone healing.
X-rays are obtained to verify that the bones are
correctly aligned.
o Open reduction: through surgical approach, the fracture
fragments are reduced. Internal fixation devices such as
pins, wires, screws, plates, nails or rods may be used to
hold the bone fragments in position.
o Fractures complications:
Factors that can impair fracture healing include:
1) inadequate fracture immobilization,
2) inadequate blood supply to the fracture site or adjacent tissue, 3)
extensive space between bone fragments,
4) interposition of soft tissue bone ends,
5) infection,
6) metabolic problems.
Compartment syndrome: occurs when there is increased tissue
pressure within a limited space (eg, cast, muscle compartment) that
compromises the circulation and the function of the tissue within the
confined area. (an anatomic compartment is an area of the body
encased by bone or fascia that contains muscles, nerves, and blood
vessels.) Is a complication that develops when pressure within a
compartment is greater than normal. The patient complains of deep,
throbbing, unrelenting pain, which continues to increase despite the
administration of opioids and seems out of proportion to the injury. A
hallmark sign is pain that occurs or intensifies with passive ROM.
The pain can be caused by reduction in size of the muscle compartment
because the enclosing muscle fascia or an increase in compartment
contents because of edema or hemorrhage. The pressure within a
muscle compartment may increase to such an extent as to decrease
microcirculation, causing nerve and muscle anoxia and necrosis.
Permanent function can be lost if the anoxic situation continues for
longer than 6 hours. Paralysis, sensory loss, and permanent disability
occur within the next 24-48 hours.
• Compartment syndrome assessment
o Frequent assessment of neurovascular function after a
fracture is essential and focuses on the 5 P: pain,
paralysis, paresthesia, pallor, and pulselessness.
Sensory deficits include: deep, throbbing, escalating
pain that increases with passive stretching.
Paresthesia (burning and tingling sensation) and
numbness are early signs of nerve involvement. Ask the
patient to move the fingers or toes. Peripheral
circulation is evaluated by assessing color, temperature,
capillary refill, swelling, and pulses.
o Medical management: prompt management of acute
compartment syndrome is essential. The physician
needs to be notified immediately if neurovascular
compromise is suspected. Is managed by elevation of
the extremity to the heart level, release of restrictive
devices. Application of cold packs. Remove restrictive
dressing (elastic bandage). Assess dressing for
drainage and tightness
o Nursing documentation: patient with right lower
extremity cast, from below the knee to the toes. Toes
with good color, warm to touch, capillary refill within 2
seconds. Pt is able to wiggle his toes with minimal
discomfort, as voiced. Right popliteal pulse present,
strong and equal to left one.
Fat embolism: at the time of fracture, fat globules may diffuse into the
vascular compartment because the marrow pressure is greater than the
capillary pressure. The fat globules may occlude the small blood vessels
that supply the lungs, brain, kidneys, and other organs. The onset of
symptoms is rapid, usually within 24 to 72 hours of injury. Presenting
features include hypoxia, tachypnea, tachycardia, and pyrexia. Cerebral
disturbances are manifested by mental status changes varying from
headache and mild agitation to delirium to coma. Immediate
immobilization of fractures, minimal fracture manipulation, adequate
support for fractured bones during turning and positioning, and
maintenance of fluid and electrolyte balance are measures that may
reduce the incidence of fat emboli.
Gas gangrene (1-14 days post fracture)
Thromboembolus: includes DVT and PE (pulmonary embolism).
Immobility, bed rest put patients at risk for thromboembolus.
Delayed complications (delayed union or no-union): nonunion results
from failure of the ends of a fractured bone to unite, whereas malunion
result from failure of the ends of fracture bone to unite in normal
alignment. Factors contributing to nonunion and malunion include
infection at the fracture site, interposition of tissue between the bone
ends, inadequate immobilization or manipulation that disrupts callus
formation, excessive space between bone fragments, limited bone
contact, and impaired blood supply resulting in AVN (avascular
necrosis)
o Cast care:
A cast is a rigid external immobilizing device that is molded to the
contours of the body. A cast is used specifically to immobilize a reduced
fracture, to correct deformity, to apply uniform pressure to underlying
soft tissue, or to support and stabilize weakened joints.
Nursing implementation:
• Observe skin at cast edges for erythema and irritation
• Assess for signs and symptoms of infection (odor and drainage
coming from under the cast)
• Elevate casted extremity
• Assess for neuro-vascular changes of the affected extremity.
• Pruritus:
o Instruct pt to gently rub the area below and above the
cast to retard the desire to scratch
o Not to stick sharp objects underneath the cast
o Use of diversional activities
• Weight bearing (as per MD orders)
• Handling the new cast
o Support the wet cast with palm of the hands to avoid
indentations that cause pressure on underlying skin
o Placed the casted extremity on pillows
A patient’s unrelieved pain must be immediately reported to the
physician to avoid possible paralysis and necrosis.
The nurse must never ignore complaints of pain from the patient in a
cast because of the possibility of problems, such as impaired tissue
perfusion or pressure ulcer formation.
o Skin traction
Skin traction is used to control muscle spams and to immobilize an area
before surgery. Skin traction is accomplished by using a weight to pull
on traction tape or on a foam boot attached to the skin.
The use of weight to exert pulling force on the affected extremity
Provides support and comfort (treatment of muscle spasm)
Temporally measure until more definitive treatment is initiated
Potential complication: skin breakdown, nerve pressure, and circulatory
impairment.
Nursing diagnosis related to fracture
• Risk for trauma related to loss of skeletal integrity, movement of
skeletal fragments, use of traction
• Acute pain related to muscle spasm, movement of bone
fragments, tissue trauma/edema, or traction/immobility device
• Risk for peripheral neurovascular dysfunction
• Impaired physical mobility related to pain, discomfort, and
restrictive devices.
o OSTEOMYELITIS
Osteomyelitis is an infection of the bone. The bone becomes infected in
one of three ways:
• Extension of soft tissue infection
• Direct bone contamination from bone surgery, open fracture, or
traumatic injury
• Hematogenous spread from other sites of infection.
Osteomyelitis is an infection of the bone that can be caused by microbial
agents. Osteomyelitis affects about two out of every 10,000 people.
Osteomyelitis etiology:
• An open injury to the bone:
o Open fracture
• An infection from elsewhere in the body:
o Spread to the bone through the blood
• A minor trauma:
o Can lead to a blood clot around the bone creating a
medium for bacteria growth
• Bacteria in the bloodstream:
o Localized infection of the bone, resulting in destruction
of the bone tissue, however new bone often forms
around the site
• A chronic open wound or soft tissue infection:
o Extending to the bone surface
Osteomyelitis risk factors:
• Diabetes
• Patients receiving hemodialysis
• Immuno-compromised patients
• Sickle cell disease
• Intravenous drug abusers
• The elderly
Osteomyelitis signs and symptoms
• Pain/and or tenderness in the infected area
• Swelling and warmth in the infected area
• Fever
• Nausea, secondarily from being ill with infection
• Drainage of pus through the skin
• Excessive sweating
• Chills
• Lower back pain
• Swelling of the ankles, feet, and legs
• Changes in gait (walking pattern that is painful, yielding a limp)
Diagnostic tools:
• Blood tests: (elevated WBC and ESR (erythrocyte
sedimentation rate)
• Blood culture: a blood culture is a test used to detect the
causative micro-organism
• Needle aspiration: to obtain a specimen for culture and
sensitivity.
• Biopsy: tissue sample
• Bone scan: a small amount of technetium 99 pyrophosphate is
injected. If the bone tissue ishealthy, the material will spread in
an uniform fashion. However, a tumor or infection in the bone
will absorb the material and show an increased concentration of
the radioactive material. Detect abnormality before x-rays.
Management:
• Goal: to control and halt the infective process. Eliminate the
infection and prevent the development of chronic infection
• Antibiotic therapy depends on the result of blood and wound
cultures
• The area affected with osteomyelitis is immobilized to decrease
discomfort and to prevent pathologic fracture of the weakened
bone.
• As soon as the culture specimens are obtained, IV antibiotic
therapy begins, based on the assumption that infection results
from a staphylococcal organism that is sensitive to a
semisynthetic penicillin.
• Surgery: destroyed bone is scrapped out. In the case of spinal
abscesses, surgery is not performed unless there is
compression of the spinal cord or nerve roots
• Some cases of chronic osteomyelitis can be so resistant to
treatment that amputation may be required.
• Chronic infectious draining sites can evolve into a squamous
cell type of skin cancer (rare)
o ORTHOPEDIC SURGERY
Many patients with musculoskeletal dysfunction undergo surgery to
correct the condition.
Conditions that may be corrected by surgery include unstabilized
fracture, deformity, joint disease, necrotic or infected tissue, and tumors.
Frequent surgical procedures include ORIF (open reduction internal
fixator) and closed reduction with internal fixation.
Orthopedic surgery goal: improving function by restoring motion and
stability and relieving pain and disability.
Surgical procedures:
• ORIF: open reduction with internal fixation
• Closed reduction with internal fixation (bone fragments are not
surgically exposed)
• Arthroplasty: the repair of joint problems through the operating
arthroscope or through open joint surgery
• Meniscectomy: the excision of damaged joint fibrocartilage
• J oint replacement: the replacement of the joint surfaces with
metal or synthetic materials
• Amputations: the removal of a body part
• Bone graft: the placement of bone tissue to promote healing to
stabilize, or to replace disease bone
• Tendon transfer: the movement of tendon insertion to improve
function
• Athrodesis: immobilizing fusion of a joint
• Fasciotomy: the incision and diversion of the muscle fascia to
relieve muscle constriction, as in compartment syndrome, or to
reduce fascia contracture.
• J oint replacement:
o Patient with severe joint and disability may undergo joint
replacement. Conditions contributing to joint
degeneration include osteoarthritis (degenerative joint
disease), rheumatoid arthritis, trauma, and congenital
deformity. Some fractures may cause disruption of the
blood supply and subsequent avascular necrosis. J oints
frequently replaced include the hip, knee, and finger
joints. Less frequently more complex joints shoulder,
elbow, wrist, ankle are replaced.
o Procedures: most joint replacement consist of metal
and high density polyethylene components. The joint
implants may be cemented in the prepared boen with
polymethyl methacrylate. Press fit, ingrowth prostheses
tha allow the patient’s bone to grow into and securely fix
the prosthesis in the bone are alternative to cement
prosthese. With joint replacement, excellent pain relief
is obtained in most patients. Return of motion and
function depends on preoperative soft tissue condition,
soft tissue reactions, and general muscle strength.
Total hip replacement: is the replacement of a severely damaged hip
with an artificial joint. Indications for this surgery include arthritis, femoral
neck fractures, and conditions resulting from congenital hip disease. The
surgeon selects the prosthesis that is best suited to the individual
patient, considering various factors, including skeletal structure and
activity level. Most consist of a metal femoral component topped by a
spherical ball fitted into a plastic acetabular socket.
Complications:
• Dislocation of the hip prosthesis, excessive wound drainage,
thromboembolism, infection, and heel pressure ulcer. Other
complications are related to immobility, heterotopic ossification
(formation of bone in the periprosthetic space), avascular
necrosis, and loosening of the prosthesis
Nursing interventions:
• Obtain baseline assessment of the affected extremity:
• Prevent infection: prophylactic antibiotics are prescribed. If
indwelling urinary catheters or portable wound sucntion devices
are used, they are removed as soon as possible to avoid
infection. Acute infection may occur within 3 months after
surgery. Adhere to strict aseptic techniques in the OR. Monitor
for sign and symptoms of infection. Avoid osteomyelitis. Hand
washing
• Monitor wound drainage: expect wound drainage of 200-500 ml
day one post. Mark borders of drainage in the dressin.
Reinforce initial surgical dressing as needed. Accurate intake
and output. Monitor for active bleeding under patient dressing
• Promote increase level of activity: assist patient with early
ambulation as ordered. OOB to bed chair, standing for short
periods to walking for progressing greater distance. Watch for
orthostatic hypotension. Weight bearing as ordered. Use of
appropriate assistive devices such as walker and or cane.
• Prevention of DVT: the incidence of DVT is 45 to 70%. The
peak occurrence is 5 to 7 days after surgery. About 20% patient
with DVT develop pulmonary embolism of which 3% of cases
are fatal. Signs of DVT include calf pain, swelling, and
tenderness. The nurse encourages the patient to consume
adequate amounts of fluids, to perform ankle and foot exercises
hourly while awake, to use elastic stockings and sequential
compression devices as prescribed. Low molecular weight
heparin.
• Preventing dislocation of hip prosthesis: the nurse teaches the
patient about positioning the leg in abductio, which helps
prevent dislocation of the prosthesis. Use pillow between the
legs to prevent dislocation. The patient hip is never flexed more
than 90 degrees. To prevent hip flexion, the nurse does not
elevate the head of the bed more than 60 degrees. For use of
the fracture bedpan, the nurse instruct the patient to flex the
good leg and use the trapeze to lift the pelvis onto the pan. High
seat chairs, semireclining wheelchairs and raised toilet seats
may be used to minimize hip joint flexion. At not time the patient
cross his or her legs. The patient should not bend at waist to put
on shoes and socks. Occupational therapist can provide the
patient with devices to assist.
• Patient education: never cross legs, avoid bending forward (no
flexion >90 degree), use high seated chair and raised toilet seat,
use assistive devices provided by OT to put on clothing (socks,
shoes, pants), keep knees apart at all times, put pillows
between legs when sleeping.
Signs and symptoms of hip dislocation:
• Increased pain at the surgical site, swelling, and immobilization
• Acute groin pain in the affected hip or increased discomfort
• Shortening of the leg
• Abnormal external or internal rotation
• Restricted ability or inability to move the leg
• Reported popping sensation in the hip
If a prosthesis becomes dislocated the nurse immediately notifies the
surgeon because the hip must be reduced and stabilize promptly so that
the leg does not sustain circulatory and nerve damage. Stresses to the
new hip joint should be avoided for the first 3 to 6 months. After close
reduction, the hip may be stabilizing with Bucks traction or a brace to
prevent recurrent dislocation.
o Total knee replacement
Total knee replacement surgery is considered for patients who have
severe pain and functional disabilities related to destruction of joint
surfaces by arthritis or bleeding into the joint.
Post op:
• Affected knee with compression dressing
• Ice to reduce edema and poss. Bleeding
• Encourage active flexion of the foot q1hr
• Monitor CPM (continuous passive motion device): the patients
leg is placed in this device, which increases circulation and
range of motion of the knee joint.
• Inspect immobilizing devices (splints, cast, or brace)
• Follow weight bearing orders
• Assist pt with ambulation, as ordered.
Nursing diagnostic
• Acute pain related to orthopedic problem
• Acute pain related to inflammation
• Risk for peripheral neurovascular dysfunction related to
inflammation and or constricting devices
• Impaired physical activity related to pain inflammation, and or
presence of immobilization device
o Hip fracture
Elderly people who have brittle bones from osteoporosis and who tend
to fall frequently have high incidence of hip fracture. The patient who
has sustained a hip fracture frequently has a comorbid condition
(cardiovascular, pulmonary, renal and endocrine). There are two major
types of hip fracture. Intracapsular fractures are fractures of the neck of
the femur. Extracapsular fractures are fractures of the trochanteric
region. Avascular necrosis is common in femoral neck fractures.
Sign and symptoms: the leg is shortened, adducted, and externally
rotated. The pt complains of pain in the hip and groin or in the medial
side of the knee.
The diagnostic of fractured hip is confirmed with an x-ray.
Management:
• Buck’s extension traction, a type of temporary skin traction, may
be applied to reduce muscle spasm, to immobilize the extremity
and to relieve pain. The goal of surgical treatment of hip
fractures is to obtain a satisfactory fixation so that the patient
can be mobilized quickly and avoid secondary medical
complications. Displacement femoral neck fractures may be
treated as emergencies with reduction and internal fixation
performed withing 12 to 24 hours after fracture. Adequate
reduction is important for fracture healing: the better the
reduction, the better the healing.
Nursing intervention:
• Attention is given to pain management, prevention of secondary
medical problems, and early mobilization of the patient. The
nurse encourages deep breathing, coughing, and foot flexion
exercises every 1 to 2 hours. Elastic compression stockings and
pneumatic compression devices are used and anticoagulants. A
pillow is placed between the legs. The patient is encourage to
exercise as much as possible by means of overbed trapeze.
Encourage the pt to drink fluids and ankle foot exercises to
prevent DVT. The nurse assess every 4 hours for DVT. Change
positions every 2 hours.
Complications: DVT, atelectasis, and pneumonia are most common
complications. Delayed complications of hip fracture include infections,
nonunion, AVN of the femoral head.


Med-surge notes (WOMEN’S HEALTH)

6/11

• OSTEOARTHRITIS (Non-inflammatory arthritis)
o Known as degenerative joint disease
o It affects women and men but women have more symptoms than men
o Women are mainly affected at: hand and knee
o Men are mainly affected at: hip
o There are changes in the joints. It happens over time. The joint become rough and softer
o The joint becomes thinner and the bones would rub together
o J oint mice: bones become spur – a small moveable stone formed in or near a joint, usually a knee.
o Risk factors:
Modifiable: obesity, repetitive joint stressor, post menopausal bone loss
Non-modifiable: age, gender, family history, trauma, fractures, infections
o By 40 years old most people have osteoarthritis pain. They are asymptomatic, asymmetrical,
redness, swelling, and tenderness at the heberden’s nodes,
o Heberden’s nodes: an abnormal cartilaginous or bony enlargement of a distal interphalaneal joint of
a finger, usually occurring in degenerative diseases of the joint.
o Patient is so stiff that takes time (usually 30 minutes or so) and a lot of activity to start the day.
They should take warm shower
o Crepitus and limited ROM in weight bearing joints. Crepitus is associated with gas gangrene,
rubbing of bone fragments, air in superficial tissues, or crackles of a consolidated area of the lung
in pneumonia.
o Manifestations:
Bad Weather affects joints - Rising humidity and falling barometric pressure often
aggravates the symptoms
Advanced groin pain
Hip most common in man
Hip: point at groin, buttocks, medial side of the thigh or knee. Pain is poorly differentiated.
Lowering the body becomes different.
Knee; pain with motion with decreased flexion, vagus deformity, crepitus.
Spine: a lot of pain. Patient tells you lower back pain. Weakness of lower extremeties,
decreases reflexives and leg pain
o Diagnostic: medical history, arthroscopy, x-ray, physical assessment
o Goal: control pain, disability, pt be able to perform ADL as much as possible with less assistance
o Treatment:
Non-drug: physical therapy (increase joint movement), occupational therapy (assistive
devices), dietitian
Aquatic exercise: increase joint flexibility, muscle strengths and increase self -confidence.
Isometric exercises: increase muscle tension
Warm bath or shower
Dietary supplements: restore and maintain cartilage, analgesics
Drug therapy: acetaminophen: first line of treatment
NSAID: avoid as possible. Inflammation is not a main sign of osteoarthritis.
• COX-2 inhibitor (less GI problem seem with NSAID)
Surgery:
• Arthrodesis: immobilization
• Arthroplasty: diseased joint components are replaced with artificial joint products
• Osteotomy – the sawing or cutting of a bone. In this case Displacement
Osteotomy in which a bone is redesigned surgically to alter the alignment or
weight-bearing stress areas.
Alternative treatments: Acupuncture, Massage therapy
Osteoarthritis Rheumatoid arthritis
Progressive, not systemic (only on
specific joints
Systemic, autoimmune condition
Primary affects weight bearing
joints
Affects all connective tissue in the
body
Pain, swelling and tenderness Warm, tender, erythematosis, and
painful joints
Crepitus, heberden’s nodes Severe joint deformities

Nursing intervention:
o Anticipate immoblization when acute problems (splint)
o Encourage to participate in ADLS, allow rest periods
o Maintaining a regular exercise program

OSTEOPOROSIS (a disorder characterized by abnormal loss of bone density and deterioration of bone tissue, with
an increased risk or fracture)
o Most common bone condition
o Female 80%
o Occurs at about 55 years of age
o 1 out of every 2 women will be affected
o 1 out of every 8 men over 50 years will develop delayed fracture
o metabolic bone disease
o types:
Primary: age related
• type 1: estrogen deficiency induced (menopause)
• type2: elderly with declined vitamin D production and decreased GI calcium
absorption (as you get older, less absorption of vitamin D and Calcium in the
GI tract)
Secondary: related to any other medical condition
Risk factors:
• nonmodifiable: age, gender, euro-american ethnicity, thin, small frame, family
Hx, Caucasians
• modifiable: chronic Ca deficiency, vitamin D deficiency, sedentary lifestyle,
smoking, ETOH, diet high in proteins and fats
o A diet high in acid forming foods is counteracted by the body by releasing calcium from the
bone into the bloodstream
o people who consumed a diet rich in alkaline forming fruits and vegetables have higher bone
mass
o secondary osteoporosis risk factors:
diabetes, chronic exercise related to suppression of menses (reduced hormones)
medications: corticosteroids, anti-seizures, aluminum, diuretics
o sign and symptoms:
called the silent thief (no warning signs). No S and S until fractures occurs
acute back pain: vertebral fracture
hip fracture spontaneous or with little trauma.
Wrist fracture: overstretching or past falls
o Complications: pain, loss of function, deformity, muscle weakness, social isolation
o X-ray is not a good tool to Dx fractures
o Bone density test (DEXA – Dual Energy Absorptiometry): an imaging technique that uses two
low-dose X-Ray beams with different levels of energy to produce a detailed image of body
components. It is used primarily to measure bone mineral density
o Labs: serum levels of calcium, phosphorus.
o Screening guidelines:
all post menopausal women under 65
all post menopausal women with fractures
women considering treatment of osteoporosis
women in hormone replacement treatment.
o Treatment:
Calcium and vitamin D
Calcium minimum: 1200-1500 mg/day for all persons.
• Sources: low fat dairy products, canned salmon, vegetables, almonds, cereals,
pasta, grains
Vitamin D 400-800 daily
• Source: milk, cereal, egg yolks, salt water fish, liver
o Calcium interferes with the absorption of iron
o Exercises: walking
o Smoking cessation
o Drugs:
Hormone replacement therapy, fosamax, calcitonin, raloxifen
o Goal: decrease pain and promote activity to minimize functional decline
Administer analgesia, provide periods of rest, assess ABD for constipation, provide
safe environment, teach pt about proper body mechanics
6/14
STD’s
Trichomoniasis (trichomonas) – a vaginal infection caused by the protozoan trichomonas vaginalis
Incubation can be years. It is symptomatic. Takes years to be diagnosed
Sign and symptoms:
o Off-white, yellow, greenish purulent discharge, foul smelling drainage, itching, irritates vagina
Some women are asymptomatic
The cervix looks like a strawberry. It is called “strawberry cervix”. Cervix has petechiae which are tiny
purple or red spots appearing on the skin as a result of tiny hemorrhages within the dermal or submucosal
layers.
Treatment:
o Single dose of metronidazole per 7 days
o If it doesn’t go away. They need to call CDS because there is resistance and they would tell what to
do. They would take report.
o You need to report STDs to the CDC
o Treat it with flagil if metronidazole doesn’t work
CHLAMYDIA (a genus of microorganisms that live as intracellular parasites, have a number of properties in
common with gram negative bacteria’s)
Most common bacterial STD in the US
Whenever you treat a patient with Chlamydia you need to treat for Gonorrhea
Chlamydia and Gonorrhea go together
Sign and symptoms
o A lot of women are asymptomatic
o Pelvic inflammatory desease (PID), it is the main sign and symptom of Chlamydia
o Men: testicular pain
o Men diagnostic test: you need to collect the first voided urine in the morning
Treatment:
o Zithromax (1 g) PO single dose
o Vibramycin 100 mg PO bid for seven days
o Erythromycin (pregnant women)
GONORRHEA
Gonorrhea is the most common venereal disease in the USA
Incubation period 3-4 days
Homosexual male has 10x greater incidence
Transmission: Direct contact with exudates via sex or neonatal passage through birth canal.
Signs and Symptoms
o Woman has no discharge
o Men has discharge. Purulent urethral discharge (white, yellow, green color)
o Complications:
Infertility
Ectopic pregnancy
Blindness for babies
Prostatitis
Sterility
Gonorrhea is the only STD that would cause low grade fever
Diagnostic test for males: you need to collect the first voided urine in the morning
When patient had low grade fever and discharge there is possibility that he/she has gonorrhea
Treatment:
o Rocephin (125 mg IM single dose)
o Oral and pharyngeal respond best to rocephin
All patient treated for gonorrhea need to be treated for Chlamydia

SYPHILIS (an STD caused by the spirochete Treponema pallidum, characterized by distinct stages of effects over
a period of years.)
Is being around for many years
Has 3 stages
Invades through intact skin or mucous membranes. Goes to the lymph nodes
Affects many organs including the integumentary system
South has the highest rate in the nation
Secondary stage is the most contagious stage (you can get it by kissing).
Incubation: about 3 weeks (range 10-90 days post exposure)
The First Stage (Primary syphilis):
o Chancre: painless ulcer (filled with spirochetes)
o Extra genital lesions may be painless
o Heals spontaneously in 1-5 weeks
The Second Stage (Secondary syphilis):
o Spirochetes have increased in number and spread throughout the body
o Rash
o Lymph nodes and nerves
o Condyloma lata: flat lesions that may appear in moist areas
Tertiary stage:
o Absence of clinical symptoms
o Appearance of soft rubber tumors, called gummas, that ulcerate and heal by scarring. Gummas
form anywhere on the surface of the body and in the eyes, liver, lungs, stomach, or reproductive
system.
o Systemic involvement with cardiovascular and CNS
Diagnosis
o RPR (rapid plasma reagin test): an agglutination examination, the test detects two groups of
antibodies. The first is a nontreponemal reagin directed against a lipoidal agent resulting from the
Treponema pallidum infection. The second is an antibody directed against the Treponemal
pallidum organism itself.
Nursing intervention
o Administer parenteral penicillin

HERPES GENITALIS (a chronic infection caused by type 2 herpes simplex virus (HSV2), usually transmitted by
sexual contact which causes painful vesicular eruptions on the skin and mucous membranes of the genitalia of
males and females.)
Type 1 and type 2
Person get herpes when person comes in contact with the vesicles
Herpes has no cure. You will always have herpes.
Assessment: tingling and itching before the vesicle appears
Complications: cervical cancer, pregnant women should have C section – HSV2 may be transmitted to the
newborn by direct contact with infected tissue during natural child birth.
Treatment: Sitz bath, analgesia, Acyclovir (an antiviral agent) taken PO results in partial control of the S&S
GENITAL WARTS (a small soft, moist pink or red swelling of the genitals that becomes pedunculated and may be
painless. The growth may be solitary, or a cauliflower-like group may be present in the same area of the genitalia.)
Etiology: Condyloma acuminate – a wart-like growth
Caused by the human papilloma virus (HPV)
Treatment: burn wart by wart
BREAST CANCER (a malignant neoplastic disease of breast tissue)
Non hormone dependant
Estrogen and progesterone receptors, are present in some breast cancers. Estrogen and progesterone
affect the rate of cells division and thus affect the risk of breast cancer by causing proliferation of breast
epithelial cells. Thus drugs that block these receptors may be useful in treating tumors with the receptors.
Tamoxifen for example.
A women’s lifetime risk for developing breast cancer is 1 in 8
Risk factors
o Genetic
o Alcohol
o Obesity
o Hormone replacement therapy
o Early menarche and late menopause (high risk). Should be late menarche and early menopause (
reduces the risk)
Screening by:
o Breast cancer genetic screening test which is a blood test used to detect the presence of breast
cancer genes.
o Breast cancer self examination: Go around the breast with your finger pads in a clock wise motion
until you reach the lymph nodes in the arm pit. Can be performed standing or in supine position.
Should be performed on the 7
th
day from the first day of your period. Look for drainage, size,
lumps, retraction
Diagnosis by:
o Mammography - Breast imaging of non-palpable lesions, Baseline mammogram between the age
of 35 – 40 years-old
o Ultrasound -Sound waves to produce an image
o MRI
o Biopsy
Treatment:
o Drug therapy - Tamoxifen if the tumor is influenced by estrogen receptor proteins, an anti-estrogen
drug is given
o Surgical
Lumpectomy – Removal of axillary node resection followed by low-dose radiation
Simple mastectomy - Removal of the entire breast and facia
Modified radical mastectomy - Removal of breast and nodes only
Radical mastectomy - Removal of breast, lymph nodes, pectoralis major and minor
o Post operative: Radiotherapy and/or chemotherapy
Post Operative Treatment:
o Implantation of a prosthesis
o Reconstructive surgery is also an option
Transverse Rectus Abdominis Myocutaneous Flap (TRAM flap): go into the abdomen,
remove muscle from the ABD and reconstruct the breast. One complication is hernia.
1
Gastritis / Peptic Ulcer Disease

Gastritis
• Gastritis is a mild irritation, inflammation, or infection of the stomach lining.
• Gastritis may be a sudden attack or chronic.
• Gastritis may be acute, lasting several hours to a few days, or chronic resulting from repeated exposure to
irritating agents or recurring episodes of acute gastritis.
• Gastritis may be the first sign of an acute systemic infection
• The gastric mucous membrane becomes edematous and hyperemic (congested with fluid and blood) and
undergoes superficial erosion. Secretes gastric juice, containing very little acid but much mucus.

Gastritis Causes:
• Acute gastritis may be caused by:
o Dietary indiscretion
o Over use of aspirin or other NSAID
o Ingestion of strong acid or alkali.
o Pyloric stenosis or obstruction.
o Tramatic injuries, burns, severe infections, hepatic renal or respiratory failure or major surgery.

• Chronic gastritis (may be cause by either benign or malignant ulcers of the stomach or by H. pylori)
o Bacterial or viral infection (infection by a virus is contagious)
o Excess stomach acid caused by:
• heavy smoking
• alcohol use
• Caffeine
o improper diet such as spicy, greasy foods
o Non-steroidal anti-inflammatory meds
o Cortisone
o Stress

Gastritis Sign and symptoms
• Abdominal discomfort
• Headache
• Lassitude
• Nausea
• Anorexia
• Vomiting
• Hiccupping
• Sour taste in the mouth
• Intolerance to spicy or fatty foods
• Malabsorption of vitamin B12

Gastritis Diagnostic tools
• GI x-ray series or endoscopy and histologic examination of a tissue specimen obtained by biopsy

Gastritis Medical management
• The gastric mucosa is capable of repairing itself after a bout of gastritis. The patient recovers in about 1
day and appetite returns 2-3 days
• Refrain from alcohol and food
• IV Fluids is administered if symptoms persist
• Modifying patient’s diet, reducing stress, recommending avoidance of alcohol and NSAIDs

Gastritis Assessment:
A diet history plus a 72 hours dietary recall. The nurse also identifies the duration of the current symptoms, any
methods used by the patient to treat these symptoms and whether the methods were effective. Signs to note during
the physical examination include abdominal tenderness, dehydration, and evidence of any systemic disorder.
2

Gastritis Nursing diagnosis
• Anxiety related to treatment
• Imbalanced nutrition, less than body requirements, related to inadequate intake of
• Nutrients
• Risk for imbalanced fluid volume related to insufficient fluid intake and excessive fluid loss subsequent to
vomiting
• Deficient knowledge about dietary management and disease process
• Acute pain related to irritated stomach mucosa

Gastritis Nursing Implementations
• Use calm approach to assess the patient and to answer all questions as completely as possible
• Monitor intake and output
• Introduce solid food as soon as possible to provide adequate oral nutrition
• Discourage the intake of caffeinated beverages, alcohol, cigarette smoking
• Assess electrolytes values every 24 hours to detect any imbalance
• Instruct the patient to avoid any food or beverages that may irritate the gastric mucosa
• Instruct the patient about the correct use of medications to relieve chronic gastritis

Peptic Ulcer Disease
• ~500,00 new cases per year
• Duodenal ulcers 95%
• Gastric ulcers less common
• Higher incidence among young adults (30-55 years of age)
• Male >Female Ratio 1.3:1
• Most common in J ewish descent
• Peptic ulcers are open sores that develop on the inside lining of your stomach, upper small intestine or
esophagus
• A person who has peptic ulcer has peptic ulcer disease.
• A peptic ulcer is an excavation that forms in the mucosal wall of the stomach, in the pylorus, in the
duodenum and esophagus
• Erosion of a circumscribed area of mucous membrane is the cause.
• Peptic ulcers are more likely on the duodenum than in the stomach.
• Peptic ulcer result from the infection of H. pylori.
• Excessive secretions of HCL in the stomach and stress may contribute to peptic ulcers
• People with type O are more susceptible to peptic ulcers than are those with blood type A, B, or AB.

Peptic Ulcer Causes
• Bacterial infection (H. pylori)
• Long-term use of nonsteroidal anti-inflammatory agents (NSAIDs)
• Cancerous tumors
• (stomach or pancreas)

Peptic ulcer disease Risk factors:
• Chronic NSAID use (increase risk of gastric ulcers)
• Corticosteroids use
• Smoking
• Stress (contributes)

Peptic ulcer disease - Helicobacter pylori
• H. Pylori is a bacterium that has adapted to living on the surface lining of the stomach.
• Impairs the ability of the stomach and duodenum to protect themselves from acid and pepsin (predisposes
these areas for ulcer formation)
• Risk factor for gastric cancer.
• ~20% of people <40 years of age
3
• ~50% of people >60 years of age
• Transmission: Overcrowded areas, from person to person
• Test: H. Pylori serum antibody.
• (+) test may persist for up to 18 Months after successful treatment.
• Meds should be held for 7 days prior serum test.

Peptic Ulcer Disease Prevention:
• Use of newer NSAID (COX2 inhibitors –spare gastric mucosal prostaglandin synthesis)
• Proton pump inhibitors BID in conjunction with NSAID –prophylaxis
• Smoking cessation
• Stress management

Peptic Ulcer Disease Diagnostic Tools:
LABS
• Endoscopy biopsy for H. Pylori
• CBC (anemia-blood loss) (leukocytosis-ulcer formation)
• Pancreatic enzyme (Amylase –excludes pancreatic involvement)
• Fasting serum gastrin level
TESTS
• Upper endoscopy
• Barium upper GI series
• Urea breath test (H. Pylori generates urease)
• Endoscopy is the preferred diagnostic procedure because it allows direct visualization of inflammatory
changes, ulcers, and lesions.

Peptic Ulcer Disease: Sign & Symptoms
Classic Sign - Dyspepsia
Possible signs of an ulcer
• Feel better when you eat or drink and then worse 1 or 2 hours later (gastric ulcer)
• Feel worse when you eat or drink (duodenal ulcer)
• Stomach pain that wakes you up at night
• Feel full fast
• Heavy feeling, bloating, burning or dull pain in your stomach
• Vomiting
• Unexpected weight loss
• Pyrosis: heartburn
• Constipation and diarrhea

Peptic Ulcer Disease Emergency Symptoms
• Sharp, sudden, persistent stomach pain
• Bloody or black stools
• Bloody vomit or vomit that looks like coffee grounds
• Signs of a serious problem
o Perforation
o Bleeding (when acid or the ulcer breaks a blood vessel)
o Obstruction (when the ulcer blocks the path of food trying to leave the stomach)

Peptic Ulcer Disease Management:
The goal of management is eradicate H. pylori and to manage gastric acidity
• Stop NSAID
• Well balanced diet
• Surgeries: Rare
• Meds:
o Proton pump inhibitors (prevacid, prilosec)
o H2 (histamine ) receptor antagonists and proton pump are used to treat NSAID induced ulcers and
others associated with H.pylori.
o Bismuth compounds
o Antacids
4

Proton Pump Inhibitors (PPI)
• Suppresses gastric acid secretion.
• Give 1 hr ac (at meal time)
• Drugs:
o Omeprazole (Prilosec)
o Lansaprazole (Prevacid)
o (Protonix)

H2 Receptor Antagonists
• Suppress basal and nocturnal gastric secretion
• Less effective inhibitor of meals stimulated acid secretion.
• Drugs:
o Ranitidine (Zantac)
o Famotidine (Pepcid)
o Nizatidine (Axid)

Bismuth Compounds
• Promotes ulcer healing
o Stimulates mucosal bicarbonate
o Stimulates prostaglandin production
o Antibacterial action against H. Pylori
• Dark stools with use

Antacids
• Provide symptom relief.

Peptic Ulcer Disease H. Pylori Treatment:
• Omeprazole 20 mg bid
• Metronidazole 500mg bid or
• Bismuth subsalicylate
• (10 to 14days)

Peptic Ulcer Disease Complications
• Internal bleeding
• Perforation (a hole through the wall of your stomach or small intestine)
• Peritonitis
• Scar tissue that can obstruct passage of food through the digestive tract. (This causes nausea, vomiting
and weight loss.)

Peptic Ulcer Disease Assessment
• The nurse asks the patient to describe the pain and the methods used to relieve it. Nurse determines how
often emesis has occurred and notes important characteristics of the vomitus. The nurse asks the patient to
list his or her usual food intake for a 72 hour period. Describe food habits, assess pt vital signs and reports
tachycardia, hypotension. Stool tested for occult blood, and physical examination including palpation of the
abdomen for localized tenderness
• Goals: relief of pain, reduced anxiety, maintenance of nutritional requirement, knowledge about the
management and prevention of ulcer recurrence, and absence of complications

Peptic Ulcer Disease Nursing Implementations
Monitor for potential complications:
• Melena (tarry stools)
• Hematemesis
• S&S anemia (dizziness, fatigue, tachycardia)
• Abd distention
• Constipation


5
Peptic Ulcer Disease Nursing Diagnosis
• Acute pain R/T effect of gastric secretion on damaged tissue
• Anxiety related to an acute illness
• Imbalanced nutrition related to changes in diet
• Deficient knowledge about prevention of symptoms and management of the condition.

The nurse reviews with the patient and family the signs and symptoms of complications to be reported. These
complications include hemorrhage (cool skin, confusion, increased heart rate, labored breathing, and blood in the
stool), penetration and perforation (severe abdominal pain, rigid, and tender abdomen, vomiting, elevated
temperature, and increased heart rate), and pyloric obstruction (nausea, vomiting, distended abdomen, and
abdominal pain)


1
Intestinal Obstruction

Caused by any condition that prevents the normal flow of chyme through the intestinal lumen

Intestinal obstruction Classifications
Simple:
• Mechanical blockage of the lumen by lesions, (most common fibrous adhesions). Is an intraluminal
obstruction or a mural obstruction from pressure on the intestinal wall occurs.
o Adhesions, hernias, tumors, inflammatory disorders, stenosis, strictures, abscess.
• Functional:
o Failure of motility (paralytic ileus). The intestinal musculature cannot propel the contents along the
bowel. The blockage can be temporary and the result from surgery.
o Examples: amyloidosis, muscular dystrophy, endocrine disorders such as diabetes and
neurological disorders such as parkinson’s disease.

• Most bowel obstructions occur in small intestine. Adhesions are the most common cause of small bowel
obstruction, followed by hernias and neoplasms. Other causes can be twisting of the bowel (
intussusception, volvulus). Most obstruction in the large bowel occur in the sigmoid colon. The most
common cause are carcinoma, diverticulitis, inflammatory bowel disorders and benign tumor.

Intestinal obstruction
↓
Sequestration of gas and fluid proximal to the obstruction
↓
Distention
↓
Colicky ABD pain
Nausea & vomiting
Decrease nutrient absorption
Decrease CHO reserve
Ketosis
↓
Loss of H2O and Electrolytes
Dehydration
Hypokalemia & Hypochloremia
↓
Intestinal bowel wall edema → Release of toxins→ Bacterial translocation
↓
Fever, hypovolemia, peritonitis
↓
Shock


Intestinal obstruction Pathophysiology
• Obstruction causes intestinal distention and loss of fluids and electrolytes
• Fluid accumulation proximal to the obstruction site
• Gas accumulation (swallowed air and bacterial fermentation)

Pathophysiology of Small Bowel Obstruction:
• intestinal contents, fluids, and gas accumulates above the intestinal obstruction. The abdominal distention
and retention of fluid reduce the absorption of fluids and stimulates gastric secretions. The pressure
increases and the pressure of venous and arteriolar capillary decreases. This causes edema, congestion,
necrosis, and eventual rupture of the intestinal wall with peritonitis. Reflux vomiting may be caused by
abdominal distention. Vomiting results in the lost of electrolytes leading to metabolic alkalosis. Dehydration
and acidosis occurs from the loss of water and sodium. With acute fluid losses, hypovolemic shock may
occur.

2

Pathophysiology of Large Bowel Obstruction:

• In the large intestine dehydration occurs more slowly than in the small intestine because the colon can
absorbs its fluids contents. Adenocarcinoid tumor account for the majority of large bowel obstructions.
Most tumors occur beyond the splenic flexure.


Intestinal obstruction Pathophysiology
• Hypochloremia: obstruction at the pylorus or higher in the small intestines leads to metabolic alkalosis due
to hydrogen ion lost from inhibition of gastric juice reabsorbtion.
• Metabolic acidosis: Develops from obstruction lower in the intestines because bicarbonate from the
pancreatic secretions and bile cannot be reabsorbed. Also due to ketosis caused by starvation
• Severe distention causes impaired arterial circulation thus causing ischemia, necrosis, and peritonitis
• Fever and leukocytosis
• Sepsis

Intestinal obstruction Sign & Symptoms
• Colicky pain that progresses to constant and severe as ischemia progresses to necrosis or perforation
• Nausea and vomiting
• ABD distention
• Partial obstruction causes diarrhea or constipation
• Lower causes vomiting or emesis containing fecal material
• Complete, increases the number of bowel sounds
• S&S of hypovolemia
• Fever

Intestinal obstruction Diagnostic tools
• Physical exam
• Ultrasound
• Radiography (CT scan and abdominal x-ray findings include abnormal quantities of gas, fluids, or both in
the intestines. Also, distended colon and pinpoint the site of obstruction
• Labs (electrolytes studies and a complete blood cell count) reveal picture of dehydration, loss of plasma
volume, and possible infection.
• Barium studies are contraindicated in large bowel obstruction

Intestinal obstruction Management
• Fluid abd electrolytes replacement
• Gastric or intestinal suction to decompressed the lumen
• Immediate surgical intervention for strangulation & complete obstruction
• When the bowel is completely obstructed, the possibility of strangulation warrants surgery
• Before surgery IV fluids is necessary to replace lost Cl, Na, K
• A colonoscopy is performed to untwist and decompress the bowel.
• A cecostomy may performed in patients who are poor surgical risk and urgently need relief form the
obstruction (opening in the cecum)
• A rectal tube may be used to decompress an area that is lower in the bowel.
• The usual treatment is surgical resection to remove the obstructing lesion.

Intestinal obstruction Nursing diagnosis
• Acute pain R/T distention/edema or ischemia of intestinal tissue as evidenced of guarding behavior or
changes in vital signs.
• Diarrhea R/T presence of obstruction as evidenced by changes in consistency and frequency of bowel
movements.
• Constipation R/T changes in peristalsis as evidenced by decreased bowel sounds and/or absence of
stools.
• Risk for deficient fluid volume R/T V&D and decrease intake.


3

Intestinal obstruction Vocabulary
• Adhesions: loops of intestines become adherent to areas that heal slowly or scar after abdominal surgery
• Intussusception: one part of the intestine slips into another part located below it
• Volvulus: bowel twists and turns on itself
• Hernia: protrusion of intestine through a weakened area in the abdominal muscle wall
• Tumor: a tumor that exits within the wall of the intestine extends into the intestinal lumen, or a tumor
outside the intestine causes pressure on the wall of the intestine.
1
Diverticular Disease
Diverticular Disease
• In the Western societies 30% of the population is affected at age 60, and 50% over age 80 (with
Diverticulosis)
• Developing countries life expectancy is much lower, no comparison is poss.
• Most cases are asymptomatic, discovered incidentally with endoscopies and barium enemas.
• The exact cause of diverticulosis has not been identified. A low intake of dietary fiber is considered a
predisposing factor
• Almost all patients have colonic involvement (it affects the lower part of the large intestine such as sigmoid
colon because that’s where more pressure is exerted on the walls of the colon) due to higher intraluminar
pressure.
• Over time the contracted colonic musculature, working against greater pressure to move small, hard stools
develop hypertrophy, thickening, rigidity, and fibrosis.
• Diverticulosis looks like swiss cheese which is why you shouldn’t eat seeds and peanuts.
• Bowel contents can accumulate in the diverticulum ( a saclike herniation of the lining of the bowel that
extends through a defect in the muscle layer.) causing inflammation and infection

Diverticular Disease Risk Factors
• Believe to arise after many years of diet deficient in fiber
• Hereditary (unknown)
• Abnormal connective tissue disorders (sclerodema, Marfan syndrome, etc)

Diverticular Disease
• Complications
o Lower GI bleeding
o Diverticulitis (infestation of the holes in the walls of colon, swelling and possible complications such
as peritonitis)
o Fistulas (tunnelling of hole to other tissue or organs
o Constipation
• Uncomplicated Diverticulosis
o More than 2/3 of patients

Sign&Symptoms
• sign and symptoms of diverticulosis are relatively mild and include bowel irregularities with intervals of
diarrhea, nausea, anorexia, and bloating or abdominal distention
• with repeated local inflammation of the diverticula the large bowel may narrow with fibrotic strictures,
leading to cramps, narrow stools, and increased constipation.
• Weakness, fatigue, and anorexia are common symptoms
• If the condition is untreated can lead to septicemia
• Chronic constipation
• ABD pain (left lower quadrant, tenderness and abdominal pain/ sigmoid involvement so either
diverticulosis or itis)
• Fluctuating bowel habits
• Mild left lower quadrant tenderness upon assessment
• Mild cramps
• Bloating

Uncomplicated Diverticulosis Management
• High fiber diets
• Fiber supplements
• Fiber Containing Foods
• Fruits
o Apple, raw, with skin1 medium =3.3 g
o Peach, raw1 medium =1.5 grams
o Pear, raw1 medium =5.1 grams
o Tangerine, raw1 medium =1.9 grams
2
• Fiber Containing Foods
• Vegetables
o Asparagus, fresh, cooked 4 spears =1.2 grams
o Broccoli, fresh, cooked1/2 cup =2.6 grams
o Brussels sprouts, fresh, cooked1/2 cup =2 grams
o Cabbage, fresh, cooked1/2 cup =1.5 grams
o Carrot, fresh, cooked1/2 cup =2.3 grams
o Cauliflower, fresh, cooked1/2 cup =1.7 grams
o Romaine lettuce1 cup =1.2 grams
o Spinach, fresh, cooked1/2 cup =2.2 grams
o Summer squash, cooked1 cup =2.5 grams
o Tomato, raw1 =1 gram
o Winter squash, cooked1 cup =5.7 grams
• Fiber Containing Foods
• Starchy Vegetables
o Baked beans, canned, plain1/2 cup =6.3 g
o Kidney beans, fresh, cooked1/2 cup =5.7 g
o Lima beans, fresh, cooked1/2 cup =6.6 g
o Potato, fresh, cooked1 =2.3 g
• Fiber Containing Foods
• Grains
• Bread, whole-wheat1 slice =1.9 grams
• Brown rice, cooked1 cup =3.5 grams
• Cereal, bran flake3/4 cup =5.3 grams
• Oatmeal, plain, cooked3/4 cup =3 grams
• White rice, cooked1 cup =0.6 grams
Diverticulitis
• Perforation of the colonic diverticulum causing infection that vary in size.
• Localized inflammation (most common) to macro-perforation with abscess and peritonitis
• The symptoms manifested generally result from complications: abscess, fistula formation, perforation,
obstruction, peritonitis, and hemorrhage

Diverticulitis Complications
• A fistula is an abnormal connection of tissue between two organs or between an organ and the skin
• E.g., diverticulitis to the bladder - feces passing thru the urine
• The organs usually involved are the bladder (most common), small intestine, and skin.
• Peritonitis ( abdominal pain, rigid-board like abdomen, loss of bowel sounds and signs and symptoms of
shock occur during peritonitis)
• abscess formation ( tenderness, palpable mass, fever, and leukocytosis)
• Bleeding ( noinflamed or slightly inflamed diverticula may erode areas adjacent to arterial branches,
causing massive rectal bleeding)

Diverticulitis Signs & Symptoms
• Mild to moderate aching ABD pain (left lower quadrant)
• Constipation or loose stools
• N&V (nausea & vomiting)
• Low grade fever and chills
• Left lower quadrant tenderness with palpation (guarding is 10 on pain scale of 0 to 10)
• (+) stool occult blood (area is irritated and could have a perforation, wbc count in the 20 & 30, fever)
• Perforation: Systemic presentation (which could lead to peritonitis and systemic infection such as sepsis)
• Leukocytosis
Test questions – you do not do a colonoscopy on someone with suspected diverticulitis because the area is so
inflamed and damaged and the scope can perferate the wall.

Diverticulitis Diagnostic tools
• KUB X-Ray: Free ABD air represents perforation (there is serous fluid and no air or gas in the peritoneum)
3
• Colonoscopy and barium enema (avoid during the initial stage because of the risk of perforation)
• ABD CT Scan (Abscess formation, wall thickening, inflammation obstruction, etc)
• CT scan is the diagnostic test of choice if the suspected diagnosis is diverticulitis; it can also reveal
abscesses.
• Laboratory tests that assist in diagnosis include a complete blood cell count, revealing and elevated WBC
(5000-10,000 normal values)

Diverticulitis Management
• Mild symptoms: outpatient with clear liquids diet and broad spectrum ABT’s. (No laxatives, no fleets
enemas and pt needs to go on liquid diet.)
• Antibiotics are prescribed for 7-10 days
• The liquid diet is recommended because increase stool volume, decrease colonic transit time, and reduce
intraluminal pressure.
• Pts with fever, increased pain and unable to tolerate PO diet needs hospitalization.
• Severe cases, immuno-suppressed, elderly, and those with co-morbid disease require acute hospitalization

Diverticulitis Hospital patients
• NPO No eating
• IVF ( intravenous fluid)
• NGT placement (ileus)
• IV ABT’s (to cover anaerobic and gram negative bacteria) for 7-10 days
• An opiod is prescribed (DEMEROL) for pain relief. Morphine is contraindicated because increase
intraluminar pressure in the colon.

Diverticulitis Surgical Management
• 20-30% of the 1/3 of cases need surgical intervention
• Required for large abscesses and peritonitis
• 1sr stage diseased segment of the colon is removed. Proximal colon brought out to form a temporary
colostomy. This is done through traditional surgical or laparoscopically.
• 2
nd
stage: After inflammation and infection subsides the colon can be reconnected electively.
• The double barrel temporary colostomy is then reanastomosed in a later procedure

Diverticulitis Prognosis
• Reoccurs in 1/3 of patients which warrant elective surgical resection.
• Assessment: ask the patient about the onset and duration of pain. Past and present elimination patterns,
review dietary habits, history of constipation with periods of diarrhea, tenesmus, abdominal bloating, and
distention. Auscultate bowel sounds, palpate four quadrants, and inspect stools for mucus, blood, pus.
Temperature, BP is monitored.

Diverticulitis Nursing Diagnosis
• Altered nutrition: Less than body requirement R/T dietary restrictions, N&D, and ABD pain (someone who is
NPO)
• Pain R/T intestinal inflammatory process, pt unable to move bowels for days, etc.
• Constipation R/T inadequate dietary intake of fiber
• Impaired skin integrity (perianal) R/T diarrhea (extremely acidic damages the skin)
• Infection, risk for (even if the infection is self evident)
Goal: attainment and maintenance of normal elimination patterns, pain relief, and absence of complications

Diverticulitis Nursing Implementation
1. Nutrition:
• Recommend daily intake of fluid at least 2 l per day (if pt doesn’t have renal or cardiac problems)
• Dietary consult
• Daily weight
• Monitor lab results (albumin) normal values are adult/elderly: 3.5-5 g/dl or 35-50 g/L
• Offer frequent small meals (6 per day, snacks and shakes like glucerna & jevity)
• Monitor Parenteral alimentation

Diverticulitis (NSG)
4
2. Pain:
• Provide optimal pain relief with prescribed analgesics (opiods like Demerol)
• Assess effectiveness of analgesics 30min after administration
• Teach non-invasive pain relief methods; relaxation techniques
• Assess location, intensity, aggravating & alleviating factors, radiation, onset

Diverticulitis (NSG)
3. Constipation:
• Teach diet high in fiber: fresh fruits with skin, whole grain breads and cereals, vegetables,
• Encourage increase fluid intake (8-10 glasses of H2O/day)
• Establish a regular time for evacuation
• Explain the hazard of enema and laxative use
• Increase ambulation and level of activity

Diverticulitis (NSG)
4. Skin integrity:
• Use of skin protecting cream
• Keep skin clean and dry
• Consult with dietitian: increase protein and CHO intake
• Monitor serum albumin level (3.5-5)
• Monitor skin integrity, turn & reposition q2h
• Protect bony prominence areas
• Refer to wound team

Diverticulitis (NSG)
5. Infection:
• Assess for S&S of infections, especially temp.
• Assess ABD for distention & bowel sounds
• Administer ABT’s as ordered
• Administer IVF as ordered
• Obtain specimen to lab ad culture for C&S
CAD
Coronary Artery Disease
• Male patients with higher incidence
• Overall ratio is 4:1 (men vs. women) but before age 40 the ratio is 8:1
• Male peak incidence is 50-60
• Female peak incidence is 60-70

CAD - Atherosclerosis formation steps
• Abnormal lipid metabolism and/or excessive intake of cholesterol and saturated fats.
• Fatty streaks (sub-endothelial accumulation of lipids and monocytes (macrophages).
• LDL (low-density lipoproteins) undergo in situ oxidation.
• Microphages migrate into the site to take up lipids
• Smooth muscle cell also migrate into the lesion
• Fibrous cap formation over the stable lesion which becomes calcified
• Lumen slowly become narrowed.

CAD: Risk Factors
• Family history
• Age
• Gender
• Elevated blood homocysteine levels
• Elevated C-reactive protein, Sedimentation rate
• Elevated serum fibrinogen
• Blood lipid abnormalities
• Metabolic syndrome
• HTN
• Diabetes mellitus
• Physical inactivity
• Cigarette smoking
• Hormone replacement therapy

CAD: Risk Factors
Abnormal lipid metabolism
• High levels of LDL cholesterol and low levels of HDL
• Ratios
• LDL: HDL (below 3 lower risk)
• LDL: HDL (above 5 high risk)

CAD: Management
• Smoking cessation
• Lowering of blood pressure
• Decrease levels of homocysteine
• Folic acid 1mg/daily (+) Vit B6 and B12
• Treatment of dyslipidemia
• Statins to decrease LDL levels
• Niacin to increase HDL levels
• Vit E as antioxidant therapy-- questionable
• Anti-platelet therapy
• ASA 81-325mg/daily
• Omega-3 fatty acid 1g/daily
• Hormone replacing therapy
• Combined estrogen-progesterone therapy in not protecting
• ACE inhibitors
• Reduces the risk for recurrent cardiac events by 20-25%

Myocardial Infarction
• Myocardial oxygen supply is severe compromised by impaired coronary blood flow.
• Myocardial cells are permanently destroyed.

Myocardial Infarction Causes:
• Coronary thrombosis 2
nd
to ruptured atherosclerotic plaque.
• Coronary spasm
• Polycythemia vera
• Decreased O2 supply (↓ BP, Anemia, acute blood loss)
• Increased O2 demand (Cocaine, amphetamines)

MI Development
↓O2 supply or ↑ O2 demand
↓
Ischemia cellular injury
↓
Necrosis (death of heart muscle)

Myocardial Infarction Incidence:
• 1 million people every year suffer of AMI.
• 25% mortality rate.
• 50% men and 63% of women with sudden cardiac death, had no previous symptoms.

Myocardial Infarction
Risk Factors:
• CAD
• 1
st
degree relative with MI prior to age 55
• Smoking
• Diabetes Mellitus
• HTN
• Hyperlipedemia
• Menopause sedentary life style
• Aging
• Personality type A

Myocardial Infarction
Diagnostic tools:
• EKG
• Cardiac Enzymes
• LDH
• Troponin
• Thallium scan
• CXR

Myocardial Infarction S&S
• Oppressive retrosternal chest pain
• Pain radiation
• Pain at rest or with minimal activity
• N/V
• Diaphoresis
• SOB
• Apprehensive
• Ashen color
• Hypotension
• Tachycardia
• New murmurs

MI - Medical Management

• M Morphine Sulphate
• O Oxygen Therapy
• N Nitroglycerin
• A Aspirin

MI - Medical Management
• Ischemic area reperfusion (Thrombolytics &/or PTCA)
• Meds ↓ O2 demand
• O2
• Bed Rest ↑ O2 supply

MI - Treatment:
Meds:
• Thrombolytics
• Analgesics
• ACE inhibitors
• Beta-Blockers

MI - NSG:
• Relieve pain
• Promote adequate tissue perfusion
• Reduce anxiety
• Monitor for potential complications
Hypertension (HTN)
Hypertension
• Blood pressure (p. 662)
• Is the product of cardiac output multiplied by peripheral resistance. (BP= CO x PVR)
• Pressure exerted on the wall of the arteries during diastole and systole.
• Influencing factors:
• cardiac output, distension of the arteries, blood volume, blood velocity, and blood viscosity.

Hypertension
• Called the silent killer because it is sometimes asymptomatic.
• Major contributor factor of death from cardiac, renal, and PVD.
• Usually accompanies Diabetes and atherosclerotic heart disease p. 855

Hypertension Definition:
• SBP>140 mm Hg & DBP>90 mm Hg
• 2 or more reading during 2 or more doctor’s visit.

Hypertension Incidence:
• 21-36% of the adult population has HTN.
• 90-95% with primary HTN
• 5-10% with secondary HTN

Hypertension
• Primary hypertension: (Unknown etiology).
• Secondary hypertension:
o Known etiology:
Chronic kidney disease
Coartation of the aorta
Thyroid/parathyroid disease
Chronic steroid therapy and Cushing syndrome.
others

Regulating Systems:
• Sympathetic Nervous System
• Renin-angiotensin-aldosterone System
• Peripheral resistance
• Insulin resistance

Hypertension Classifications:
• Pre-hypertension:
o SBP 120-139 & DBP 80-89 mm Hg
• Stage 1 HTN:
o SBP 140-159 & DBP 90-99 mm Hg
• Stage 2 HTN:
• SBP >160 & DBP> 100

Hypertension Risk factors:
• Cigarette smoking (increases the risk of dying from a cardiac event)
• Obesity
• Physical inactivity
• ETOH
• African American
• Family history

Hypertension Target organ damage:
• Left ventricular hypertrophy
• Angina
• Heart failure
• CVA
• Kidney failure
• Peripheral arterial disease
• Retinopathy

Hypertension: S&S
• Retinal changes
• Papilledema (optic nerve edema)
• R/T target organ damage (CVA, Kidneys,…)
• Morning headaches & cervical pain

Hypertension p. 858, table 32-3

Hypertension: Life style modification
• Weight reduction (BMI 18.5-24.9 kg/m2)
• Change eating habits:
• Diet rich in fruits, vegetables, low fat dairy products and reduce saturated fats.
• Reduction of dietary sodium intake to 2.4g/day
• Limit ETOH intake, 2drinks/male/day & 1/female
• Regular aerobic exercises, 30 minutes Monday to Friday.

Hypertension: MEDS
• Diuretics
• Β- blockers
• ACE inhibitors
• Angiotensin 2 antagonists
• Calcium channel blockers
• vasodilators
Hypertension: NSG
• Obtain V/S BP in both arms, apical and peripheral pulses.
• Assist in identifying modifiable risk factors
• Assist in developing a health maintenance plan (set realistic goals) (smoking, exercise, diet, and stress)

Hypertension:
• HTN animation
• Hypertension case study


Hypertensive Urgency (p.865)
• “Situation in which blood pressure must be lowered within few hours.” (Brunner & Suddarth)
• Close Hemodynamic monitoring is required, most patients are admitted to intensive care units.
• Life threatening side effect of medications is a sudden drop in blood pressure which requires immediate
action to restore blood pressure to allow appropriate tissue perfusion.
o SBP>90 mm Hg
Congestive Heart Failure (CHF)
• Inability of the heart to pump sufficient blood to meet the needs of the tissues of oxygen and nutrients.
• Fluid overload and inadequate tissue perfusion.
• Heart abnormality that leads to decreased systole and/or diastole (contraction and/or filling)

CHF Etiology:
• Primary cause: Atherosclerosis.
• Causes: CAD, HTN, Valvular disorders.
• Incidence increases with age. Most common cause of hops. of people older than age 65 (p. 789)

Congestive Heart Failure (CHF)
Positioning: (p.803)
• Increase head of the bed 8-10 inches with the use of pillows of blocks under the bed with arms
supported by pillows.
• OOB sitting in armchair.
• High fowlers with feet dangling.
Advantage:
• Venous return to the heart (preload) is reduced.
• Pulmonary congestion is alleviated.
• Impingement of the liver in the diaphragm is minimized.

CHF: Diagnostic tools
• Echocardiogram (EF)
• Cardiac cath
• CXR
• ECG
• Labs:
• Electrolytes
• BUN and Creat.
• BNP
• TSH
• CBC
• U/A

CHF: Diagnostic tools
BNP
• B-type natriuretic peptide
• Marker of ventricular systolic and diastolic dysfunction.
• Elevated with ventricular volume expansion and fluid overload.


CHF: Medical Management
• Goal:
o Reduce the workload on the heart by reducing afterload and preload.
• Meds:
o ACE inhibitors
o ARB (angiotensin 2 receptor blocker)
o Digitalis
o Β-blockers
o Diuretics

CHF: NSG
• V/S
• Daily weights
• Educate about Na restriction
• Educate to avoid excessive fluid intake (fluid restriction), smoking cessation, and ETOH.
• O2 based on pt’s condition.
• Accurate I&O
• Auscultate lungs
• Monitor for dehydration & hypotension due to meds
• Assess skin turgor and mucous membranes
• Assist with ADL’s

Angina Pectoris
Angina Pectoris
• Clinical syndrome characterized by pain or pressure in the anterior chest.
• Result of insufficient blood flow R/T significant obstruction of a major coronary artery.
• Coronary oxygen needs exceeds the supply.
• Most often caused by arteriosclerosis & atherosclerosis.

Angina Pectoris
• Arteriosclerosis
o Thickening, hardening, loss of elasticity, and calcification of the arterial wall.
• Atherosclerosis
o Yellowish plaque of lipids and cellular debris in the inner layer of the arterial wall.

Angina Pectoris Influencing Factors:
• Physical exertion: ↑ myocardial oxygen demand
• Exposure to cold: ↑ Oxygen demand due to vasoconstriction, which ↑ BP.
• Eating a heavy meal: ↑ blood flow to the mesenteric area which ↓ blood supply to the coronaries.
• Stress/emotions: ↑BP, ↑HR, ↑ myocardial workload.

Angina Pectoris S&S
• Chest pain subsides with rest and/or nitroglycerin.

Angina Pectoris Management:
• Surgery:
o PTCA
o CABG
o Intra-coronary stents.

Angina Pectoris Medications:
• Nitroglycerin:
• Dilates veins and arteries (systemic vasodilator)
• ↓ myocardial oxygen consumption
• ↑ coronary blood flow
• ↓ preload
• Beta adrenergic blocking agents:
• ↓myocardial Oxygen consumption by blocking β-adrenergic sympathetic stimulation
• ↓BP, ↓ myocardial stimulation
• Use cautiously with Asthma and Diabetes (mask hypoglycemia symptoms)
• Calcium Channel Blockers
o ↓SA node automaticity and/or AV node conduction
o Relax blood vessels. Prevent/treat vasospasm
o Dilates smooth muscle wall of coronary arteries
o ↓Workload of the heart
• Anti-platelets & anticoagulant
• ASA
• Plavix
• Ticlid
• Heparin

Angina Pectoris Oxygen administration:
• Increase oxygen delivered to the myocardium to decrease pain



EKG
EKG - Properties of Cardiac Cells
• Automaticity:
o Ability to spontaneously generate and discharge an electrical impulse
• Excitability:
o Ability to respond to an electrical impulse
• Conductivity:
o Ability to transmit an electrical impulse from one cell to another
• Contractility
o Ability to shorten and lengthen its muscle fibers
• Extensibility:
o The ability of the cell to stretch.

EKG - Electrical Impulses
• Depolarization
o Contraction of the cardiac cell (electrical activation)
o systole
• Repolarization
• Relaxation of the myocardial cell (recovery)
• Diastole

• Depolarization of one electrical cell stimulates adjacent cells causing a propagation of the electrical
stimulus producing an electrical current.

EKG
Records the electrical current of the cardiac cells as waves in a paper/strip.

EKG - Electrical Conduction System
• SA node (sinoatrail)
o Called the pacemaker cells because they poses the highest level of automaticity.
o Discharge impulses at a rate of 60-100 beats/min
• AV node (atrioventricular)
o Escape pacemaker. Discharge impulses at a rate of 40-60 beats/min
• Bundle of His (R +L branches)
• Purkinje fibers
o Escape pacemaker. Discharge impulses at a rate of 30-40 beats/min
• P wave: (atrial contraction)
o Atrial depolarization. Spread of the impulse from the SA node through the atria.
• QRS wave: (ventricular contraction)
o Ventricular depolarization. Spread of the impulse through the ventricles.
• T wave:
o Later phase of ventricular Repolarization

One heart beat = P-QRS-T sequence

Peripheral Vascular Disease

Types Arterial Occlusion
• Type 1:
o 10-15% of patients.
o Plaque formation limited to the aorta and the common iliac arteries.
o Higher incidence among young adults (ages 40-55)- heavy smokers +hyperlipidemia.
• Type2:
o 25% of patients
o Involves the aorta, the common iliac artery, and external iliac artery.
• Type 3:
o Most common, affects 60-70% of patients.
o Affects the aorta, iliac, femoral, popliteal, and the tibial arteries.

Peripheral Vascular Disease S&S
• Impotence (iliac arteries occlusion)
• Claudication
• Rest pain
• Gangrene
• Atrophy of skin, subcutaneous tissue and muscles of the calves
• Hair loss
• Coolness of the skin
• Dependent Rubor

Claudication
• Pain and numbness or weakness in the calves, thighs, or buttocks produced by exercise and relieve after a
few minutes of rest.
• Reproducible pain

Ischemic Rest Pain
• Pain at rest, nocturnal located across the dorsum of the foot at the metatarsal heads.
• Relieve by placing the affected extremity in a dependent position.
• Impending gangrene.

PVD - Medical Management: Meds
• Pentoxifylline 400 mg TID
o Deforms RBC.
• Phosphodiesterase inhibitor cilostazol 100mg BID
o Impairs platelet aggregation and increases Ca-mediated vasodilatation.
o Improves walking distance
• Propionyl-L-carnitine 1g BID
o Increases walk distance
• Ginko biloba extract 120mg daily
o Increases walk distance
o Risk of bleeding
• ASA 325 mg daily

PVD - Medical management: Sx
• Stent angioplasty
• Thomboendarterectomy
• Arterial bypass
• Lumbar sympathectomy (reserve for symptomatic patients)
• Hyperbaric oxygen

PVD - Surgery Complications
Percutaneous procedures:
• Distal emboli
• Contrast nephropathy
• Puncture site complications:
• Hematoma
• Pseudo aneurysm
• Arteriovenous fistulas
• Retroperitoneal hemorrhage
• Occlusion

PVD - Prognosis
• 25% will develop Claudication and rest pain
• 10% will face amputations
• Pts with CAD: 50% survival/5years

PVD - Acute Limb Ischemia
Etiology:
• Emboli
• Thrombus
• Trauma

PVD - Acute Limb Ischemia
Characteristics of acute ischemia (6 P’s)
• Pain (common early symptom)
• Pallor
• Pulselessness
• Paresthesias (common early symptom)
• Poikilothermia
• Paralysis

PVD - Arterial Embolism
• 80%-90% arise from the heart
• 60%-70% of patients suffer from A.Fib
• Non-cardiac: R/T atherosclerosis

PVD - Arterial Embolism: Treatment
• Heparin sodium to prevent distal thrombosis
• Emergent embolectomy
• Percutaneous thrombolysis &/or thrombolytic therapy
• Endarterectomy

PVD - Arterial Embolism: Complications
• Compartment syndrome post embolectomy
• Foot drop 2
nd
to peroneal nerve ischemia
• Renal failure
• Amputations

PVD - Arterial Embolism: Prognosis
• 25%-30% in hospital mortality (heart disease)
• Depends on the location of the occlusion.

PVD - Acute Arterial Thrombosis
• Usually results from atherosclerosis
• Other Risk Factors:
• Trauma
• Low flow rate: hypovolemia & Cardiogenic shock
• Polycythemia
• Dehydration
• Hypercoagulopathy

PVD - Venous Disease: DVT
• 80% of thrombosis begins in the deep vein of the calf.
• 25% of cases progression in to the popliteal and femoral veins.
• 30% of post/op patients develop asymptomatic thrombosis.
• 3% of post/op patients develop S&S of thrombosis.

PVD - DVT: Risk Factors
• Total hip replacement
• Cardiac failure
• Stroke
• Ventilatory support
• Pelvic bone or limb fracture
• Paralysis
• Extended air travel
• Lengthy surgery
• Hypercoagulopathy R/T malignancy, etc

PVD - DVT: Risk Factors
• It is estimated that about 20% of patients with new DVT have an underlying malignancy.

Others:
• Advance age
• A blood group
• Obesity
• Multiple pregnancies
• Oral contraceptives
• IBS


PVD - DVT: S&S
• 50% of patients do not present with S&S
• Dull ache
• Tightness
• Calf pain (pronounced with walking)
• Edema of the affected extremity
• Low grade fever
• Tachycardia
• (+) Homan’s sign (50% of patients)

PVD - DVT: Diagnostic Tools
• Duplex ultrasound

PVD - DVT: Complications
• Pulmonary Embolism
• Varicose veins
• Chronic venous insufficiency

PVD - DVT: Treatment
• Anticoagulation with Heparin to reach a goal of PTT (partial thromboplastin time) of 1.5-2 times normal).
• Warfarin after heparinization.
• Exonaprin (does not require monitor labs)

Comparison
Arterial vs. Venous
• Arterial Occlusion
• Claudication and rest pain
• Hair loss, coolness of the skin.
• Unequal peripheral pulses.
• R/T atherosclerosis mainly
• Dx with Duplex Ultrasound

DVT (venous)
• Pain and edema of the calf and /or thigh
• 50% of patients are asymptomatic
• Hx of CHF, recent Sx, trauma, neoplasia, oral contraceptives, and/or prolonged inactivity.
• Dx with Duplex ultrasound