Running head: PAIN CASE STUDY

Case Study: Pain
Amit Dhir, Omeid Heidari, Sean Mayer, Ololade Ikuomola & Adam Boyce
NR110.542 Physiological/Pathophysiological Basis for Advanced Nursing Practice I
09/29/2015
Johns Hopkins University School of Nursing

On our honor, we pledge that we have neither given nor received any unauthorized assistance on this assignment.
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Running head: PAIN CASE STUDY

CASE STUDY
Pain

Use this document in documenting your response to the Patient Case Questions. CHIEF COMPLAINT
“My back is killing me. The pain is mostly sharp and stabbing, and sometimes it’s a dull ache.
You’ve got to do something. Those Tramadol pills aren’t cutting it and they’ve bound me up.” “I am not sleeping because of the pain.” MEDICAL HISTORY
P.M. is a retired, 81­year­old male being seen for a routine health maintenance visit. He has a history of lower back pain, morbid obesity, hypertension, hypothyroid, occipital lobe stroke, bilateral total knee arthroplasty, GERD and sleep apnea. Now reporting pain in feet. He has been a smoker for the past 64 years, reporting 1­2 ppd. He is accompanied by his wife of 62 years. CURRENT MEDICATIONS
Tramadol 50­100 mg p.o. Q 12 hrs prn back pain
Atenolol 25 mg p.o. Q a.m.
Levothyroxine sodium 125 mcg p.o. Q a.m.
Clopidogrel 75 mg p.p. Q a.m.
Ibuprofen 600 mg ii p.o. prn knee pain
Aspirin 650 mg p.o. prn “when I can’t get to sleep”
Multi­vitamin i p.o. Q a.m. PHYSICAL EXAM
Vital Signs
Blood pressure: 112/68; A­rate: 86; respirations: 20; oral temperature: 97.2º F; height: 70”; weight: 320 pounds; BMI: 45.9

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General
: morbidly obese man in distress; winces and supports lower back with his hands. Head and neck normal. Lungs are clear to auscultation. Abdominal exam positive for tenderness over epigastric region. Bilat lower legs with ruborous edema with +2 ­ +3 pitting over dorsal feet.
Dorsalis pedis and posterior tibial pulses are +1 bilat. Musculoskeletal exam with reduced ROM of back, limited by pain in lower lumbar region with flexion and extension. Straight leg raise testing is negative to 50 degrees elevation, limited by pain in knees. There is increased tone in the lumbar paraspinal muscles diffusely, but no focal tenderness. Crepitus is present in the right knee. ROM of the knees is limited by pain. Neurological exam: alert and oriented X 3. Cranial nerves intact with exception of absence of lateral peripheral vision. Grip strength good and equal bilaterally. Leg strength 5/5 proximally and distally. Sensation is intact to light touch, sharp, position and vibration in arms and legs. Reflexes are ++ at biceps, triceps, patellae and ankles.
Gait is slightly unsteady with wide base of support and reduced step height.
Laboratory Results
: CBC WNL. Fasting glucose = 175; Thyroid profile WNL. BUN = 20;
Creat = 1.4. Spinal x ray shows decreased intervertebral height, endplate sclerosis, osteophyte formation. 3

Running head: PAIN CASE STUDY

I. Provide a brief and concise history of the patient’s problem and description of the disease? Brief History:
P.M. is a morbidly obese 81­year­old man who presents with complaints of increased non­specific lower back pain, which is sharp, stabbing, and sometimes dull, with a tendency to wake him up at nights. The pain unrelieved by his current pain medications i.e.
Tramadol. Pt. reports “Tramadol is just not cutting it.” Pt. also explains presence of epigastric pain, which possibly due to history of GERD, which is exacerbated by being obese, smoking and other lifestyle habits. He also presents with a new onset of bilateral feet pain, which could be due to a possible undiagnosed diabetes and lower leg pitting edema. During physical exam PM’s
ROM and reflexes are limited with presence of crepitus in bilateral knees. Pt. is experiencing these deficits due to pain in the lower back, pain in his knees and also largely due to the possible underlying progressive degenerative disease process he is presenting with. Straight leg testing is negative to 50 degrees elevation limited by pain in knees. There is increased tone in the lumbar paraspinal muscles diffusely, but not focal tenderness. Spinal x­ray shows decreased intervertebral height, endplate sclerosis, osteophyte formation. Pt.’s back pain and ineffective medication effect is believed to be exacerbated by other presenting symptoms as well i.e. epigastric pain, limited ROM, feet pain. In the presence of spine disease process, pt. is otherwise neurologically intact.
Pathogenesis:
The case study identifies a given abnormality. How does the pain process evolve? Describe the sequence of cellular and tissue events that take place from the time of initial contact with an etiological agent until the ultimate expression of pain.
The sensation of pain is comprised of at least two elements: the local irritation
(stimulation of peripheral nerves) and the recognition of pain (within the CNS). Free nerve endings called nociceptors are located in the skin, muscle, joints, bones, and viscera. Nociceptors respond to tissue injury (Hitner & Nagle, n.d.). When there is no injury, there is no pain stimulus, so the nociceptors are quiet. When a pain­generating event happens, biochemical changes occur within the localized area of the injury. Usually, prostaglandins, histamine, bradykinins, serotonin, and Substance P are among the peripheral neurotransmitters released that trigger nociceptors to wake up. Nociceptors alert the brain to the intensity of the pain by increasing the frequency of signals sent to specialized areas within the CNS (Hitner & Nagle, n.d.). The signals travel through the spinal cord into the area called the dorsal horn where they are rerouted to the appropriate area of the brain that can interpret the intensity and quality of pain present. Pain signals are sent up A­delta nociceptor and C­nociceptor fibers in the ascending pathways to the brain. If the signal is passed through the A­delta fibers (myelinated), the pain is consciously experienced as sharp. If the signal is passed through C fibers (unmyelinated), dull, aching pain is felt.

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Nociceptive pain can only occur when all neural equipment (nerve cells, nerve endings, spinal cord, and brain) is working properly (McCance, Huether & Brashers, 2014).
Pain duration is either acute or chronic. Acute pain usually appears in association with an observable injury (e.g., sunburn, broken foot, muscle sprain, or headache) and disappears when the injury heals. Chronic pain persists for weeks, months, or years even with analgesic therapy
(Munson, n.d.). Nociceptive pain can be either acute or chronic while neuropathic pain is chronic, even though it may be intermittent. If an injury doesn't heal or the pain is not adequately inhibited, nociceptors get "really irritated", a condition known as peripheral sensitization, and send so many signals through the CNS that the patient over responds to even normal stimuli, such as a feather or brush touched to the area. In neuropathic conditions sensitization can also occur within the spinal neurons observed as over responsiveness (hyperalgesia), prolonged pain, or the spread of pain to an uninjured area (referred pain) (McCance, Huether & Brashers, 2014). Therefore, pain is the result of a complex series of steps from a site of injury to the brain, which interprets the stimuli as pain. Pain that originates outside the nervous system is termed nociceptive pain; pain in the nervous system is neurogenic or neuropathic pain (Munson, n.d.). Neurogenic pain is associated with neural injury. Pain results from spontaneous discharges from the damaged nerves, spontaneous dorsal root activity, or degeneration of modulating mechanisms. Neurogenic pain doesn't activate nociceptors, and there's no typical pathway for transmission (Munson, n.d.) Nociception begins when noxious stimuli reach pain fibers. Various agents, such as chemicals, temperature, or mechanical pressure, stimulate sensory receptors called nociceptors—which are free nerve endings in the tissues—. If a stimulus is sufficiently strong, impulses travel via the afferent nerve fibers along sensory pathways to the spinal cord, where they initiate autonomic and motor reflexes. The information also continues to travel to the brain, which perceives it as pain. Several theories have been developed in an attempt to explain pain
(Munson, n.d.). Nociception consists of four steps: transduction, transmission, modulation, and perception (McCance, Huether & Brashers, 2014). . Transduction ­ Transduction is the conversion of noxious stimuli into electrical impulses and subsequent depolarization of the nerve membrane. Algesic substances that sensitize the nociceptors and are released at the site of injury or inflammation create these electrical impulses.
Examples include hydrogen ions and potassium ions, serotonin, histamine, prostaglandins, bradykinin, and substance P.

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Transmission ­ A­delta fibers and C fibers transmit pain sensations from the tissues to the
CNS.
A­delta fibers are small diameter, lightly myelinated fibers. Mechanical or thermal stimuli elicit a rapid or fast response. These fibers transmit localized, sharp, stinging, or pinpricking type pain sensation. A­delta fibers connect with secondary neuron groupings on the dorsal horn of the spinal cord (McCance, Huether & Brashers, 2014). C fibers are smaller and unmyelinated. They connect with second order neurons in lamina
I and II (the latter includes the substantia gelatinosa, an area in which pain is modulated). C fibers respond to chemical stimuli, rather than heat or pressure, triggering a slow pain response, usually within 1 second. This dull ache or burning sensation isn't localized and leads to two responses: an acute response transmitted immediately through fast pain pathways, which prompts the person to evade the stimulus, and lingering pain transmitted through slow pathways, which persists or worsens (McCance, Huether & Brashers, 2014). The A­delta and C fibers carry the pain signal from the peripheral tissues to the dorsal horn of the spinal cord. Excitatory and inhibitory interneurons and projection cells (neurons that connect pathways in the cerebral cortex of the CNS and peripheral nervous system) carry the signal to the brain by way of crossed and uncrossed pathways. An example of a crossed pathway is the spinothalamic tract, which enters the brain stem and ends in the thalamus. Sensory impulses travel from the medial and lateral lemniscus (tract) to the thalamus and brainstem.
From the thalamus, other neurons carry the information to the sensory cortex, where their pain is perceived and understood (McCance, Huether & Brashers, 2014). Another example of a crossed pathway is the ascending spinoreticulothalamic tract, which is responsible for the psychological components of pain and arousal. At this site, neurons synapse with interneurons before they cross to the opposite side of the cord and made their way to the medulla and, eventually, the reticular activating system, mesencephalon, and thalamus.
Impulses then are transmitted to the cerebral cortex, limbic system, and basal ganglia (Hitner &
Nagle, n.d.). After stimuli are delivered, responses from the brain must be relayed back to the original site. Several pathways carry the information in the dorsolateral white columns to the dorsal horn of the spinal cords. Some corticospinal tract neurons end in the dorsal horn and allow the brain to pay selective attention to certain stimuli while ignoring others. This allows transmission of the primary signal while suppressing the tendency for signals to spread to adjacent neurons. Modulation ­ Modulation refers to modifications in pain transmission. Some neurons from the cerebral cortex and brainstem activate inhibitory processes, thus modifying the transmission. Substances—such as serotonin from the mesencephalon, norepinephrine from the pons, and endorphins from the brain and spinal cord—inhibit pain transmission by decreasing the release of nociceptive neurotransmitters. Spinal reflexes involving motor neurons may initiate a
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protective action such as withdrawal from a pinprick or may enhance the pain, as when trauma causes a muscle spasm in the injured area (McCance, Huether & Brashers, 2014). Perception is the end result of pain transduction, transmission, and modulation. It encompasses the emotional, sensory, and subjective aspects of the pain experience. Pain perception is thought to occur in the cortical structures of the somatosensory cortex and limbic system (McCance, Huether & Brashers, 2014). Alertness, arousal, and motivation are believed to result from the action of the reticular activating system and limbic system. No matter what type of pain is present, relief from pain is the therapeutic goal. The specialized medical discipline of pain management has changed the spectrum of therapy and the types of drugs used, especially to achieve satisfactory analgesia as soon as possible. Inadequate control of pain can delay healing. With chronic pain, psychological and emotional changes occur that cause the patient to become tired and irritable; patients develop insomnia, significant stress responses such as increased heart rate and blood pressure, depression, impaired resistance to infection, and even increased sensitization to pain. The psychological component associated with the inability to permanently relieve the pain intensifies the response to pain by stimulating the
CNS.

Epidemiology: What are the incidence, prevalence, mortality, and morbidity of pain?
Incidence:
Persistent Pain:116 million (IOM, 2011)
Prevalence:
More than one­quarter of Americans (26%) age 20 years and over ­ or, an estimated
76.5 million Americans ­ report that they have had a problem with pain of any sort that persisted for more than 24 hours in duration (NCHS, 2011). Adults age 45­64 years were the most likely to report pain lasting more than 24 hours (30%). Twenty­five percent (25%) of young adults age
20­44 reported pain, and adults age 65 and over were the least likely to report pain (21%)
(NCHS, 2011).
Recent Center for Disease Control and Prevention (CDC) and National Center for Health
Statistics (NCHS) data suggest substantial rates of pain from the various causes and that most people in chronic pain have multiple sites of pain. For U.S. adults reporting pain, causes include: severe headache or migraine (16.1%), low back pain (28.1%), neck pain (15.1%), knee pain
(19.5%), shoulder pain (9.0%), finger pain (7.6%), and hip pain (7.1%) (NCHS, 2011).
Mortality/Morbidity:
There is not strong research on morbidity and mortality of pain. While pain is not associated with mortality, morbidity in terms of lost productivity, use of medical services, and cost to society is staggering.
The total annual incremental cost of health care due to pain ranges from $560 billion to
$635 billion (in 2010 dollars) in the United States, which combines the medical costs of pain care and the economic costs related to disability days and lost wages and productivity. Lost
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Running head: PAIN CASE STUDY

productive time from common painful conditions was estimated to be $61.2 billion per year, while 76.6% of lost productive time was explained by reduced work performance, not absenteeism (American Productivity Audit, 2010).
More than half of all hospitalized patients experienced pain in the last days of their lives and although therapies are present to alleviate most pain for those dying of cancer, research shows that 50­75% of patients die in moderate to severe pain (American Productivity Audit,
2010).
Risk Factors:
Increased age, morbid obesity, smoking, spinal x ray showing decreased intervertebral height, endplate sclerosis, osteophyte formation, likely osteoarthritis and possible tolerance to narcotics II. Selected Case Study Questions Note: faculty will select specific questions to be answered Describe the results of the pertinent laboratory tests relative to pathophysiology. Why were these tests important? How do these tests indicate an alteration in the normal physiology?
By performing a spinal x­ray to reveal osteophyte formation and decreased intervertebral height the practitioner may have revealed the process of degeneration of the spine, commonly classified as lumbar spine osteoarthritis (Good, Carey & Jordan, 2013). Many imaging techniques can be used to diagnose and quantify osteoarthritis; however, plain film radiographs are frequently utilized due to their inexpensive nature and the fact that they are easily obtained
(Goode, Carey & Jordan, 2013). X­rays can be suggestive of not only malignancy, but also fracture and infection. As an initial study of choice, they also can be analyzed for signs of osteophytes, foraminal narrowing, end plate sclerosis, and disk space narrowing (Madigan,
Vaccaro, Spector & Milam, 2009). In the spine, the presence of both intervertebral disc degeneration and osteophyte formation at the vertebral level has been used to characterize lumbar spine osteoarthritis­­also referred to as spondylosis (Goode, Carey & Jordan, 2013).
These changes and development of vertebral osteophytes, facet joint osteoarthritis, and disc space narrowing all have adequate nerve supply and are frequently associated with instances of lower back pain (Goode, Carey & Jordan, 2013).
Specifically, a vertebral osteophyte is a bony outgrowth that arises at the junction of bone and cartilage. These growths can form without cartilage damage in healthy joints; however, the fact that osteophytes are seen in our patient with decreased intervertebral height may be indicative of increased load on facet joints and have led to cartilage alteration (Goode, Carey &
Jordan, 2013). The role of vertebral osteophytes in combination with intervertebral disc degeneration still constitute a debated pathophysiological process and a specific definition that combines these features in relation to spinal osteoarthritis is still unknown (Goode, Carey &
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Jordan, 2013). The fact that endplate sclerosis is also seen in the presenting patient may indicate areas of degeneration where fat has been replaced by sclerotic bone (Madigan et al., 2009).
However, by utilizing a plain film radiograph, practitioners gain more information regarding the origin of lower back pain from innervated structures. One can then more efficiently associate lower back pain with pathological processes such as degenerative disc disease or spondylolysis as mentioned above (McCance, Huether & Brashers, 2014).
By checking the patient’s kidney function the practitioner has attempted to rule out any intraabdominal pathology such as renal stones. They also have found that the CBC is within normal limits. This is relevant in this particular case due to the fact that a practitioner would need to rule out the possibility of osteomyelitis­­which can be associated with diabetes mellitus or the elderly (Papdakis & McPhee, 2016). In fact, in older patient populations the most common sites of hematogenous osteomyelitis are the thoracic and lumbar vertebral bodies
(Papadakis & McPhee, 2016).
What else would you like to know from this patient? I would like to know if the pain from the patient’s lower back radiates down into his sacroiliac region. I would inquire into this because lower back pain often affects the area between the lower rib cage and the gluteal muscles while radiating to the thighs (McCance,
Huether & Brashers, 2014). I would also ask if the pain he reports in his feet is only when moving around and walking, or if it is also at rest as lower extremity claudication is typically absent unless lumbar stenosis is also present (Madigan et al., 2009). In addition to both of these questions I would inquire into his wide­based gait. A wide­based gait (in conjunction with pseudoclaudication and thigh pain after lumbar extension) can be associated with spinal stenosis
(Chou, 2014).
In general I would ask about any unexplained weight changes related to hypothyroidism.
The patient is described as being morbidly obese­­which could also be a contributing factor to our laboratory finding of decreased intervertebral height. I would ask if he is having any pain at night, night sweats, fevers, any history of localized tenderness, history of cancer and also bacterial infections. Any urinary and GI complications such as blood in urine or stool, pain upon urination, new onset incontinence, urinary retention, or saddle anesthesia should also be inquiries as many of these can evoke suspicion of spinal infection associated with lower back pain
(McCance, Huether & Brashers, 2014). By asking if the patient has used any injection drugs recently I would also be gathering information regarding the possibility of osteomyelitis­­which could rapidly progress and present as fever, pain and sensory and motor dysfunction (Papadakis
& McPhee, 2016). Finally, I would inquire into any history of depression or psychosocial distress as patients with psychosocial stress are at increased risk for chronic lower back pain and poorer functional outcomes (Chou, 2014).

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What exam findings are especially pertinent for this case? What additional assessment would you like to perform?
One of the major exam findings that is especially pertinent for this case is the musculoskeletal exam. This yielded a reduced range of motion of the patient’s back­­particularly upon flexion and extension. This is a significant finding due to the fact that pain upon extension of the back may be associated with facet joint disease (Madigan, et al., 2009). Also very important is the assessment of the patient’s grip, upper extremity and lower extremity strength.
The patient exhibits adequate grip strength and 5/5 leg strength, which both rule against involvement of sciatic nerve or lumbar and sacral nerve roots (McCance, Huether & Brashers,
2014).
Acute back pain that involves these nerves often can manifest with both neurosensory and motor deficits, or marked weakness (McCance, Huether & Brashers, 2014). The patient exhibits 2+ reflexes of his biceps, triceps, patellae and achilles, and does not necessarily manifest sensory symptoms such as focal tenderness upon palpation. This is an important finding since impaired patellae and achilles reflexes could possibly be indicative of degenerative disc disease with herniation (Chou, 2014). His straight leg raise testing is limited by knee pain, likely due to history of bilateral total knee arthroplasty. However, I would like to perform a crossed­straight leg test. This would assess for a herniated disc by passively raising one leg to see if the elevation produces pain in the opposite leg (Chou, 2014). I also would evaluate the patient’s lymph nodes for inflammation and possibly a prostate exam to rule out other malignancies based on the patient’s responses to my inquires about genitourinary function. Finally, I think it is important to auscultate for an aortic bruit on this patient due to the epigastric pain that he complained of upon performance of an abdominal examination.
Which nociceptor(s) is/are likely responsible for the pain?
A­delta fibers, stimulated by mechanical deformation (mechanonociceptors), transmit,
“well­localized ‘fast’ pain sensations.” C­fibers are unmyelinated and transmit the dull, aching sensations that are longer lasting and generalized. (McCance, Huether & Brashers, 2014). Pain transmission is the conduction of pain impulses along the A­delta and C fibers into the dorsal horn of the spinal cord and to the brainstem, thalamus, and cortex. (McCance, Huether &
Brashers, 2014).
Describe any drug­drug or drug­disease interactions that you should address.
● Multivitamins/Minerals with
Clopidogrel may enhance the antiplatelet effect of Agents with Antiplatelet Properties. (Lexicomp, 2015)
● Ibuprofen (an NSAID) may enhance the anticoagulant effect of Anticoagulants
(Clopidogrel and ASA) (Solomon, 2015)
● Ibuprofen (an NSAID) may diminish the antihypertensive effect of Beta­Blockers
(Atenolol) (Solomon, 2015)
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● Aspirin has shown to enhance the antiplatelet effect of Ticagrelor (a drug in the same class as Clopidogrel) Low doses should be recommended (Lexicomp, 2015)
● Ibuprofen (NSAID) may enhance the adverse effect of Salicylates (ASA). An increased risk of bleeding may be associated with use of this combination (potentiated by the use of
Clopidogrel) (Solomon, 2015) Describe the disease process you would discuss with the patient and his wife.
This question will be addressed in section IV. III. Pertinent diagnostic and laboratory tests relative to pathophysiology What diagnostic testing would you like to perform and what specific pathophysiology will you be looking for?
It is essential to note that pain especially in the back and legs can be a result of acute and chronic disease processes. As P.M. presents with new onset leg pain and debilitating back pain, further imaging and diagnostic studies must be performed to determine the etiology of these symptoms taking into account his medical history and current presentation. An MRI,
Electromyogram, Venous Ultrasound, and Bone scan will be used to evaluate for typical and atypical presentation of several conditions.
MRI
With positive findings of decreased intervertebral height and endplate sclerosis on spinal
X­ray, there is need for an MRI of the Thoraco­Lumbar Spine. MRI testing has been relied upon to provide advanced imaging beyond the scope of X­Rays. Walker expresses the accuracy of
MRI testing and its usage in viewing soft tissue structures, ligaments and neural anatomy
(Walker, 2012). An MRI in this case can be used to diagnose spinal stenosis or degenerative disc disease. Sciatica can be ruled out because of lack or neurosensory symptoms. Osteophyte formation, which was found on the X­ray, has been found to be a precursor to spinal stenosis. In spinal stenosis, there is a narrowing of the spinal canal, which can be secondary to bone enlargement (McCance, Huether & Brashers, 2014). Positive MRI findings that support spinal stenosis include narrowing of the spinal canal or a pinched nerve which could be the cause of back and or leg pain (McCance, Huether & Brashers, 2014). .
P.M. also presents with risk factors that predispose him to DDD such as his age, 81 years old, and a longstanding history of smoking. MRI diagnostics in this case can also prove to be helpful in getting to the root of the issue. Degenerative changes may be apart of the normal aging process of an individual. Cigarette smoke , a key risk factor in P.M’s history, significantly
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decreases overall blood supply during disk formation leading to distorted disk structures
(McCance, Huether & Brashers, 2014). Positive MRI findings that support DDD include disc space collapse of greater than 50%, disc desiccation, an annular tear or cartilaginous endplate erosion (Walker, 2012). Electromyogram P.M.’s limited range of motion and pain on musculoskeletal examination can also call for an Electromyogram to possibly rule out a herniated disc as well as assess nerve damage associated with chronic back pain (Walker, 2012). Lower back and calf/ foot pain pose as incidental findings that correlate with herniated discs, which also appeared in PMs assessment.
Positive findings from Electromyogram that support nerve damage include reduced nerve conduction especially in lower limbs (Walker, 2012). Positive findings that support herniated disc disease as diagnosed by EMG is impulsive electrical activity secondary to loss of typical innervation (
Candotti et.al, 2008).
Venous Ultrasound/D­Dimer
A patient with a warm red painful leg raises a suspicion of a possible DVT. Patients are deemed high risk for clots if they are post operative, sedentary, have a previous history of a clotting disorder, a smokers, and hypertensive (
Bonner & Johnson, 2014). Presence of artificial limb also poses as a risk for developing a clot.
Lab tests that will rule out clotting disorders such as DVT include D­dimer. Elevated D­dimer proves as a positive finding. Venous duplex
(Venous Ultrasound) is another diagnostic study that serves to rule out thrombosis in patients. A positive finding includes a visible clot in the image (
Bonner & Johnson, 2014)
.
Bone Scan A bone scan may also be indicated to assess bone structure, view stress fractures caused by repetitive trauma and visualize current status of skeletal structures as well as rule out malignancies and infections. This exam is of interest because of P.M’s skeletal pain and history of hypothyroidism, which predisposes him to an increased risk for fractures (
Dhanwal, 2011)
.
Obesity also increases the stress on bones and joints that can lead to fractures and progression of chronic disease processes. Pathological findings on a bone scan include presentation of “Hot” and “Cold” spots on film to demonstrate level of radioactive material absorbed.
IV. Patient / Family Education Pain is a very difficult issue for practitioners to address because its origins can often be undefined and may be relenting and unrelieved by certain drugs after a tolerance has built up over time (Swica, 2002) It is important to discriminate between a tolerance and an addiction to pain medication when dealing with patients who are experiencing chronic pain. A tolerance
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occurs when a higher dosage of the same drug is needed to achieve the same effect that a smaller dosage had previously achieved (Swica, 2002). The patient and family need to be educated realistically on the course of this disease through stating what is believed to be the current cause of the pain. With the shortening of the spine on the x­ray it can be concluded that the patient has less CSF in his spinal cord which could be causing vertebrae to rub together causing pain (Levin,
2014). This coupled with the fact that the patient is morbidly obese increases the compression of the spinal cord which could be increasing pain (Chou, 2013).
The osteophyte formation on the patient’s spine could also be a reason that the pain is happening.The pathophysiology behind the formation of osteophytes in unclear but is generally thought to be related to osteoarthritis and the formation of new bone turning into spurs which can sometimes lead to pain when they form around nerve endings in the spine (Schnieder, 2015).
Both of these disease processes are progressive but can be slowed through different interventions that can be performed by the patient (Chou, 2013). Next, I would suggest that this patient be placed on around the clock pain control with a different medication because his back pain is a chronic issue that is affecting his lifestyle and sleeping habits. With the presence of sleep apnea I would not prescribe a medication that caused respiratory depression especially if it needed to be taken at night in order to provide pain relief for sleep because respiratory depression is a side effect of many opioids that limit its usefulness in cases of already impaired breathing (Phillips et al., 2012). The prognosis for this disease course is not a positive outlook because of the progressive state of the disease but should not be presented to the patient and family in that matter. The disease process can be slowed down and pain can be alleviated by lifestyle changes and this is how the family should be educated (Chou, 2013). First, I would educate the family on what may be causing the pain and tell them how the disease typically progresses as have been stated above. You would tell the family that the process of a full recovery from this is unlikely but that the pain can be relieved and the patient can live a largely pain free life. You would then teach different interventions to them that address the patient’s overall health and well­being which would ultimately help to reduce his pain. The patient needs to be taught non­pharmacologic pain management strategies that will help decrease his pain and ultimately increase his overall life satisfaction (Chou, 2013).
The first and most basic thing to teach the patient is to take his pain medication when the pain is beginning instead of waiting until he cannot bear the pain because it will help to maintain better control of the pain (Chou, 2013). He needs to be told not to sit in one place for extended periods because because getting up and walking around every hour or so can prevent stiffness and increase blood flow to different regions of the body which can improve pain relief (Chou,
2013). Remaining active is positive for him but he should not exercise after episodes of pain because it can exacerbate the pain and cause it to be prolonged (Chou, 2013). While the patient should be encouraged to not exercise after an episode of pain it is important to distinguish for him that weight loss will help to decrease the amount of pressure on his back which will help to
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alleviate the pain, so he should not use a slight discomfort of his lower back as an excuse not to exercise (Chou, 2013). He needs to sit in a chair with a straight back on it so that it will help to brace his back and lessen his pain. He also needs to reduce the amount of stress in his life and avoid activities that may aggravate the pain and make it worse (Chou, 2013). I would also speak to the patient about smoking cessation because this is a risk factor for because it is a risk factor for the degenerative process of his back. Even if the patient did not feel that he could stop it would be beneficial for him to cut his smoking down because any amount of decrease could mean great improvements (Chou, 2013). Through these interventions for pain control the patient will be able to live a life that is largely pain free and ultimately slow the course of his disease.
Overall, the way that the patient views and manages his own health will be what determines the course of his disease and education is a key step in this process.

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th
V. Use of evidence­based studies/references using Publication Manual of the APA (6 ed) Bonner, L., & Johnson, J. (2014). Deep vein thrombosis: diagnosis and treatment.
Nursing
Standard 8
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Electromyography for assessment of pain in low back muscles.
Physical Therapy 8
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Chou, R. (2014). Low Back Pain.
Annals of Internal Medicine.
160(11).

doi:10.7326/0003­4819­160­11­201406030­01006
Chou, R. (2013). Patient Information: Low back pain in adults (beyond the basics).
Wolters Kluwer
. Retrieved from http://www.uptodate.com/contents/low­back­pain­in­adults­beyond­the­basics?source=se arch_result&search=Patient information: Back pain

Dhanwal, D. K. (2011). Thyroid disorders and bone mineral metabolism.
Indian Journal of Endocrinology and Metabolism 5
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Goode, A. P., Carey, T. S., & Jordan, J. M. (2013). Low back pain and lumbar spine osteoarthritis: how are they related?
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Hitner, H., & Nagle, B. (n.d.).
Pharmacology: An introduction (6th ed., pp. 195­199).

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