MEDICAL-SURGICAL NURSING:
CARE OF CLIENTS WITH PROBLEMS IN THE OXYGENATION, FLUID & ELECTROLYTE, INFECTIOUS, INFLAMMATORY,
IMMUNOLOGY RESPONSE, CELLULAR ABERRATION
MODULE 1: 1. CATEGORIZED ACCORDING TO DURATION
CONCEPT OF PAIN 2. CLASSIFIED ACCORDING TO INFERRED PATHOLOGY
INTRODUCTION
A. PAIN
 Pain is defined as an unpleasant sensory and emotional
experience associated with actual or potential tissue damage
or described terms of such damage (American Pain Society,
2018).
 Pain can be localized, affecting a specific area of the body, or
it can be general. Most of the time, pain is the reason and the
first manifestation that makes client seek medical attention.
Pain sensation varies individually. It is influenced by beliefs,
attitude and social factors.
TYPES AND CATEGORIES OF PAIN
1.
ACUTE PAIN  differs from chronic pain primarily in its
duration.
 For example, tissue damage as a result
of surgery, trauma, or burns produces
acute pain, which is expected to have a
relatively short duration and resolve with
normal healing.
CHRONIC PAIN  subcategorized as being of cancer or
noncancer origin and can be time limited
(e.g., may resolve within months) or
persist throughout the course of a
person’s life.
 Examples of noncancer pain include
peripheral neuropathy from diabetes,
back or neck pain after injury, and
osteoarthritis pain from joint
degeneration. Some conditions can
produce both acute and chronic pain.
CANCER-  For example, some patients with cancer
RELATED have continuous chronic pain and also
experience acute exacerbations of pain
periodically —called breakthrough pain
(BTP)—or endure acute pain from
repetitive painful procedures during
cancer treatment
NOCICEPTIVE  normal functioning of physiologic
systems that leads to the perception of
PAIN
noxious stimuli (tissue injury) as being
(PHYSIOLOGIC) painful
NEUROPATHIC  pathologic and results from abnormal
PAIN processing of sensory input by the
nervous system as a result of damage to
(PATHOLOGIC) the peripheral or central nervous system
(CNS) or both
 Neuropathic pain is sustained by
mechanisms that are driven by
damage to, or dysfunction of, the
peripheral or central nervous
system and is the result of
abnormal processing of stimuli
MIXED PAIN  Patients may have a combination of
(COMBINATION nociceptive and neuropathic pain. For
example, a patient may have
OF nociceptive pain as a result of tumor
NOCICEPTIVE growth and also report radiating sharp
AD and shooting neuropathic pain if the
tumor is pressing against a nerve
NEUROPATHIC)
plexus. Sickle cell disease pain is
usually a combination of nociceptive
pain from the clumping of sickled cells
and resulting perfusion deficits, and
neuropathic pain from nerve ischemia
NOCICEPTIVE PAIN
TRANSDUCTION
 Transduction refers to the processes by which noxious
stimuli, such as a surgical incision or burn, activate
primary afferent neurons called nociceptors, which are
located throughout the body in the skin, subcutaneous
tissue, and visceral (organ) and somatic
(musculoskeletal) structures
 These neurons have the ability to respond selectively to
noxious stimuli generated as a result of tissue damage
from mechanical (e.g., incision, tumor growth), thermal
(e.g., burn, frostbite), chemical (e.g., toxins,
chemotherapy), and infectious sources. Noxious stimuli
cause the release of a number of excitatory compounds
(e.g., serotonin, bradykinin, histamine, substance P, and
prostaglandins), which move pain along the pain
pathway
 Prostaglandins are lipid compounds that initiate
inflammatory responses that increase tissue swelling
and pain at the site of injury. They form when the
enzyme phospholipase breaks down phospholipids into
arachidonic acid. In turn, the enzyme cyclo- oxygenase
(COX) acts on arachidonic acid to produce
prostaglandins
 COX-1 and COX-2 are isoenzymes of COX and play an
important role in producing the effects of the nonopioid
analgesic agents, which include the nonsteroidal anti-
inflammatory drugs (NSAIDs) and acetaminophen
(Tylenol). NSAIDs produce pain relief primarily by
blocking the formation of prostaglandins in the periphery
  Other analgesic agents work at the site of transduction mechanism analgesic agents, such as tramadol (Ultram)
by affecting the flux of ions. For example, sodium and tapentadol (Nucynta), bind to opioid receptor sites
channels are closed and inactive at rest but undergo and block the reuptake of serotonin and/or
changes in response to nerve membrane depolarization. norepinephrine
Transient channel opening leads to an influx of sodium
that results in nerve conduction. Local anesthetics
reduce nerve conduction by blocking sodium channels.
Anticonvulsants also produce pain relief by reducing
the flux of other ions, such as calcium and potassium
2. TRANSMISSION
 Transmission is another process involved in nociception.
Effective transduction generates an action potential that is
transmitted along the A- delta (δ) and C fibers. A-δ fibers
are lightly myelinated and faster conducting than the
unmyelinated C fibers. The endings of A-δ fibers detect
thermal and mechanical injury, allow relatively quick
localization of pain, and are responsible for a rapid reflex
withdrawal from the painful stimulus. Unmyelinated C
fibers are slow impulse conductors and respond to
mechanical, thermal, and chemical stimuli. They produce
poorly localized and often aching or burning pain. A-beta
(β) fibers are the largest of the fibers and respond to
touch, movement, and vibration but do not normally
transmit pain
 Noxious information passes through the dorsal root
ganglia and synapses in the dorsal horn of the spinal cord.
An action potential is generated, and the impulse ascends
up to the spinal cord and transmits the information to the
brain, where pain is perceived. Extensive modulation
occurs in the dorsal horn via complex neurochemical
mechanisms. The primary A-δ fibers and C fibers release
various transmitters including glutamate, neurokinins, and
substance P. Glutamate is a key neurotransmitter because
it binds to the N- methyl-D-aspartate (NMDA) receptor and
promotes pain transmission.
 The drug ketamine, an NMDA receptor antagonist,
produces analgesia by preventing glutamate from binding
to the NMDA receptor sites. Endogenous and exogenous
opioids bind to opioid receptor sites in the dorsal horn to
block substance P and thereby produce analgesia. The
opioid methadone (Dolophine) binds to opioid receptor
sites and has NMDA antagonist properties.

3. PERCEPTION
 Perception is the result of the neural activity associated
with transmission of noxious stimuli (Apkarian, Bushnell,
Schweinhardt, et al., 2013). It requires activation of higher
brain structures for the occurrence of awareness,
emotions, and drives associated with pain. The physiology
of perception of pain continues to be studied but can be
targeted by mind–body therapies, such as distraction and
imagery, which are based on the belief that brain
processes can strongly influence pain perception

4. MODULATION
 Modulation of the information generated in response to
noxious stimuli occurs at every level from the periphery to
the cortex and involves many different neurochemicals
 For example, serotonin and norepinephrine are inhibitory
neurotransmitters that are released in the spinal cord and
the brain stem by the descending (efferent) fibers of the
modulatory system. Some antidepressants provide pain
relief by blocking the body’s reuptake (resorption) of
serotonin and norepinephrine, extending their availability
to fight pain. Endogenous opioids are located throughout
the peripheral and central nervous systems, and like
exogenous opioids, they bind to opioid receptors in the
descending system and inhibit pain transmission. Dual-

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 NEUROPATHIC PAIN

 Nociceptive injury or inflammation may result in an altered

physiologic response within the nociceptive system. These
changes cause release of inflammatory cytokines that may
alter gene expression and sensitivity in nociceptive fibers. In
turn, these alter nociceptive activity, causing neuropathic
pain.

1. PERIPHERAL MECHANISMS

 At any point from the periphery to the CNS, the

potential exists for the development of neuropathic
pain. Hyperexcitable nerve endings in the periphery
can become damaged, leading to abnormal
reorganization of the nervous system called
neuroplasticity, an underlying mechanism of some
neuropathic pain states. Changes in the number and
location of ion channels can occur. For example,
sodium channels abnormally accumulate in injured
nociceptors, which can lower the threshold for nerve
depolarization and increase response to stimuli,
setting off ectopic nerve discharges
 These and many other processes lead to a
phenomenon called peripheral sensitization, which
is thought to contribute to the maintenance of
neuropathic pain. Topical local anesthetics, such as
lidocaine patch 5% (Lidoderm), produce effects in the
tissues right under the site of application by
“dampening” neuropathic pain mechanisms in the
peripheral nervous system

2. CENTRAL MECHANISMS
 Central sensitization is defined as abnormal
hyperexcitability of central neurons in the spinal cord,
which results from complex changes induced by
incoming afferent barrages of nociceptors. Extensive
release and binding of excitatory neurotransmitters,
such as glutamate, activate the NMDA receptor and
cause an increase in intracellular calcium levels into
the neuron, resulting in pain. Similar to what happens
in the peripheral nervous system, an increase in the
influx of sodium is thought to lower the threshold for
nerve activation, increase response to stimuli, and
enlarge the receptive field served by the affected
neuron.
 As in the peripheral nervous system, anatomic
changes can occur in the CNS. For example, injury to
a nerve route can lead to reorganization in the dorsal horn
of the spinal cord. Nerve fibers can invade other locations
and create abnormal sensations in the area of the body
served by the injured nerve.
 Allodynia, or pain from a normally nonnoxious stimulus
(e.g., touch), is one such type of abnormal sensation and a
common feature of neuropathic pain. In patients with

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 allodynia, the mere weight of clothing or bedsheets on the ANALGESIC AGENTS
skin can be excruciatingly painful NON-OPIOID  Paracetamol and NSAIDS

PAIN ASSESSMENT TOOLS  NSAIDS Decrease pain by inhibiting COX pathway

Combined with opioids
Nephrotoxic
 The highly subjective nature of pain causes challenges in
assessment and management; however, the patient’s self- COX-1 mediates prostaglandin formation
report is the undisputed standard for assessing the existence involved in maintenance of physiologic
and intensity of pain. Self-report is considered the most function
reliable measure of the existence and intensity of the patient’s
pain. Accepting and acting on the patient’s report of pain are COX-2 mediates prostaglandin formation
sometimes difficult. Because pain cannot be proved, the that results in symptoms of pain,
health care team is vulnerable to inaccurate or untruthful inflammation and fever
reports of pain. OPIOID Acts on CNS to SIDE EFFECTS:
(NARCOTICS) inhibit activity  Respiratory
 COMPREHENSIVE PAIN ASSESSMENT: PATIENT ascending Depression and
INTERVIEW nociceptive sedation
pathways o Nausea and
o Location of Pain vomiting
o Intensity o Constipation
o Quality (Sharp, Shooting, Burning) o Inadequate
o Onset and Duration pain relief
o Aggravating and Relieving Factors o Tolerance and
o Effect of pain on function and quality of life Addiction
o Comfort-function (pain intensity) goal o Pruritus
o Other information (culture, past pain experiences, o Urinary
pertinent medical history, laboratory tests, diagnostic Retention
studies)

1. PAIN INTENSITY
NUMERIC The NRS is most often presented as a
RATING horizontal 0- to-10-point scale, with word
SCALE (NRS) anchors of “no pain” at one end of the scale,
2. PATIENTS UNABLE TO SLEF-REPORT PAIN “moderate pain” in the middle of the scale, and
“worst possible pain” at the end of the scale.
FLACC indicated for use in young children. Scores WONG- The FACES scale consists of six cartoon faces
are assigned after assessing Facial BAKER with word descriptors, ranging from a smiling
expression, Leg movement, Activity, Crying, FACES PAIN face on the left for “no pain (or hurt)” to a
and Consolability, with each of these five RATING frowning, tearful face on the right for “worst
categories assigned scores from 0 to 2, SCALE pain (or hurt).” Patients are asked to choose
yielding a total composite score of 0 to 10. the face that best reflects their pain. The faces
Scores of “0” are interpreted as reflecting are most commonly numbered using a 0, 2, 4,
that the patient is relaxed and comfortable, 6, 8, 10 metric, although 0 to 5 can also be
scores of “1” to “3” are interpreted as used. Patients are asked to choose the face
consistent with mild discomfort, scores from that best describes their pain. The FACES
“4” to “6” are considered consistent with scale is used in adults and children as young
moderate pain, and scores from “7” to “10” as 3 years
are considered consistent with severe FACES PAIN The FPS-R has six faces to make it consistent
discomfort or pain. SCALE- with other scales using the 0 to 10 metric. The
PAINAD (PAIN indicated for use in adults with advanced REVISED faces range from a neutral facial expression to
ASSESSMENT dementia (FPS-R) one of intense pain and are numbered 0, 2, 4,
IN ADVANCED 6, 8, and 10 Faces scales have been shown to
DEMENTIA) Patterned after FLACC be reliable and valid measures in children as
young as 3 years of age; however, the ability to
CPOT indicated for use in patients in critical care optimally quantify pain (identify a number) is
(CRITICAL units not acquired until approximately 8 years of age
CARE PAIN VERBAL A VDS uses different words or phrases to
OBSERVATION Patterned after FLACC DESCRIPTOR describe the intensity of pain, such as “no pain,
TOOL) SCALE (VDS) mild pain, moderate pain, severe pain, very
severe pain, and worst possible pain.”
PAIN MANAGEMENT VISUAL The VAS is a horizontal (sometimes vertical)
ANALOG 10-cm line with word anchors at the extremes,
1. PHARMACOLOGICAL SCALE such as “no pain” on one end and “pain as bad
as it could be” or “worst possible pain” on the
other end. Patients are asked to make a mark
Page 4 of 6 on the line Although often used in research, the
VAS is impractical for use in daily clinical
practice and rarely used in that setting.
 3. NEUROLOGIC AND NEUROSURGICAL INTERVENTIONS
LOCAL ANESTHETIC Rapidly absorbed - Indicated for intractable pain
AGENTS Blocks nerve conduction
- Indicated for prolonged and severe intractable pain
Vasoconstrictive
 STIMULATION PROCEDURES
 TOPICALS - Applied to the site of injury with a o Intermittent electrical transmission of a tract or center to
vasoconstricting agents
inhibit the transmission of pain impulses (Spinal cord or
- EMLA (Eutectic Mixture of local
deep brain stimulation)
anesthetic)
o Reversible
 INTRASPINAL - directly applied to the nerve root  INTERRUPTION OF PAIN PATHWAYS
through an epidural catheter - permanent
o CORDOTOMY
- Division of certain tracts of the SC
ANTIDEPRESSANTS For neurologic pain and - Interrupt the transmission of pain
unresponsive to opioids o RHIZOTOMY
 TRICYCLIC - sensory nerve roots are destroyed when they enter
ANTIDEPRESSANTS Amitriptyline (Elavil) or the SC reducing nociceptive input
Imipramine (Trofanil) –
therapeutic effect may not
occur before 3 weeks

 SNRIs Duloxetine (Cymbalta) and
venlafaxine (Effexor) first-line
options for neuropathic pain
treatment
ANTICONVULSANTS Gabapentin (Neurontin) and
pregabalin (Lyrica) are first-
line analgesic agents for
neuropathic pain

KETAMINE (KETALAR) Dissociative anesthetic with

dose-independent analgesic,
sedative and amnestic
properties

Third-line analgesic agent for

refractory acute pain

2. NON- PHARMACOLOGICAL

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