Nervous System – Spinal Cord Injury

Spinal cord injuries

 Can have a devastating effect on health & well-being
 SCI is divided into traumatic (result of external physical impact) & non-traumatic (result of disease, infection, or
tumor) categories
 Etiology & pathophysiology of initial injury
o Spinal cord is wrapped in tough layers of dura
o Rarely torn or transected by direct trauma
o Spinal cord injury due to cord compression by:
 Bone displacement
 Interruption of blood supply to cord
 Tumor
o Penetrating trauma (gunshot wound or stab wounds)
o Primary injury  initial mechanical disruption of axons as a result of stretch or laceration
o Secondary injury  ongoing, progressive damage that occurs after initial injury
o Apoptosis occurs & may continue for weeks or months after initial injury
o Complete cord damage in severe trauma related to auto destruction of cord
 Petechial hemorrhage are in central grey matter of cord shortly after injury
o By 24 hours or less after injury, the development of edema above & below the level of injury as a result
of ischemic damage may cause permanent cord damage
 Edema secondary to inflammatory response is harmful because of lack of space for tissue
expansion
 Resultant compression of cord & extension of edema above & below injury increase ischemic
damage
o This ongoing destructive process makes it critical that the initial care & management of the client with a
spinal cord injury be initiated as soon as possible to limit further destruction of the spinal cord
o Resulting hypoxia reduced oxygen tension below level that meets metabolic needs of spinal cord
o Lactate metabolites
o Increased vasoactive substances = norepinephrine, serotonin, dopamine
 At high levels, these vasoactive substances cause vasospasms & hypoxia, leading to subsequent
necrosis
 Unfortunately, the spinal cord has minimal ability to adapt to vasospasm
o Extent of neurological damage caused by spinal cord injury results from:
 Primary injury damage (actual physical disruption of axons)
 Secondary damage (ischemia, hypoxia, microhemorrhage, & edema)
 Because secondary injury processes occur over time, the extent of injury & prognosis for
recovery are most accurately determined 72 hours or longer after injury

Spinal & Neurogenic shock

 Spinal shock
o Temporary neurological syndrome = this syndrome lasts days to months & may mask post-inuury
neurological function
o Characterized by:
 Decreased reflexes
 Loss of sensation
 Flaccid paralysis below level of injury
o Experienced by about 50% of people with acute SPI
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 Neurogenic shock
o Loss of vasomotor tone caused by injury
o Characterized by hypotension, hypothermia, & bradycardia (important clinical cues)
o Loss of sympathetic nervous system innervation causes:
 Peripheral vasodilation
 Venous pooling
 Decreased cardiac output
 These effects are generally associated with a cervical or high thoracic injury
 Classification of SPI
o Classified by mechanism of:
 Injury
 Flexion
 Hyperextension
 Flexion-rotation (the most unstable of all injuries because the ligamentous structures that
stabilize the spine are torn – most often implicated in severe neurological deficits)
 Extension-rotation
 compression
 Skeletal level of injury
 Injury is at the vertebral level, where there is most damage to vertebral bones &
ligaments
o Cervical, thoracic, or lumbar (cervical and lumbar most common)
 Neurological level of injury
 Lowest segment of spinal cord with normal sensory & motor function on both sides of
the body
 Paralysis of all 4 extremities occurs (tetraplegia, quadriplegia) if cervical cord is involved
 Paraplegia results if thoracic or lumbar cord is damaged
 Completeness or degree of injury
 Degree of spinal cord involvement may be:
o Complete cord involvement – results in total loss of sensory & motor function
below level of lesion (injury)
o Incomplete (partial) cord involvement – results in mixed loss of voluntary motor
activity & sensation & leaves some tracts intact
 Clinical Manifestations
o Generally direct result of trauma that causes cord compression, ischemia, edema, & possible cord
transection
o Related to level & degree of injury
o Client with an incomplete lesion may demonstrate a mixture of symptoms
o Higher the injury, the more serious the sequelae
 Proximity of cervical cord to medulla & brain stem
o Movement & functional goals are related to specific location of SCI
o Immediate postinjury problems include:
 Maintaining a patent airway
 Adequate ventilation
 Adequate circulating blood volume
 Preventing extension of cord damage (secondary injury)
o Respiratory system
 Respiratory complications closely correspond to level of injury
 Cervical injury (above level of C4)
 Presents special problems because of total loss of respiratory muscle function
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  Mechanical ventilation is required to keep client alive
 Cervical injury (below level of C4)
 Diaphragmatic breathing if phrenic nerve is functioning
 Spinal cord edema & hemorrhage can affect function of phrenic nerve & cause
respiratory insufficiency
 Hypoventilation almost always occurs with diaphragmatic breathing
 Cervical & thoracic injuries cause paralysis of abdominal muscles & intercostal muscles
 Client cannot cough effectively  leads to atelectasis or pneumonia
 Artificial airway provides direct access for pathogens
 Important to reduce infections
 Neurogenic pulmonary edema may occur
 Pulmonary edema may occur in response to fluid overload
o Cardiovascular system
 Any cord injury above level T6 greatly reduces the influence of the sympathetic nervous system
 Bradycardia(<40 bpm) occurs – atropine may be necessary to increase HR & prevent hypoxemia
 Peripheral vasodilation results in hypotension
 Relative hypovolemia exists because of increase in venous capacitance
 Cardiac monitoring is necessary
 Peripheral vasodilation:
 Decreased venous return of blood to heart
 Decreased cardiac output
 IV fluids or vasopressor drugs may be required to support BP
o Urinary system
 Urinary retention common
 Bladder is atonic & overdistended
 In-dwelling catheter inserted (increased risk of infection)
 Bladder may become hyperirritable
 Loss of inhibition from brain
 Reflex emptying
o Gastrointestinal system
 If cord injury is above T5, primary GI problems are related to hypomotility
 Decreased GI motor activity contributes to development of:
 Paralytic ileus
 Gastric distension (NGT may relieve this)
 Stress ulcers common
 Intra-abdominal bleeding may occur
 Difficult to diagnose
 Indications of bleeding
o Continued hypotension despite treatment
o Decreased hemoglobin & hematocrit
 Expanding girth may also be noted
 Histamine H2 receptor blockers (ranitidine & famotidine) and proton pump inhibitors
(omeprazole/lansoprazole) are frequently used to prevent the occurrence of ulcers during the
initial phase
 Less voluntary neurogenic control over bowel results in a neurogenic bowel
 Injury level of T12 or below:
 Bowel is areflexic
 Decreased sphincter tone
 As reflexes return,

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  Bowel becomes reflexic
 Sphincter tone is enhanced
 Reflex emptying occurs
o Integumentary system
 Consequence of lack of movement is skin breakdown
 Pressure ulcers can occur quickly
 Can lead to major infection or sepsis
o Thermoregulation
 Poikilothermism
 Adjustment of body temperature to room temperature
 Occurs in SCI’s because sympathetic nervous system interruption prevents peripheral
temperature sensations from reaching hypothalamus
 With spinal cord disruption, there is decreased ability to sweat & shiver
 Degree of poikilothermisms depends on level of injury
 Clients with high cervical injuries have a greater loss of the ability to regulate temperature than
do those with thoracic or lumbar injuries
o Metabolic needs
 Nasogastric suctioning may lead to metabolic alkalosis
 Reduced tissue perfusion may lead to acidosis
 Monitor electrolyte levels until suctioning is discontinued & normal diet is resumed
 Loss of body weight is common
 Nutritional needs much greater than expected for immobilized person
 Positive nitrogen & high-protein diet
 Prevents skin breakdown & infection
 Decreases rate of muscle atrophy
o Peripheral vascular problems
 Deep vein thrombosis problem – common during first 3 months post SPI
 Pulmonary embolism is a leading cause of death
 DVT assessments
 Doppler examination
 Measurement of legs & thigh girth
 It is more difficult to detect a DVT in a person with a spinal cord injury because the usual signs
and symptoms, such as pain and tenderness, will not be present.
 Diagnostic studies
o CT scan may be used to assess stability of injury, location, & degree of bone injury
o MRI is gold standard for imaging neurological tissues – used to assess for soft tissue & neural changes
o A comprehensive neurological exam is performed along with assessment of head, chest, & abdomen for
additional injuries or trauma
o Clients with cervical injuries who demonstrate altered mental status may also need vertebral angiography
to rule out vertebral artery damage
 Collaborative care
o Immediate goals are to sustain life & prevent further cord damage
 Patent airway
 Adequate ventilation
 Adequate circulating blood volume
o Systemic & neurogenic shock must be treated to maintain BP
o Thoracic & lumbar vertebrae injuries
 Systemic support less intense than cervical injury
 Respiratory compromise not a severe
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  Bradycardia is not a problem
 Specific problems treated symptomatically
o After stabilization, history is obtained
 Emphasis on how injury occurred
 Extent of injury as perceived by client immediately after event
o Assessment
 Test muscle groups with & against gravity, alone & against resistance, & on both sides of the
body
 Note spontaneous movement
 Sensory examination
 Position sense & vibration
 Brain injury may have occurred – assess history for unconsciousness, signs of concussion, &
increased intracranial pressure
 Planning
o Maintain an optimal level of neurological functioning
o Have minimal to no complications of immobility
o Learn skills, gain knowledge, & acquire behaviors to care for self
o Return to home & community

Autonomic dysreflexia
 Massive uncompensated cardiovascular reaction mediated by sympathetic nervous system
 Occurs in response to visceral stimulation
 Life-threatening
 The return of reflexes after the resolution of spinal shock means that clients with an injury level at T6 or higher
may develop autonomic dysreflexia
 If resolution doesn’t occur, this condition can lead to status epilepticus, stroke, MI, & even death
 Most common precipitating factor is distended bladder or rectum
o Contraction of the bladder or rectum, stimulation of the skin, or stimulation of the pain receptors may also
cause autonomic dysreflexia
 Manifestations:
o Hypertension
o Blurred vision
o Throbbing headache (take BP)
o Marked diaphoresis above lesion level
o Bradycardia
o Piloerection (erection of body hair) resulting from pilomotor spasm
o Flushing of skin above lesion
o Spots in visual field
o Nasal congestion
o Anxiety
o Nausea
 Nursing interventions
o Elevate head of bed at 45 degrees, or sit client upright
o Notify physician
o Assess cause
o Provide immediate catheterization
o Teach client & family causes & symptoms

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 o The most common cause is bladder irritation – immediate catheterization may be necessary to relieve
bladder distension
o Stool impaction can result in autonomic dysreflexia – a DRE should be performed only after application
of an anesthetic ointment to decrease rectal stimulation & to prevent an increase in symptoms

Respiratory Rehabilitation
 Phrenic nerve stimulators or electronic diaphragmatic pacemakers increase mobility
o These devices are not appropriate for all ventilator-dependent clients but may be helpful for those with an
intact phrenic nerve
 Teach cervical level injury clients who are not ventilator dependent
o Assisted coughing
o Regular use of spirometry or deep breathing exercises

Neurogenic bladder
 Any type of bladder dysfunction related to abnormal or absent bladder innervation
 Common problems:
o Urgency, frequency, incontinence, inability to void, & high bladder pressures resulting in reflux of urine
into kidneys

Neurogenic bowel
 Voluntary control may be lost
 High-fibre diet & adequate fluid intake
 Suppositories, small-volume enemas, or digital stimulation by client or nurse
 Carefully record bowel movements
 In the client with an upper motor neuron lesion, digital stimulation is necessary to relax the external sphincter to
promote defecation
 Valsalva maneuver & manual stimulation are useful in clients with lower motor neuron lesions

Neurogenic skin
 Prevention of pressure ulcers & other types of injury to insensitive skin is essential
 Teach these skills & provide information about daily skin care
 Careful positioning & repositioning should be done every 2 hours with gradual increase in time
 A comprehensive visual and tactile examination of the skin should be done twice daily, with special attention
given to areas over bony prominences. The areas most vulnerable to breakdown include the ischia, trochanters,
heels, and sacrum.
 Pressure-relieving cushions must be used in wheelchairs
 Protect skin by avoiding thermal injury
 Assess nutritional status regularly – both body weight loss & weight gain can contribute to skin breakdown

Sexuality
 Important issue regardless of client’s age or gender
 Injury level & completeness of injury are needed to understand the male client’s potential for orgasm, erection, &
fertility, & the client’s capacity for sexual satisfaction
 Treatment for erectile dysfunction include drugs, vacuum devices, & surgical procedures
 Effects of SPI on female sexual response are less clear
 Woman of child-bearing age remains fertile & has the ability to become pregnant or to deliver normally through
the birth canal

Grief & depression

 May feel an overwhelming sense of loss
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  May believe they are useless & burdens to their families
 Response & recovery differ from those experiencing loss from amputation or termina illness
 Working through grief is difficult, lifelong process
 Needs support & encouragement

Head Injuries & Brain Tumors

Glasgow coma scale
 The GCS is a tool for assessing a clients neurologic response to stimuli
 Score of 15 = indicates normal neurologic status
 Score of 10-14 = compromised neurological status
 Score of <7 = severe neurologic deficits & most likely coma

Head injuries
 Broad classification that includes injury to the scalp, skull, or brain
 Can lead to conditions ranging from scalp lacerations or mild concussion to coma & death
 Brain damage from traumatic injury takes two forms: primary or secondary injury
 Can range from mild to sever
 Cranial vault is 3 main components:
o Brain
o Blood
o CSF
 Nursing assessment – GCS, neurological status, presence of CSF leak
 Overall goals:
o Maintain adequate cerebral perfusion
o Remain normothermic
o Be free from pain, discomfort, & infection
o Attain maximal cognitive, motor, & sensory function
 Acute intervention
o Major focus on nursing care related to increased ICP
o Eye problems
o Hyperthermia
o Raise the head of the clients leaking CSF
o Maintain cerebral perfusion
o Prevent secondary cerebral ischemia
o Monitor for changes in neurological status
o Treatment of life-threatening conditions will initially take priority in nursing care

Concussion
 Type of closed head injury
 Brain is compressed by a portion of the skull at time of blow & temporary ischemia of brain tissue results
 Clinical manifestations
o Transient loss of consciousness
o Confusion/amnesia
o Slurred or incoherent speech
o Headache & dizziness
o Nausea & vomiting
 Treatment
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 o Seek medical attention – rule out more serious injury
o Prolong unconsciousness means emergency
 Nursing care
o Glasgow coma scale
o Education
o Reduced activity & stimulation
o Turn q 2 hours to avoid complications

Contusion
 More serious than concussion
 Results in bruising & sometimes hemorrhage of superficial cerebral tissue

Increased Intracranial pressure

 Life-threatening situation resulting from an increase in brain tissue, blood, CSF
 Cerebral edema
o Increased accumulation of fluid in the extravascular spaces of the brain tissue
 Cerebral response to ICP
o As ICP increases, autoregulation (brains ability to alter the cerebral vascular resistance to blood flow
through changes in the diameter of its blood vessels, to maintain a constant blood flow despite
fluctuations in mean arterial BP) & decreased production & flow of CSF are compensatory mechanisms
 Nursing management
o Acute invtervention – respiratory function, fluid & electrolyte balance, monitoring ICP, body position,
protection from injury, psychological consideration
o Evaluation – maintain cerebral perfusion, normal ICP, no complication of immobility

Pharmacology
 Most frequently ordered drugs include:
o Osmotic diuretics –
o Loop diuretics –
o Histamine H2 recetpor antagonist or PPI’s –
o Antiemetics –
o Anticonvulsants –
o Barbiturates –

Cranial surgery
 Cranial surgery may be indicated for a brain tumor, CNS infection, vascular abnormalities, craniocerebral trauma,
epilepsy, or intractable pain
 Types:
o Stereotactic surgery
 Stereotactic is a precision apparatus that assists the surgeon to targe a very precise area of the
brain
o Craniotomy (surgical removal of part of the skull to expose the brain)
 Purpose – most commonly performed surgery for brain tumor removal – may be done to remove
a blood clot & control hemorrhage, inspect the brain, perform a biopsy, or relieve pressure inside
the skull
o Burr holes

Primary brain tumors

 Cause unknown
 Only risk factor is exposure to radiation
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  Classifeid:
o Those arising from the covering of the brain (eg. Dural meningioma)
o Those developing in or on the cranial nerves (eg. Acoustic neuroma)
o Those originating within brain tissue (eg. Glioma) these are the most common
 Clinical manifestations
o Depends on which area of the brain has the tumor
 Diagnostics – neurological exam, CT with contrast, MRI, PET, biopsy, EEG, cytological studies of CSF
 Medical management
o Chemotherapy
o Radiation (tends to be cornerstone treatment for many types)
o Brachytherapy (surgical implantation of radiation to deliver high doses at a short distance)
o Surgical resection
o Drug therapy
 Nursing management
o Assessment – LOC, cognitive function, motor abilities, sensory perception, integrated function, balance &
proprioception, coping abilities

Burns
Burns
 Occur when injury to the tissue of the body is caused by heat, chemicals, electrical current, or radiation – the
resulting affects are influenced by temperature of the burning agent, duration of contact time, & type of tissue that
is injured
 Should be viewed as preventable
 Types of burn injuries:
o Thermal burns
o Chemical burns
o Smoke inhalation injury
o Electrical burns
o Cold thermal injury

Classifications of burn injury

 Severity of injury is determined by:
o Depth of burn
o Extent of burn in percent of TBSA
o Location of burn
o Patient risk factors
 Depth of burn
o Burns have been defined by degrees (1st, 2nd, 3rd, & 4th)
o American Burn Association advocates categorizing the burn according to depth of skin destruction
 Superficial partial-thickness burn – involves the epidermis
 Deep partial-thickness burn – involves the dermis
 Full-thickness burn – involves fat, muscle, & bone
 Extent of burn
o Two commonly used guides for determining the total body surface area
 Lund-Browder chart – considered most accurate because the patient’s age, in proportional to
relative body-area size is considered
 Rule of nines – considered adequate for initial assessment of adult patients

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  Location of burn
o Location of the burn is related to the severity of the injury
o Circumferential burns of the extremities can cause circulatory compromise
o Patients may also develop compartment syndrome
 Patient risk factors
o Older adults heal more slowly than younger adults
o Pre-existing cardiovascular, respiratory, & renal diseases contribute to poorer prognosis
o Diabetes mellitus contributes to poor healing & gangrene
o Physical debilitation renders patient less able to recover
o Concurrent fractures, head injuries, or other trauma also lead to poor prognosis

Phases of burn managmenet

 Prehospital care
 Emergent (resuscitative) – can start 20 minutes post-burn
o Emergent phase is the period of time required to resolve immediate problems resulting from the injury
o Pathophysiology
 Fluid & electrolyte shifts
 Inflammation & healing
 Immunological changes
o Clinical manifestations
o Complications
o Nursing management
 From the onset of the burn event until the patient is stabilized, nursing and collaborative
management predominantly consists of airway management, fluid therapy, and wound care.
 Airway management frequently involves early endotracheal (preferably orotracheal) intubation.
Early intubation eliminates the necessity for emergency tracheostomy after respiratory problems
have become apparent. In general, the patient with major injuries involving burns to the face and
neck requires intubation within 1 to 2 hours after burn injury.
 After intubation, the patient is placed on ventilatory assistance, and the delivered oxygen
concentration is determined by assessing ABG values. Extubation may be indicated when the
edema resolves, usually 3 to 6 days after burn injury, unless severe inhalation injury is involved.
 Escharotomies of the chest wall may be needed to relieve respiratory distress secondary to
circumferential, full-thickness burns of the neck and trunk.
 Within 6 to 12 hours after injury in which smoke inhalation is suspected, a fibreoptic
bronchoscopy should be performed to assess the lower airway. Significant findings include the
appearance of carbonaceous material, mucosal edema, vesicles, erythema, hemorrhage, and
ulceration.
 When intubation is not performed, treatment of inhalation injury includes administration of 100%
humidified O2 as needed. Place the patient in a high Fowler’s position, unless contraindicated
(e.g., spinal injury), and encourage coughing and deep breathing every hour. Reposition the
patient every 1 to 2 hours, and provide chest physiotherapy and suctioning as necessary. If
respiratory failure develops, intubation and mechanical ventilation are initiated.
 Hands and arms should be extended and elevated on pillows to minimize edema. Splints may
need to be applied to burned hands and feet to keep them in positions of function.
 Ears should be kept free of pressure because of their poor vascularization and predisposition to
infection. The patient with ear burns should not use pillows because pressure on the cartilage may
cause chondritis, and the ear may stick to the pillowcase, causing pain and bleeding.
 The patient’s head can be elevated using a rolled towel placed under the shoulders, with care
taken to avoid pressure necrosis.

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  The same holds true for the patient with neck burns. Pillows are removed and a rolled towel is
placed under the shoulders to hyperextend the neck and prevent neck wound contraction.
 Drug therapy
 Analgesics are ordered to promote patient comfort.
 Early in the postburn period, IV pain medications should be given because:
o (1) onset of action is fastest with this route
o (2) GI function is slowed or impaired as the result of shock or paralytic ileus,
o (3) intramuscular (IM) injections will not be absorbed adequately in burned or
edematous areas, causing pooling of medications in the tissues. When fluid
mobilization begins, the patient could be inadvertently overdosed from the
interstitial accumulation of previous IM medications.
 The need for analgesia must be reevaluated frequently as patients’ needs may change and
tolerance to medications may develop over time. Initially, opioids are the drug of choice
for pain control. When given appropriately, these drugs should provide adequate pain
management.
 Sedative/hypnotics and antidepressant agents can also be given with analgesics to control
the anxiety, insomnia, and/or depression that patients may experience.
 Analgesic requirements can vary tremendously from one patient to another. The extent
and depth of burn may not correlate with pain intensity.
 Tetanus toxoid is given routinely to all burn patients because of the likelihood of
anaerobic burn wound contamination. If the patient has not received an active
immunization within 10 years before the burn injury, tetanus immune globulin should be
considered.
 Antimicrobial agents
 VTE prophylaxis
 Nutritional therapy
 Fluid replacement takes priority over nutritional needs
 Early & aggressive nutritional support within hours of burn injury
 Resting metabolic expenditure may be increased by 50-100% above normal
 Core temperature is elevated
 Caloric needs are increased dramatically
 Hypermetabolic state
 Acute (wound healing)
o The acute phase begins with the mobilization of extracellular fluid & subsequent diuresis
o The acute phase is concluded when the burned area is completely covered by skin grafts, or when the
wounds are healed
o Pathophysiology
o Clinical manifestations
 Partial-thickness wounds form eschar, which begins separating fairly soon after injury. Once the
eschar is removed, re-epithelialization begins at the wound margins & appears as red or pink scar
tissue
 Epithelial buds from the dermal bed eventually close in the wound, which then heals
spontaneously without surgical intervention, usually within 10-21 days
 Margins of full-thickness eschar takes longer to separate – as a result, full-thickness wounds
requires surgical debridement & skin grafting for healing
o Lab values
o Complications
 Same complications can be present in the emergent phase & may continue into the acute phase
 Infection
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 o Nursing & collaborative management
 Wound care
 Excision & grafting
 Pain management
 Physical & occupational therapy
 Good time for exercise is during wound cleaning
 Passive & active ROM
 Splints should be custom-fitted
 Nutritional therapy
 Psychosocial care
 Rehabilitative (restorative)
o The rehabilitation phase begins when:
 Burn wounds are healed
 Patient can resume a level of self-care activity
o Complications
 Skin & joint contractures
 Role of exercise cannot be overemphasized
 Constant encouragement & reassurance
 Address spiritual & cultural needs

Emotional needs of the Patient & family

 A common emotional respond is regression
 Early psychiatric intervention
 Assess psychoemotional cues
 Issue of sexuality must be met with honesty
 Family & patient support groups

Burn shock

HIV & Infection

Transmission of hiv
 Fragile virus transmitted only through contact with body fluids  blood, semen, vaginal secretions, & breast milk

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  Subtypes:
o HIV-1 – mutates easily, frequently
o HIV-2 – less transmittable; HIV to AIDs interval longer

Pathophysiology of hiv
 RNA viruse (retrovirus) discovered in 1983
 Binds to specific CD4 & chemokine receptors to enter the cell
 HIV is surrounded by an envelope made up of proteins (including gp120) and contains a core of viral RNA and
proteins.
 HIV has gp120 glycoproteins that attach to CD4 and chemokine CXCR4 and CCR5 receptors on the surface of
CD4+ T cells.
 Viral RNA then enters the cell, produces viral DNA in the presence of reverse transcriptase, and incorporates
itself into the cellular genome in the presence of integrase, causing permanent cellular infection and the
production of new virions.
 New viral RNA develops initially in long strands that are cut in the presence of protease and leave the cell
through a budding process that ultimately contributes to cellular destruction.
 Cells with CD4 receptor sites are infected
o CD4+ T cells (t-helper cells), lymphocytes, monocytes/macrophages, astrocytes, oligodendrocytes
o Immune dysfunction in HIV disease is caused predominantly by damage to and destruction of CD4 + T
cells. These cells are targeted because they have more CD4 receptors on their surfaces than other CD4
receptor-bearing cells.
 Immune problems start when CD4_ T-cell counts drop to below 500 cells/L
o Normal range is 800-1200 cells/L
 Allows for opportunistic diseases/infections

Viral load in the blood

 Initial infection
o Viremia (large viral levels in blood) for 2-3 weeks
 Transmission is more likely when viral load is high
o Followed by prolonged periods (years) of low viral load
o During the time of low viral load, which may last for 10–12 years or longer, clinical symptoms can be
limited. Even without symptoms, however, HIV replication occurs at a rapid and constant rate in the
blood and lymph tissues.
o A major consequence of rapid replication is that errors can occur in the copying process, causing
mutations that contribute to treatment difficulties.

Clinical manifestations & Complications

 Acute infection
o Flu-like symptoms
 Fever, swollen lymph glands, sore throat, headache, malaise, nausea, muscle & joint pain,
diarrhea, or a diffuse rash
 Occurs about 1-3 weeks after infection
 Lasts for 1-2 weeks
o Some people develop neurologic complications such as aseptic meningitis, peripheral neuropathy, facial
palsy, or Guillain-Barre syndrome
o During this time, a high viral load is noted & CD4+ T cell counts fall temporarily but quickly return to
baseline
 Early chronic infection
o Generally asymptomatic

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  Fatigue, headache, low-grade fever, & night sweats often occur
 Most are not aware of infected status
 Intermediate chronic
o CD4+ T cells drop to 200-500 cells/L
 Viral load increases
o HIV advances to a more active state
o Thrush, oral hairy leukoplakia, persistent vaginal candida infections, herpes, bacterial infections, Kaposi’s
sarcoma
 Late chronic or AIDS
o Immune system severely compromised
o Great risk for opportunistic disease
o Possible malignancies, wasting, & dementia

Diagnostic Studies
 Most useful screening tests detect HIV-specific antibodies (may take 2 months to detect antibodies)
 Enzyme immunoassay (EIA) – detects serums & antibodies that bind to HIV antigens on test plates
o IF EIA blood is found positive, the test is repeated
o If both EIA results are found positive, a more specific test is performed:
 Immunofluorescence assay (IFA) – used to identify HIV in infected cells; blood is treated with a
fluorescent antibody against p17 & p24 antigen
 Western blot (WB) – involves the use of gel electrophoresis on purified HIV antigens, then
incubated with serum samples. If antibody in serum is present, can be detected
 Blood that is reactive in all 3 steps is reported as positive for HIV antibodies
 Abnormal blood tests common – neutropenia, thrombocytopenia, anemia & altered liver function tests

Collaborative care
 Monitoring HIV disease progression & immune function
 Initiating & monitoring antiretroviral therapy
 Preventing, detecting, & treating opportunistic infections
 Manage symptoms
 Prevent further transmission
 Drug therapy
o Decrease viral load
o Maintain/raise CD4+ counts
o Delay HIV-related symptoms & opportunistic infections
o Prevent transmission

Hiv testing & counselling

 Testing is the only sure method to determine infection
o Negative results = opportunity for prevention education
o Positive results = treatment & education to protect sexual & drug-using partners
 All testing should be accompanied by pretest & post-test education

Shock Syndrome
Shock
 Syndrome characterized by decreased tissue perfusion & impaired cellular metabolism
o Imbalance in supply/demand for O2 & nutrients

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Classification of shock
 Low flow
o Cardiogenic – systolic or diastolic dysfunction & compromised cardiac output
 Precipitating causes
 Myocardial infarction
 Cardiomyopathy
 Blunt cardiac injury
 Severe systemic or pulmonary hypertension
 Cardiac tamponade
 Myocardial depression from metabolic problems
 Early manifestations  tachycardia, hypotension, narrowed pulse pressure, pulmonary
congestion
 Physical examination
 Tachypnea, pulmonary congestion
 Pallor, cool clammy skin
 Decreased capillary refill time
 Anxiety, confusion, agitation
 Diagnostic studies:
 Lab tests – cardiac enzymes, troponin levels, B-type natriuretic peptide (BNP)
 ECG, chest x-ray, echocardiogram
 Collaborative care
 Restore blood flow to the myocardium by restoring the balance between O2 supply &
demand
 Thrombolytic therapy
 Angioplasty with stenting
 Emergency revascularization
 Valve replacement
 Hemodynamic monitoring
 Drug therapy (eg. Diuretics to reduce preload)
 Circulatory assist devices (eg. Intra-aortic balloon pump, ventricular assist device)
o Hypovolemic – loss of intravascular fluid volume
 Hemorrhage, GI loss (vomiting/diarrhea), fistula drainage, hyperglycemia, diuresis
 Relative hypovolemia (third-spacing)
 Results when fluid volume moves out of the vascular space into extravascular space (eg.
Interstitial or intracavitary space)
 Response to acute volume loss depends on:
 Extent of injury o r insult
 Age
 General state of health
 Clinical manifestations = anxiety, tachypnea, increase in CO & HR, decrease in SV, PAOP, &
urinary output
 If loss is >30%, blood volume is replaced
 Collaborative care
 Management focuses on stopping the loss of fluid & restoring the circulating volume
 Fluid replacement is calculated using a 3:1 rule (3 mL of isotonic crystalloid for every 1
mL of estimated blood loss)
 Distributive
o Neurogenic

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  Hemodynamic phenomenon that can occur within 30 minutes of a SCI at the T5 vertebrae or
above and can last up to 6 weeks
 Can occur in response to spinal anesthesia
 Results in massive vasodilation, leading to pooling of blood in vessels
 The injury results in massive vasodilation without compensation due to the loss of SNS
vasoconstrictor tone
 Clinical manifestations
 Hypotension, bradycardia
 Temperature dysregulation (resulting in heat loss)
 Dry skin
 Poikilothermia (taking on temperature of the environment)
 Collaborative care
 In spinal cord injury: spinal stability
o Treatment of the hypotension & bradycardia with vasopressors & atropine
o Fluids used cautiously as hypotension generally is not related to fluid loss
o Monitor for hypothermia
o Anaphylactic
 Acute, life-threatening hypersensitivity reaction
 Massive vasodilation
 Release of mediators
 Increased capillary permeability – as capillary permeability increases, fluid leaks from
the vascular space into the interstitial space
 Clinical manifestations
 Anxiety, confusion, dizziness
 Sense of impending doom
 Chest pain
 Incontinence
 Swelling of the lips & tongue, angioedema
 Wheezing, stridor
 Flushing, pruritus, urticaria
 Respiratory distress & circulatory failure
 Collaborative care
 Epinephrine first line of treatment
 H1-anithistamines (Benadryl) and H2-antihistamines (Zantac) second line of treatment
 Maintaining patent airway – nebulized bronchodilators & endotracheal intubation may be
necessary
 Aggressive fluid replacement
o Septic
 Infection  spread of response  coagulation cascade  myocardial depression  chocking
cells  increased lactase
 Sepsis = systemic inflammatory response to documented or suspected infection
 Severe sepsis = sepsis & organ dysfunction, hypoperfusion or hypotension
 Septic shock
 Presence of sepsis with hypotension despite fluid resuscitation
 Presence of tissue perfusion abnormalities
 Septic shock has 3 major pathophysiological effects:
o Vasodilation
o Presence of tissue perfusion abnormalities

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 o Myocardial depression
 Clinical manifestations
 Increased coagulation & inflammation
 Decreased fibrinolysis (formation of microthrombi & obstruction of microvasculature)
 Clinical presentation of sepsis is complex & no single symptom or group of symptoms is
specific to the diagnosis
 Hyperdynamic state = increased CO & decreased SVR
 Tachypnea, hyperventilation
 Temperature dysregulation
 Decreased urine output
 Altered neurological status
 GI dysfunction
 Respiratory failure is common
 Collaborative care
 Fluid replacement to restore perfusion (hemodynamic monitoring)
 Vasopressor drug therapy
 Vasopressin for clients refractory to vasopressor therapy
 IV corticosteroids for clients who require vasopressor therapy, despite fluid resuscitation,
to maintain adequate BP
 Antibiotics after cultures are obtained (eg. Blood, wound exudate, urine, stool, sputum)
 Glucose levels <10 mmol/L
 Stress ulcer prophylaxis with H2-receptor blockers
 DVT prophylaxis with low-dose unfractionated heparin or low-molecular weight heparin

Stages of shock
 Initial stage
o Usually not clinically apparent
o Metabolism changes from aerobic to anaerobic
 Lactic acid accumulates & must be removed by blood & broken down by the liver
 Process requires unavailable O2
 Compensatory stage
o Clinically apparent but overlapping stages
o Attempts are aimed at overcoming consequences of anaerobic metabolism & maintaining homeostasis
o Baroreceptors in carotid & aortic bodies activate SNS in response to decreased BP
 Vasoconstriction while blood to vital organs maintained
o Decrease in blood to kidneys activates renin-angiotensin system
 Increased venous return to heart, CO, BP
o Impaired GI motility – risk for paralytic ileus
o Cool, clammy skin from blood – except sept client who is warm & flushed
o Shunting blood from lungs increases physiological dead space
 Decreased arterial O2 levels
 Increase in rate/depth of respirations
 V/Q mismatch
o SNS stimulation increases myocardial O2 demands
o If perfusion deficit corrected, client recovers with no residual sequelae
o If deficit not corrected, client enters progressive stage
 Progressive stage
o Begins when compensatory mechanisms fail

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 o Aggressive interventions to prevent multiple organ dysfunction syndrome
o Change in client’s mental status are important findings in this stage
o Hallmarks of decreased cellular perfusion & altered capillary permeability
 Leakage of protein into interstitial space
 Increased systemic interstitial edema
o Anasarca
 Fluid leakage affects solid organs & peripheral tissues
 Decreased blood flow to pulmonary capillaries
o Movement of fluid from pulmonary vasculature to interstitium
 Interstitial edema
 Bronchoconstriction
 Decreased residual capacity
o Fluid moves into alveoli
 Edema, decreased compliance, worsening V/Q mismatch, tachypnea, crackles, increased work of
breathing
o CO begins to fall
 Decreased artery, cerebral, & peripheral perfusion
 Hypoperfusion
 Weak peripheral pulses
 Ischemia of distal extremities
o Myocardial dysfunction results in:
 Dysrhythmias & ischemia
 Myocardial infarction
 Result = complete deterioration of cardiovascular system
o Mucosal barrier of GI system becomes ischemic
 Ulcers
 Bleeding
 Risk of translocation of bacteria
 Decreased ability to absorb nutrients
o Liver fails to metabolize drugs & waste
 Jaundice, elevated enzymes
 Loss of immune function
 Risk for DIC & significant bleeding
 Refractory stage
o Exacerbation of anaerobic metabolism
o Accumulation of lactic acid
o Increased capillary permeability
o Profound hypotension & hypoexemia
o Tachycardia worsens
o Failure of one organ system affects others
o Recovery unlikely
o Failure of liver, lungs, & kidneys will result in accumulation of waste products such as lactate, urea,
ammonia, and carbon dioxide

Shock diagnostic studies

 Thorough history & physical examination
 No single study to determine shock
o Blood studies – elevation of lactate & base deficit
o 12-lead ECG

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 o Chest x-ray
o Hemodynamic monitoring

Collaborative care
 Successful management includes:
o Indentification of clients at risk for shock & prompt intervention
o Integration of the client’s history, physical exam, & clinical findings to establish a diagnosis
o Interventions to control or eliminate the cause of decreased perfusion
o Protection of target & distal organs from dysfunction
o Provision of multisystem supportive care
 General management strategies
o Ensure patent airway
o Maximize oxygen delivery
 Cornerstone of therapy for septic, hypovolemic, & anaphylactic shock = volume expansion
o Isotonic crystalloids (eg. Normal saline) & colloids (eg. Albumin) for initial resuscitation of shock
 Volume expansion
o Complications of fluid resuscitation  hypothermia & coagulopathy
 Primary goal of drug therapy – correction of decreased tissue perfusion
o Vasopressor drugs (eg. Norepinephrine)
 Achieve/maintain MAP >65 mmHg
 Reserved for clients unresponsive to fluid resuscitation
o Vasodilator therapy (eg. Nitroglycerin, nitroprusside)
 Achieve/maintain MAP >65mmHg
 Nutrition is vital to decreased morbidity from shock
o Initiate enteral nutrition within the first 24 hours
o Protein-calorie malnutrition is one of the main manifestations of hypermetabolism in shock
o Initiate parenteral nutrition if enteral feedings are contraindicated or fail to meet caloric requirements
o Monitor weight, protein, nitrogen balance, BUN, glucose, & electrolytes

Shock evaluation
 Normal or baseline ECG, BP, CVP
 Normal temperature
 Warm, dry skin
 Urinary output >0.5 mL/kg/hour
 Normal RR & SaO2 >90%
 Verbalization of fears & anxiety

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