Study Guide for Integument: Nursing Care of Individual with Burns – Mod 7

1. What population is most likely to get burned? Which has the highest survival rate
and mortality rate?
• Children 4 years and younger, adults over age 65 = highest fatality rates
• 3rd leading cause of unintentional injury-related death  children 14 years and younger
• Greatest risk are children under 5  limited control of environment, limited ability to act
promptly

2. What are the most critical types of burn wounds?

• Full thickness Skin Destruction: 3rd and 4th degree (See below)

3. How do partial thickness burns differ from full thickness burns? How do first,
second, third degree burns differ in terms of signs and symptoms? How about healing
and scarring?
Partial Thickness Skin Destruction Full Thickness Skin Destruction
• Superficial (first-degree): • Third-and fourth degree burn:
o Clinical Appearance: o Clinical Appearance:
 Erythema, blanching on  Dry, waxy white, leathery, or
pressure, pain and mild hard skin; visible thrombosed
swelling, no vesicles or blisters vessels; insensitivity to pain 
(skin may blister and peel after nerve destruction; possible
24h) involvement of muscles,
o Cause: tendons, bones
 Superficial sunburn; quick heat o Cause:
flash  Flame; scald, chemical; tar;
o Structures involved: electric current
 Superficial epidermal damage o Structure involved:
w/ hyperemia. Tactile and pain  All skin elements; local nerve
sensation intact. endings destroyed; coagulation
o Healing: 3 to 5 days necrosis present; surgical
• Deep (second-degree): intervention needed for healing
o Clinical Appearance: o Healing: Weak to months
 Fluid-filled vesicles that are
red, shiny, wet (ruptured
vesicles); severe pain (nerve
injury); mild/moderate edema
o Cause:
 Flame; Flash; Scald; Contact
burns; Chemical; Tar
o Structure involved:
 Epidermis/dermis; skin
elements (epithelial
regeneration occurs)
o Healing: 2 to 6 weeks

4. Describe the injuries suffered by someone with an electrical burn.

• Result of intense heat generated from electrical current – direct damage to nerves and
vessels, causing tissue anoxia and death can occur
• Assessment findings include:
o Leathery, white, charred skin o Minimal or absent pain
o Burn odor o Dysrhythmias
o Impaired touch sensation o Cardiac arrest
 o Location of contact points
o Diminished peripheral circulation in
injured extremity
o Thermal burns if clothing ignites
o Fractures or dislocations from force
of current
o Head or neck injury if fall occurred
o Depth and extent of wound difficult
to visualize; assume injury greater
than what is seen

5.Describe first aid for the patient with thermal burns.

• Ensure patent airway
• Stabilize cervical spine
• Assess for inhalation injury
• Monitor vital signs, LOC, respiratory
status, O2 sat, cardiac rhythm
• Assess ABCs
• Remove nonadherent clothing, shoes,
watches, jewelry, glasses, contact lenses,
if face exposed
• Establish IV access w/ 2 large-bored caths
for >15% TBSA burn
• Begin fluid replacement
• Insert urinary cath
• Elevate burn limbs above heart to
decrease edema
• Adminsiter IV analgesia and assess
effectiveness freq
• Identify and treat other assoc injuries
• Cover burned areas w/ dry dressing or
clean sheet

6. How do chemical burns look? How does treatment for chemical burns differ from
that of thermal burns?
• Burning; redness and swelling of injured tissue; degeneration of exposed tissue; discoloration
of injured skin; localized pain; edema of surrounding tissue; respiratory distress if chemical
inhaled; decreased muscle coordination; paralysis
• Tx:
o Anticipate intubation w/ significant
inhalation injury, circumferential full-
thickness burns to neck/chest; large TBSA
burn
o Brush dry chemical from skin before
irrigation
o Flush chemical from wound and
surrounding area w/ saline solution of
water
o Contact poison control center for
assistance

7. How is burn surface area estimated using

the rule of nines? Is this method useful for
children?

• Considered accurate for adults

• For irregular burns, palmer surface of hand is
approx 1% TBSA
• Not accurate for pediatrics

8. What signs and symptoms tell you that a

person has suffered from an inhalation injury?
• Hx of being burned in an enclosed space or
clothing catching fire
• Rapid, shallow respirations
• Increasing hoarseness
• Coughing
• Singed nasal or facial hair
• Darkened oral/nasal membranes
• Smoky breath
• Carbonaceous sputum
• Productive cough w/ black, gray, or bloody sputum
• Irritation of upper airways or burning pain in throat or chest
• Difficulty swallowing
• Restlessness, anxiety
• Altered mental status, incl confusion, coma
• Decreased O2 sat
• Dysrhythmias

9. Why do we give tetanus prophylaxis treatment?

• Given routinely – due to anaerobic burn wound contamination

10. What are the most important nursing care problems for the patient with a burn?
Which systems are affected?
• Hypovolemic shock and edema formation
o Hypovolemic shock is caused by massive shift of fluids out of blood vessels 
increased permeability
o Water, sodium, and later plasma proteins move into interstitial spaces
o Colloidal osmotic pressure decreases w/ progressive loss of protein from vascular space
 more fluid shifting out of vascular space into interstitial spaces (second spacing –
fluid in interstitium)
o Third spacing results (ex: exudates and blister formation; edema in nonburned areas)
o Decreased BP; increased pulse
o If not corrected = irreversible shock and DEATH
o Circulatory status impaired  hemolysis of RBCS; thrombosis in capillaries  loss of
circulating RBCs
o Na+ shifts to interstitial spaces and remains there until edema formation ceases
(hyponatremia)
o K+ shifts develops because injured cells and hemolyzed RBCs release K+ into
circulation (hyperkalemia)

11. What are the goals of treatment for patients in the emergent phase, acute phase
and rehabilitative phase? Be sure you can prioritize the goals.
Emergent Phase Acute Phase Rehabilitation Phase
Fluid Therapy: Fluid Therapy: • Counsel/teach pt/family
• Assess fluid needs • Continue to replace fluids, • Encourage/assist pt in
• Begin IV fluid replacement depending on pt’s clinical resuming self-care
• Insert urinary cath response • Prevent or minimize
Wound Care:
• Monitor urine output
Wound Care:
• Start hydrotherapy or
wound cleansing
• Debride as necessary
• Assess extent/depth of
burns
• Initiate appropriate wound
care
• Admin tetanus
toxoid/tetanus antitoxin
Pain & Anxiety:
• Assess/manage
pain/anxiety
Psychosocial Care:
• Provide support to pt/family
during crisis phase
Physical/Occupational
Therapy:
• Place pt in position that
prevents contracture
formation
• Assess need for splints
Nutritional Therapy:
• Assess nutritional needs;
feed pt by most
appropriate route
• Continue contractures; assess
hydrotherapy/cleansing likelihood of scarring
• Assess wound daily/adjust • Discuss possible
dressing protocols PRN reconstructive sx
• Observe for complications • Prepare for discharge
• Continue debridement home/transfer to rehab
• Continue assessing for tx
pain/anxiety
Early Excision and Grafting
• Provide temp homografts
• Provide permanent
autografts
• Care for donor sites
Nutritional Therapy:
• Cont to assess diet to
support wound healing
Physical/Occupational
Therapy:
• Begin daily therapy
program for maintenance
of ROM
• Assess for splints/anti-
contracture positioning
• Counsel/teach pt/family
about physical/psychosocial
aspects of care
• Encourage/assist pt w/ self-
care as possible

12. Describe fluid and electrolyte shifts during the emergent phase of burns. (when
capillaries are very permeable and when diuresis begins).
***I explained this in Question 10***

13. What processes cause acid-base disturbances in a burn patient?

• Hypermetabolism—increased metabolic rate after major trauma and burns is r/t ANS
response and subsequent release of hormones from adrenal glands, hypothalamus, and
pituitary gland
o results in increased heat production and elevation of body temperature
o demonstrated by tachycardia, tachypnea, low grade fever
• Metabolic acidosis - anaerobic metabolism from decreased tissue perfusion  increase in
lactic acid end products. Also decreased renal function due to renal ischemia  retention of
these acid products
o loss of serum bicarbonate

14. Describe fluid therapy for the burn patient in the emergent phase. When do we
use crystalloids, colloids? How do we know if the person is getting enough fluid
replacement?
• IV therapy = adult pt w/ burns > 15% TBSA
• Determined by size and depth of burn; age of pt; indiv considerations (dehydration,
preexisting chronic illness)
Crystalloids Colloids (Albumin)
• First 24 Hrs • Second 24 Hrs
o Brook (Modified) – o 0.3-0.5 ml/kg/%TBSA
  LR sol: 2.0 ml/kg/%TBSA burn o 20%-60% of calculated plasma
 ½ given during 1st 8 hr volume
 ½ given during next 16 hr
o Parkland (Baxter) –
 LR sol: 4 ml/kg/%TBSA burn
 ½ given 1st 8 hr Adequate Fluid Replacement:
 ¼ given each next 8 hr
• Urine output: 30 to 50 ml/hr adult; 75-100
• Example of Parkland: ml/hr for electrical burn pt w/ evidence of
o For a 70kg pt w/ 50% TBSA burn: hemoglobinuria/myoglobinuria
o 4ml X 70kg X 50% = 14,000 ml  • Cardiopulmonary factors: BP (sys >90
14L in 24 hr mmHg), pulse (<120bpm)
o ½ in 1st 8hr = 7000 ml (875 ml/hr)
o ¼ in 2nd 8hr = 3500 ml (436 ml/hr)
o ¼ in 3rd 8hr = 3500 ml (436 ml/hr)

15. What are the dietary needs of a burn person during the healing process? What
types of food should we encourage the person to eat?
• Priority = fluid replacement in emergent phase over nutritional needs
• Non-intubated pts w/ <20% TBSA burn able to eat enough to meet nutritional req
• Intubated pts/those w/ larger burns = need add support 
o Enteral feedings – preserves GI function, increases intestinal blood flow, promotes
optimal conditions for wound healing

16. Why do Curling’s ulcers or stress ulcers develop in people with burns?
• Curling’s Ulcer – type of gastroduodenal ulcer  diffuse superficial lesions (incl mucosal
erosion) caused by generalized stress response  results in decreased production of mucus
and increased gastric acid secretion
• Due to decreased blood flow to GI tract during hypovolemic shock phase
• Tx: prevention; prophylactic use antacids, H2-histamine blockers; PPIs

17. How are medications given to persons with severe burns?

• Given IV 
o GI function is slowed/impaired due to shock/paralytic ileus
o IM will not be absorbed adequately in burned/edematous areas  causes pooling of
meds  pt can be overdosed from accumulation

18. How is pain managed?

• Analgesia: morphine, hydromorphone, fentanyl, oxycodone, methadone, NSAIDs, Adjuvant
Analgesics
• Sedatives: Haldol, Ativan, Versed

19. What are skin grafts; what are the types and why are they used?
• Transplantation of skin
• Types of Grafts
Source Coverage
• Porcine • Temp (3 days – 2 wk)
• Cadaveric Skin • Temp (3 days – 2wk)
• Patient’s Own skin • Permanent
• Patient’s own skin and cell cultures • Permanent
• Porcine collagen bonded to silicone • Temp (10-21 days)
membrane • Temp (10-21 days)
• Human, dermal fibroblast-derived matrix w/
growth factors • Permanent
• Bovine collagen and glycosaminoglycan
bonded to silicone membrane • Permanent
• Acellular dermal matrix derived from
donated human skin

20. What is an escharotomy and why is it done?

• Scalpel incision through full thickness eschar
• Restore circulation to compromised extremities

21. What are pressure garments and why are they worn? How long are they worn each
day?
• Pressure garments prevent and control the formation of hypertrophic scars by applying
counter pressure to the wounded area.
• Pressure garments aid in reducing the effects hypertrophic scarring there by reducing
scarring and deformities.
• Pressure garments should be worn at least 23 hours a day, removing them for bathing and
cleaning of the garments only.
• Most patients will need to wear pressure garments for 12 to 18 months.
Study Guide for Altered Level of Consciousness: Head Injury – Mod 8

1. Which type of head injury is transient in nature? How else are head injuries
classified?
Type: closed Description S/S
Concussion Sudden transient mechanical head injury Disruption in LOC, retrograde
with disruption of neural activity and a amnesia, headache, vomiting
change in the LOC
Contusion Bruising of the brain tissue within a focal Coup-site of impact
area, usually closed head injury Contrecoup- opposite side
Brain stem contusion is much more away from injury
serious, disturbs RAS and can cause coma. *assessment may have focal or
generalized findings, seizures
are common complication
Laceration Actual tearing of the brain tissue; usually Focal and generalized signs;
occur with depressed, open, and hemorrhage common
penetrating injuries
SKULL FRACTURES: all are open Cause
Linear Break in continuity of bone w/out Low-velocity injuries
alteration of relationship of parts
Depressed Inward indentation of the skull Powerful blow
Simple Linear or depressed skull fracture w/out Low to moderate impact
fragmentation or communicating
lacerations
Comminuted Multiple linear fractures with Direct, high-momentum impact
fragmentation of bone into many pieces
Compound Depressed skull fracture and scalp Severe head injury
laceration with communicating pathway to
intracranial cavity

2. When a person is first treated in the ER for a head injury, why do we avoid placing
an NG tube or suctioning the nasopharynx?
-Due to the high risk of meningitis when there is a CSF leak

3. What are the signs of a basilar skull fracture?

-possible cranial nerve deficits
-Battle’s sign (postauricular ecchymosis)
-periorbital ecchymosis (raccoon eyes)
If there’s a tear in the dura:
-rhinorrhea: CSF leakage from the nose
-otorrhea: CSF leakage from the ear

4. What test is most often used to diagnose head injuries?

CT Scan because it allows rapid diagnosis and intervention in the acute setting.

5. What would you do if a person with a head injury begins to vomit?

Give antiemetics.

6. How is an epidural hematoma different from a subdural, type of bleeding and s/s?
Highest risk for a chronic subdural hematoma?
Type Bleeding S/S
Epidural Between the dura and inner Venous: develop slowly
Hematoma surface of the skull, neurological Arterial: develops rapidly, under high
emergency and usually involved pressure
a major artery Unconsciousness, followed by brief lucid
 period, then decrease in LOC
Possible headache, N/V
Subdural Between the dura mater and Decreasing LOC, headache, ipsilateral
Hematoma arachnoid layer of the meninges, pupil dilates and fixates if ICP is elevated
usually venous and develops
slower, 3-21 days
Chronic Develops over wks-mths; most Why? Larger subdural space due to brain
Subdural at risk are those 50s-60s and atrophy
Hematoma alcoholics

7. What is the most important aspect of neuroassessment? What other pieces of data
do we gather in a good neuroassessment? What is the Glasgow coma scale?
Most Important: LOC

Neuroassessment:
Area Normal Response
Pupils Brisk, consensual constriction CNIII
High ICP- fixed or if both
pupils dilate
Eye Mvmt.; Doll’s Turn head and eyes should move Aid in locating intracranial
Eye Reflex across midline to opposite side lesion
(oculocephalic)
Motor strength- Raises arms if weak palmar surface Test all four extremities for
Palmar Drift Test turns downward and arm drifts any weakness
downward
Spontaneous Pain stimulus, passive ROM
Movement
Always Check Vital Cushings Triad: systolic htn w/wide pulse pressure, bradycardia w/full
Signs and bounding pulse, altered respiration

Glasgow Coma Scale:

1. opening of the eyes
2. best verbal response
3. best motor response
Highest score possible=15
Less than or = 8 indicates coma

8. What is an ICP monitor? What is normal ICP?

ICP monitoring should be used on all patients with a GCS of 8 or less and within abnormal CT
scan or MRI

Normal ICP= 0-15 mm Hg; total pressure exerted by 3 components in skull (brain tissue, blood,
CSF)
Monroe-Kellie Doctrine: relatively constant volume in the rigid skull; body can adapt to changes

Type of Description Extra Stuff

Monitor
Ventriculosto Catheter inserted into the right High risk for infection; can be
my lateral ventricle; fluid coupled distorted by bubbles or excessive
system; “gold standard”; allows for tube length
sampling and drug admin
Fiberoptic Sensor transducer placed within the
Catheter ventricle or brain tissue
Subarachnoid -Be sure drainage devices are
bolt closed for 6 mins for accurate
Epidural reading
wedge -P2>P1= possible noncompliance
and risk for increased ICP
-Inaccurate Readings: CSF
leakage, obstruction (tissue or
clots), kinks, incorrect height of
drainage/pt
LICOX brain Placed in frontal white matter; PbtO2=37-47 normal
tissue measures pressure of oxygen in brain Low=ischemia
oxygenation tissue
catheter
Jugular Placed in internal jugular; measure SjvO2 = 60-80%
venous bulb jugular venous o2 sat which indicates <50-55% indicates impaired
catheter cerebral oxygen supply and demand cerebral oxygenation

9. What would happen if intracranial pressure (ICP) continues to rise? What are the
late signs of increased ICP? If your patient experiences these late signs, what do you
do?

Late Signs Very Late

Decreased LOC Coma
Change in pupil size, equality, Pupils dilated and fixed
reactivity; possible bilateral pupillary
dilation
Decorticate posture Decerebrate and/or absence of motor
response
Inc systolic htn, dec pulse rate, altered Dec systolic bp, inc pulse, respiratory arrest
resp pattern
Rigidity, unilateral decerebrate posture Absence of motor response
CARE:
-HOB to 30 degree; head in neutral position
-intubation and mechanical vent
-ICP monitoring
-Cerebral Oxygenation Monitoring (LICOX, SjvO2)
-PaO2 greater than 100mg
-Maintain Fluid and Electrolyte Balance
-Systolic between 100-160
-CPP >60
-reduce cerebral metabolism
-Drug therapy (mentioned below)

10. Describe the difference between decerebrate and decorticate posturing.

Posture Description Outcome
Decerebrat EXTENSOR; arms extended, More serious; disruption of fibers in
e adducted, hyperpronated, midbrain and brainstem; think “e”
extension of legs w/plantar flexion extension/emergency
Decorticat FLEXOR; internal rotation, Interruption of voluntary motor
e adduction of arm, flexion of tracts in cerebral cortex
elbows, wrists and fingers
11. What drugs are used to manage increased ICP? How do they work?
Drug MOA
Mannitol Plasma expansion, osmotic Monitor fluid and electrolyte
(Osmitrol) effect; reduces blood viscosity balance
which increases CBF also moves May be contraindicated with
fluid from tissue to vessels renal failure
Need a filter and Foley
Corticosteroids Control vasogenic edema, Not for use in head injuries
possibly improve neuronal fnc. Should also be given anti-ulcer
drugs
High Dose Reduces metabolic rate which Total burst suppression (no
Barbiturates reduces CBF spikes) on EEG shows maximal
(tals,ex. May also reduce edema and therapeutic effect
Phenobarbital) provide more uniform blood
supply
AntiSeizure Reduction in seizure, Seizures can increase ICP
Drugs (Dilantin) prophylactic
Others:
Tylenol and ASA are given for hyperthermia.
Paralytic agents are sometimes given to control restlessness and to ensure controlled ventilation
of the patient. Watch out for this though - do you know what problem this causes for you as the
nurse?
Opioids such as morphine and Fentanyl
Benzos are avoided due to hypotensive effects.

12. Why is hyperventilation sometimes used to treat increased ICP?

Hyperventilation lowers the PaCO2 which leads to constriction of cerebral blood vessels, which
reduces CBF and ICP.
Recommended: less aggressive, time limited, transient therapy (PaCO2= 30-35mmHg)
Be sure there is adequate intravascular volume and systemic BP

13. What nursing interventions help control ICP?

•Positioning:
-Provide rest and quiet to prevent increases in ICP.
-Keep stimulation to a minimum.
-Head and neck in proper alignment to promote venous return from the
head to the heart. (This will help lower ICP).
-Turn carefully.
•Support of respiratory function:
-Monitor respiratory status.
-Protect the airway.
-Suction VERY judiciously, only when necessary.
-Vent pts, monitor settings and ABG’s carefully.
-Hyperventilation, hypocapnea, and respiratory alkalosis help constrict
blood vessels in the brain and lower ICP.
-Hypoventilation should be avoided.
•Maintain fluid and electrolyte balance
•Monitor ICP
•Protect from injury
•Maintain nutrition

14. What are complications regarding fluid and electrolyte status in the patient with a
head injury? Why do these complications occur?
Diabetes insipidus (decreased ADH) results in fluid loss
SIADH (increased ADH) results in fluid overload.
Both of these are complications of head injury and damage to the pituitary gland.

15. What should the nurse do if he/she suspects SIADH in a patient with a head
injury?
Notify physician, goal is to restore balance, possible fluid restriction, or severe IV hypertonic
saline solution

16. If a patient with a head injury has a seizure, what do you do first?
Couldn’t find this exactly but from previous tests you should stand and watch. No attempts to
provide privacy should be made! 

Some notes from ppt and other stuff:

Intracranial monitoring devices must be a closed system to prevent infection. The patient must
be positioned correctly and the drain must be patent.
Cerebral perfusion pressure (CPP) indicates how well the circulatory system is proving nutrients
(oxygen and glucose) in particular) to and removing wastes from the brain. The formula for
calculating CPP follows:
CPP = MAP - ICP MAP is mean arterial pressure. As you can see if the ICP rises to the level of
arterial pressure, CPP ceases - not a good deal.
In surgery hematomas are evacuated and bleeding vessels are ligated . Post-op care is the
same as for any craniotomy patient.

Factors affecting Autoregulation (Monroe-Kellie) include:

1. decreased oxygen in the blood - causes dilation of vessels resulting in more blood flow in
the brain - this is usually something we try to avoid in head injuries.
2. acid pH also causes dilation of vessels.
3. increased carbon dioxide in the blood - causes dilation of vessels - we try to avoid this
also
4. increased oxygen and decreased carbon dioxide cause constriction of vessels and lower
the pressure in the brain.
concussion - mild - very seldom permanent; headache, vomiting Watch overnight - wake every
hour and check neurostatus.
Brainstem contusion - comatose immediately - affects RAS; unsure about prognosis,
sometimes wakes up after a day or so; sometimes never wakes up; always hospitalized.
Laceration of brain - tearing of vessels resulting in secondary hemorrhage; could cause the
victim to bleed to death if not treated. Port of entry for infection
SECONDARY INJURIES (remember they occur as a result of the injury and include epidural and
subdural injuries- check #6
PRIMARY INJURIES include open and closed injuries.
Open include fractures: linear - simple, clean, little line - 80% of fractures, usually heal well.
comminuted - more serious, small breakage, indentation, spider linear fracture like you would
get with a baseball bat! compound - external opening, very serious injury.
basilar - occurs at the base of skull along paranasal sinuses and results in CSF leakage in the
nose and ears; also periorbital ecchymosis and ecchymosis behind the mastoid bone.
penetrating skull wound - gunshot wound with entrance and exit wounds; usually massive
internal damage although the outer wounds may not look too bad.
NO NG TUBES UNTIL FRACTURE STATUS IS DETERMINED