Class 12: Fractures, inflammation/immunity & burns Flashcards
In infants, fractures are…
Rare
The highest incidence of fractures is in blanks and blank
Young males (15-24) and old people (>65)
Etiology of fractures
-Direct blow, crushing force & torsion
-Cancer, osteoporosis & Cushing’s syndrome
Classification of fractures
-Name of the bone, location of injury, orientation of the fracture & condition of the overlying tissues
Location of injury in fractures includes
Metaphysial, diaphysial and epiphyseal
Orientation of fracture includes the…
Type
Condition of the overlying tissues in a fracture includes..
Open or closed
Fracture identification sentence
A (orientation) (fragmentation) fracture of the (side) (location) of the (bone)
Example of a fracture identification sentence
A (transvere) (segmental) fracture of the (medial) (diaphysis) of the (tibia)
Closed fracture
Skin is intact
Complete fracture
The bone is separated in 2 pieces
Depressed fracture
Bone fragments are driven inward
Impacted fracture
A part of the fractured bone is driven into another bone
Oblique fracture
The fracture line runs at an angle across the axis of the bone
Pathological fracture
The fracture results from weakening of the bone structure by pathological processes such as neoplasia
Transverse fracture
The bone is fractured straight across
Comminuted fracture
The bone is splinted or crushed, creating numerous fragments
Compression fracture
A fractured bone is compressed by another bone
Greenstick fracture
One side of the bone is broken and the other is bent; common in children
Incomplete fracture
The fracture line does not extend through the full transverse width of the bone
Open fracture
The skin is not intact, bone is exposed and infection/soft tissue injury are common
Spiral fracture
The break partially encircles the bone
A broken bone can…
Cause damage to the surrounding tissue, periosteum and blood vessels in the cortex and marrow
Bone tissue destruction…
Triggers an inflammatory response
Procallus formation
A bony callus formation that is part of bone remodeling
Fracture healing time (neonates to later childhood)
-Neonatal period; 2-3 weeks
-Early childhood; 4 weeks
-Later childhood; 6-8 weeks
Fracture healing time (adolescence to adults)
-Adolescence; 8-12 weeks
-Adults vary depending on risk factors
Clinical manifestations of fractures
-Often numbness up to 20 minutes following injury
-Unnatural alignment, swelling, muscle spasms, tenderness, pain, impaired sensation, loss of function, discolouration, bleeding and crepitus
5 P’s to assess in fractures
-Pain & point of tenderness
-Pulse distal to the fracture site
-Pallor
-Paresthesia: Sensation distal to the fracture site
-Paralysis: Movement distal to the fracture site
Assessing injured limb: CSM
-C: Circulation
-S: Sensation
-M: Motion
Positive local factors influencing bone healing
Immobilization, timely reduction, application of ice and electrical stimulation
Positive systemic factors influencing bone healing
-Adequate amounts of growth hormone, vitamin D and Ca+
-Adequate blood supply, younger age and moderate activity level prior to injury
Negative local factors influencing bone healing
Delayed reduction, open fracture (increased risk for infection) and presence of foreign body at the fracture site
Negative systemic factors influencing systemic factors
Immunocompromised, decreased circulation (DM & PVD), malnutrition, osteoporosis and advanced age
Complications of fracture
Avascular necrosis, compartment syndrome, fat embolism, infection and osteomyelitis, PE, nerve compression, delay union/nonunion and skin breakdown
Fat emboli subjective data
-Dyspnea & chest pain
-Confusion, aLOC, numbness, feeling faint, DM & obesity
Fat emboli objective data
-Cyanosis, chest petechiae, pallor & cold extremeties
-Pupillary changes, buccal cavity, conjunctiva and soft palate
-Muscle twitching, shock & vomiting
Nerve compression subjective data
Discomfort, pain, referred pain, burning, tingling, “stinging sensation”, numbness, aSensation & inability to distinguish touch
Nerve compression objective data
Diminished movement & reflexes, weakness, paralysis, irritability, colour changes r/t impaired circulation
Avascular necrosis subjective data
Tenderness & pain, especially on passive motion
Avascular necrosis objective data
Edema, swelling, bleeding from wound, decreased colour, temperature & mobility
Delayedunion/nonunion subjective data
Pain
Delayed union/nonunion objective data
Lack of callus formation on x-ray & poor alignment
Skin breakdown subjective data
Pain
Skin breakdown objective data
-Elevated temp & HR, erythema, edema-cast edges, exposed distal portion of limb within cast and hyperactive reflexes
-Draining and foul odour from break in skin; crepitus
Compartment syndrome subjective data
Severe, unrelenting pain, unrelieved by narcotics and associated with passive stretching of muscle and paresthesias
Compartment syndrome objective data
Edema, paralysis, decreased/absent peripheral pulses, poor cap refill, and limb temp change
Innate & adaptive immunity are..
The 2 main defence systems
Innate immunity
-1st line of defence
-Natural or native immunity
-Inflammation (2nd Line of Defense); biochemical and cellular mechanisms
Adaptive immunity
-3rd line of defence
-Slower but more specific process
Innate & adaptive immunity are blank
Separate but also interdependent
Innate immunity is..
Non specific & always prepared to act quick
First line of defence
Physical (ie. skin)
Common bacteria we encounter
-Staph. aureus
-MRSA, streptococci, VRE & STI
Second line of defense
-Inflammation: First response to injury, quick & non specific
Inflammation vascular response
Vasodilation, increased permeability, and WBC adhere to vessel walls
Inflammation plasma protein systems
Complement system, clotting system & kinin system
Second line of defence: Cell components + leukocytes (1)
-Granulocytes (neutrophils): Band cells/immature neutrophils, eosinophil, basophil (histamine), and mast cells (released during inflammation & healing)
Second line of defence: Cell components + leukocytes (2)
Agranulocytes (monocytes & macrophages): Precursors of macrophages, slower than neutrophils, and better suited for long term defence
Second line of defence: Cell components + leukocytes (3)
B&T cells
Acute inflammation symptoms + local
Swelling, pain, heat & redness
Early/mild inflammation + local
Serous exudate
Severe inflammation + local
Fibrinous & purulent exudate
Fever + systemic signs
-Normal temperature 36-37
-Leukocytes and macrophage; pyrogen
-Pyrogen “fire”
-Mild-moderate vs high fever (39.4-41.1)
Leukocytosis + systemic signs
-Increase in circulating WBC
Inflammation with wounds
-Normal response of living tissue to injury
-Starts- Tissue damage (but NOT destroyed)
-Until healing starts
Infection & wounds
Maggots, cleaning MRSA infection and group A streptococcus
Burns
A traumatic injury to the skin or other organic tissue primarily caused by thermal or other acute exposures
Types of burns
Thermal, cold, electrical, radiation (sunburn), chemical and inhalation (flash burns from fire & steam, hot smoke & CO)
Most common type of burn in children is…
From a scald injury (thermal)
The most common type of burn in adults is…
From a flame
Males are blank..
Twice as likely to be burn victims than females
Childrens skin is…
Thinner & burns 4x more quickly & deeply than adult skin
Children’s rapid physical growth means ..
They also scar more easily
Superficial burn
-1st degree, involing only the epidermis, no blisters
-Painful, dry, red, and blanch with pressure
-Commonly seen with sunburns
Partial thickness burns
-2nd degree involving the epidermis & dermis
-Superficial or deep, caused by prolonged exposure (>10 seconds) to intense heat
Characteristics of partial thickness burns
Blister, moist, serous, edema, pink or red mottling, blanching and very painful
Full thickness burns
-3rd degree extending through all layers of dermis & SC tissue
Characteristics of full thickness burns
Waxy white to leathery gray to charred & black, dry, inelastic, does not blanch, no vesicles or blister formation
Fourth degree burns
Potentially life threatening burns extending through the skin into underlying tissues & fascia, muscle and/or bone
Severity of the burn is determined by…
-Location, pt age, causative agent, contact duration, presence of respiratory involvement and pt general health
Minor burn
3rd degree appear on <2% of the TBSA, 2nd degree burns appear on <10% of a child’s TBSA
Moderate burn
3rd degree burns appear on 2-10% of TBSA regardless of the body size, 2nd degree burns appear on 10-20% of a child’s TBSA
Major burn
20% of TBSA in most adults are major burns, 2nd degree burns covering >20% of a child’s TBSA
Burn assessment tools
-Pt palmer surface, lund-browder chart and rule of nines
-These assessments are used to estimate the % of TBSA involved in a burn injury
Pt palmer surface (hand chart)
-The hand chart is a practical method to determine the extent of a burn, since the palm of the human hand comprises 1% of BSA. Use the patients own hand when using this assessment tool. It can be used to accurately measure the extent of burns that have occurred over many different areas of the body.
-From finger tips to wrist
Rule of nines, look at picture online
Divides the body surface into areas of equal 9% or multiples of 9% of TBSA. This chart is used for adult patients only as BSA proportions do not follow this 9% configuration for children less than 14 years of age
Factors influencing a positive outcome in burns
Multidisciplinary team involved, airway, rehydration, depth and extent of burns, nutrition, pain control, activity, psychological impact on patient and family
Airway + burns
-The first priority of burn care is airway maintenance
-If there is evidence of respiratory involvement, 100% oxygen is administered and blood gas values are drawn including carbon monoxide levels
-If the child is displaying signs of respiratory distress, intubation is performed
The following suggest inhalation of noxious agents or respiratory burns
-Thermal injuries to the face, nares, and upper torso
-A hx of injury in an enclosed space
-An examination of the oral and nasal membranes that reveals edema or blisters
-Evidence of trauma to the upper respiratory passage
CO poisoning
-Colorless, odorless and tasteless gas that has an affinity for hemoglobin 200 x greater than that of oxygen
-Oxygen molecules are displaced and carbon monoxide reversibly binds to hemoglobin to form carboxyhemoglobin (tissue hypoxia)
Mild CO poisoning
-1-10 is normal and 11-20% is mild
-Headache, flushing, aVisual acuity, aCerebral functioning and slight breathlessness
Moderate CO poisoning
-21-40%
-Headache, N/V, drowsiness, tinnitus, vertigo, confusion & stupor, pale to reddish-purple skin, decreased BP, increased & irregular HR
Severe CO poisoning
-41-60%
-Coma & seizures
Fatal CO poisoning (61-80)
Death
Infection control + burns
-Hand & forearm washing is the best
-Large burns may require iso
Infection control + burns cont’d
-Chief danger is wound infection, generalized sepsis and bacterial pneumonia
-Ongoing assessment is crucial
Assessments in burn pts
-ABC
-Signs of shock (hypovolemic and septic), increased temperature
-Intake (both IV and PO), U/O (minimum 1-2 cc/kg/hr), pain control, wound & dressing assessments and psychosocial support
Burn size is…
Essential to guide therapy
The most accurate assessment of TBSA burn in children & adults is the…
Lund-Browder chart
3rd line of defence
-Adaptive immunity
-Slower than innate
-Antigen: Substance capable of stimulating antibodies
3 benefits of adaptive immunity
-Specific: Engages a particular target
-Systemic: Not restricted to a local site
-Memory: It remembers
Adaptive defence system
-Humoral: B lymphocytes
-Cell mediated: T lymphocytes
Lymph nodes
B & T lymphocytes act as surveillance, lymph nodes are widespread
Adaptive immunity: Humoral immunity
-Humoral: Virus free in the fluids of our bodies
-Plasma cells secrete antibodies (immunoglobulin) that binds to antigens
-Memory cell that prevents future re-exposures
Adaptive immunity: Humoral immunity steps
-Bone marrow; B lymphocytes; memory cells & plasma cells
-Plasma cells; antibodies
Humoral immunity
-Antibody circulates in the blood and binds to antigens on infectious agents
-Either directly inactivates the microorganism or activates the inflammatory mediators
-Antibodies are primarily responsible for protection
Adaptive immunity: Cell-mediated immunity T lymphocytes
-Helper: Activates B cells, cytotoxic T cells, NK cells & macrophages
-Cytotoxic (killer): Cell lysis
-Suppressors Th: Expressed as CD4 & T regulatory cells
Adaptive immunity: Cell-mediated immunity
-Cellular: Virus infected cells
-T cells activate lymphocytes & macrophages
-Memory produced
Adaptive immunity: Cell-mediated immunity steps
Bone marrow; T lymphocyte; helper T cell, suppressor T cell, cytotoxic T cell and memory cells
Active & passive immunity
-Adaptive immunity can be either
-Active (active acquired) immunity is produced after either natural exposure to an antigen or after immunization
-Passive (acquired) immunity occurs when preformed antibodies or T lymphocytes are transferred from donor to recipient
To recognize & respond
-Antigen is a molecule that reacts with antibodies or antigen receptors on B and T cells
-Most antigens are immunogenic
-Must be recognized by and bound to an antibody
To recognize & respond cont’d
-Antibodies are aka immunoglobulins
-There are 5 molecular classes of immunoglobulins
5 molecular classes of immunoglobulins
-GAMED
-IgG, IgA, IgM, IgE & IgD
IgG
Most abundant & crosses the placenta
IgA
Found in the blood & body secretions
IgM
Biggest size & first to respond in a primary response
IgE
Least concentrated but specific to allergic responses & in the defense against parasitic infections
IgD
Found in low concentrations with limited knowledge of function
Live/attenuated
Measles, mumps, rubella (MMR), varicella (chicken pox), zosters (shingles), influenza (nasal spray), rotavirus and yellow fever
Inactivated/killed
Polio (IPV), hepatitis A and rabies
Toxoid (inactivated toxin)
Diphtheria, tetanus (DTaP)
Subunit/conjugate
Hepatitis B, influenza (injection), haemophilus influenza type B (Hib), pertussis (DTaP), pneumococcal & meningococcal & HPV
Early & late signs in fractures
-Early: Numbness & tingling
-Late: Cyanosis
Pain is not always….
Congruent with the injury
Avascular necrosis
Fracture interrupts blood supplu to the bone leading to bone death
Fat embolism
Only occurs in larger limbs (ie. Femur) and will develop 48-72hr after the injury
PE in fractures occurs as a result of…
Fat emboli
Compartment syndrome timeline
-Early symptom is numbness & tingling
-4-6 hours after compartment syndrome develops, it is irreversible
The kinin system..
Responds to pain
Inflammation steps
-1. Protect tissue
-2. Limits inflammatory response to a specific area
-3. Interacts with adaptive immune response
-4. Starts the healing process
Agranulocytes live…
Longer than granulocytes in acidic environments
Pt palmer surface burn assessment tool pros & cons
It is the most innacurate but easiest way to measure burns in children
Hourly U/O is used to determine…
Fluid resuscitation in burn pts
IgM & IgG are…
Most common
IgM is the first to…
respond when getting a vaccine and turns into IgG antibodies
Immunocompromised people cannot get…
Live vaccines
