HIV Clinical Stage  Moderate unexplained weight loss (<10%

2 of presumed or measured body weight)

 Recurrent respiratory infections (sinusitis,
I. GENERAL MEDICAL BACKGROUND tonsillitis, otitis media, and pharyngitis)
 Herpes zoster
A. Definition  Angular cheilitis
 Recurrent oral ulceration
 Papular pruritic eruptions
HIV stands for human immunodeficiency virus. It  Seborrheic dermatitis
is the virus that can lead to acquired immunodeficiency  Fungal nail infections
syndrome, or AIDS, if not treated. Unlike some other
viruses, the human body can’t get rid of HIV completely,
even with treatment.

HIV attacks the body’s immune system, Clinical Stage  Unexplained severe weight loss (>10% of
3 presumed or measured body weight)
specifically the CD4 cells (T cells), which help the  Unexplained chronic diarrhea for >1 month
immune system fight off infections. Untreated, HIV  Unexplained persistent fever for >1 month
reduces the number of CD4 cells (T cells) in the body, (>37.6°C, intermittent or constant)
 Persistent oral candidiasis (thrush)
making the person more likely to get other infections or  Oral hairy leukoplakia
infection-related cancers. Over time, HIV can destroy so  Pulmonary tuberculosis (current)
many of these cells that the body can’t fight off infections  Severe presumed bacterial infections (e.g.,
pneumonia, empyema, pyomyositis, bone
and disease. or joint infection, meningitis, bacteremia)
 Acute necrotizing ulcerative stomatitis,
gingivitis, or periodontitis
B. Classification  Unexplained anemia (hemoglobin <8 g/dL)
 Neutropenia (neutrophils <500 cells/µL)
 Chronic thrombocytopenia (platelets
CDC Classification System for HIV-Infected Adults and <50,000 cells/µL)
Adolescents Clinical Stage  HIV wasting syndrome, as defined by the
4 CDC (see Table 1, above)
 Pneumocystis pneumonia
CD4 Cell Clinical Categories  Recurrent severe bacterial pneumonia
Count  Chronic herpes simplex infection (orolabial,
Categories A  B C genital, or anorectal site for >1 month or
Asymptomatic, Symptomatic AIDS- visceral herpes at any site)
Acute HIV, or Conditions, not Indicator  Esophageal candidiasis (or candidiasis of
trachea, bronchi, or lungs)
PGL A or C Conditions
 Extrapulmonary tuberculosis
 Kaposi sarcoma
 Cytomegalovirus infection (retinitis or
(1) ≥500 A1 B1 C1 infection of other organs)
cells/µL  Central nervous system toxoplasmosis
(2) 200-499 A2 B2 C2  HIV encephalopathy
 Cryptococcosis, extrapulmonary (including
cells/µL
meningitis)
(3) <200 A3 B3 C3  Disseminated nontuberculosis
cells/µL mycobacteria infection
Abbreviations: PGL = persistent generalized lymphadenopathy  Progressive multifocal
leukoencephalopathy
 Candida of the trachea, bronchi, or lungs
 Chronic cryptosporidiosis (with diarrhea)
 Chronic isosporiasis
 Disseminated mycosis (e.g.,
histoplasmosis, coccidioidomycosis,
WHO Clinical Staging of HIV/AIDS for Adults and penicilliosis)
Adolescents  Recurrent
nontyphoidal Salmonella bacteremia
 Lymphoma (cerebral or B-cell non-
Clinical Stage Clinical Conditions or Symptoms Hodgkin)
 Invasive cervical carcinoma
 Atypical disseminated leishmaniasis
Primary HIV  Asymptomatic  Symptomatic HIV-associated nephropathy
Infection  Acute retroviral syndrome  Symptomatic HIV-associated
cardiomyopathy
 Reactivation of American trypanosomiasis
(meningoencephalitis or myocarditis)
Clinical Stage  Asymptomatic
1  Persistent generalized lymphadenopathy

C. Epidemiology

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 Since the beginning of the epidemic, more of endothelial cells, is also a common finding in
than 70 million people have been infected with the patients with AIDS.
HIV virus and about 35 million people have died of
HIV. Globally, 36.7 million [30.8–42.9 million] people G. Complications
were living with HIV at the end of 2016. An
HIV infection weakens your immune system,
estimated 0.8% [0.7-0.9%] of adults aged 15–49
making you highly susceptible to numerous
years worldwide are living with HIV, although the
infections and certain types of cancers.
burden of the epidemic continues to vary
considerably between countries and regions. Sub- Infections common to HIV/AIDS
Saharan Africa remains most severely affected, with
nearly 1 in every 25 adults (4.2%) living with HIV
 Tuberculosis (TB). In resource-poor nations,
and accounting for nearly two-thirds of the people
TB is the most common opportunistic infection
living with HIV worldwide.
associated with HIV and a leading cause of death
among people with AIDS.
D. Etiology  Cytomegalovirus. This common herpes virus
is transmitted in body fluids such as saliva, blood,
HIV is a retrovirus that infects and replicates urine, semen and breast milk. A healthy immune
primarily in human CD4+ T cells and macrophages. system inactivates the virus, and it remains
HIV can be transmitted via blood, blood products, dormant in your body. If your immune system
sexual fluids, other fluids containing blood, and weakens, the virus resurfaces — causing damage
breast milk. Most individuals are infected with HIV to your eyes, digestive tract, lungs or other organs.
through sexual contact, before birth or during  Candidiasis. Candidiasis is a common HIV-
delivery, during breast-feeding, or when sharing related infection. It causes inflammation and a thick,
contaminated needles and syringes (intravenous white coating on the mucous membranes of your
drug users). Sexual intercourse is the most mouth, tongue, esophagus or vagina.
common, albeit inefficient, mode of HIV
 Cryptococcal meningitis. Meningitis is an
transmission. The risk of transmission per exposure
inflammation of the membranes and fluid
is low; estimates are on the order of 0.1% per
surrounding your brain and spinal cord (meninges).
contact for heterosexual transmission, but this varies
Cryptococcal meningitis is a common central
considerably and increases with concurrent
nervous system infection associated with HIV,
ulcerative STDs, high HIV viral load in the host, and
caused by a fungus found in soil.
lack of antiretroviral therapy
 Toxoplasmosis. This potentially deadly
E. Pathophysiology infection is caused by Toxoplasma gondii, a
parasite spread primarily by cats. Infected cats
Infection occurs across mucosal surfaces pass the parasites in their stools, and the parasites
covered with stratified squamous epithelium, may then spread to other animals and humans.
including the vagina, cervix and anus. Dendritic  Cryptosporidiosis. This infection is caused by
cells, with coreceptor CCR5, bind HIV and transport an intestinal parasite that's commonly found in
it to the lymphoid tissues where it encounters the animals. You contract cryptosporidiosis when you
CD4 T cells. When the virus enters the host cell, the ingest contaminated food or water. The parasite
viral RNA is transcribed into complementary DNA, grows in your intestines and bile ducts, leading to
which then integrated into the host cell, stimulating severe, chronic diarrhea in people with AIDS.
replication of this provirus. The virus undergoes Cancers common to HIV/AIDS
rapid replication, associated with the generation of
many viral mutations. These mutations are  Kaposi's sarcoma. A tumor of the blood
numerous and can occur within a day, promoting the vessel walls, this cancer is rare in people not
development of antigenic variation.
F. Clinical Manifestations
As the disease progresses, the CD4T-cell
number gradually declines, promoting significant
immunosuppression. The loss of CD4 Tcells is
caused by the killing of infected cells by viruses,
the apoptosis (programmed cell death) of infected
cells and the killing of CD4 Tcells by CD8
cytotoxic T lymphocytes. Cell-mediated immunity
is lost when the CD4 T cell level is too low,
contributing to the rink of opportunistic infection.
Resistance is lost to many common pathogens,
including the fungi Candida. Activation of latent
viruses may occur, promoting symptoms and
disease. Pneumonia, especially the type caused
by Pneumocystis carinii, is a common
opportunistic infection. Kaposi’s sarcoma, a tumor

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 infected with HIV, but common in HIV-positive c. Plasma HIV RNA Assay — Most sensitive and
people. reliable measurement of plasma viral load.

Kaposi's sarcoma usually appears as pink, red or I. Differential Diagnosis

purple lesions on the skin and mouth. In people
with darker skin, the lesions may look dark brown or Many individuals with HIV/AIDS may remain
black. Kaposi's sarcoma can also affect the internal asymptomatic for years, with a mean time of 10
organs, including the digestive tract and lungs. years between exposure and development.
Virtually, all the findings in the initial onset of
 Lymphomas. This type of cancer originates in AIDS may be found/mimic other diseases such
your white blood cells and usually first appears in as:
your lymph nodes. The most common early sign is
painless swelling of the lymph nodes in your neck,  Fever
armpit or groin.  Headaches
Other complications  Night sweats
 Fatigue
 Wasting syndrome. Aggressive treatment  Hypertension
regimens have reduced the number of cases of  Back pain
wasting syndrome, but it still affects many people  Pulmonary complications ex. cough and SOA
with AIDS. It's defined as a loss of at least 10  GI complaints (change in bowel habits and
percent of body weight, often accompanied by function)
diarrhea, chronic weakness and fever.  Cutaneous complaints (dry skin, new rashes,
 Neurological complications. Although AIDS nail bed changes)
doesn't appear to infect the nerve cells, it can  Poor wound healing
cause neurological symptoms such as confusion,  Thrush
forgetfulness, depression, anxiety and difficulty  Easy Bruising
walking. One of the most common neurological  Weight loss
complications is AIDS dementia complex, which  Herpes Simplex virus
leads to behavioral changes and diminished mental  Cytomegalovirus
functioning.  Lymphoma
 Kidney disease. HIV-associated nephropathy
(HIVAN) is an inflammation of the tiny filters in your All of these signs/symptoms may be associated
kidneys that remove excess fluid and wastes from with other diseases.
your bloodstream and pass them to your urine. A combination of complaints is more suggestive
Because of a genetic predisposition, the risk of of HIV infection than any one symptom alone.
developing HIVAN is much higher in blacks.
J. Prognosis
Regardless of CD4 count, antiretroviral therapy
should be started in those diagnosed with HIVAN.
 From the time of seroconversion, 10%-20% of
HIV-infected individuals will progress to AIDS in
3-6 years.
H. Diagnosis  Once the patient has constitutional symptoms,
herpes zoster, thrush or lower CD4+ lymphocyte
 Licensed tests for diagnosing HIV infection count, chances are >40% of progressing to AIDS
 If one cannot afford WBA, confirm results by after 3 years of follow-up and >50% after 5 years.
repeating ELISA after 4-12 wks (3 mos.) for  Prognosis can be modified by antiretroviral
secroonversion to occur. If still (+) then therapy and general medical support.
indicative of (+) HIV infection.

A. Enzyme-Linked Immunosorbent Assay (ELISA) II. GENERAL HEALTH CARE MANAGEMENT

 Standard screening test
 Extremely sensitive test A. Medical, Surgical and Pharmacological
 Disadvantage: Low specificity Management

B. Western Blot Assay ( WBA)

 Most common confirmatory test Medication
 Tests for assessing disease progression
Classes of drugs for HIV
 CD4+ T-cells count & plasma HIV RNA assay
There are many different types of drugs used to
are the most accurate assessment for disease
treat HIV. Your doctor will figure out the best
progression & time death
medications for you. This decision will depend on your
viral load and strain as well as the extent and severity
a. CD4+ T-cell count
of your infection.
b. p24 Antigen Capture Assay - Simplest test

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 Many people with HIV need to take more than its job, the virus can’t complete the process that
one drug. Attacking HIV from multiple directions makes new copies. This reduces the number of
reduces the viral load more quickly. It also helps viruses that can infect more cells.
prevent resistance to the drugs being used. This means
that your medications may work better to treat your HIV. Protease inhibitor drugs include:

Multiclass combination drugs  tipranavir (Aptivus)

Combination drugs combine medications from different  indinavir (Crixivan)
groups into one drug form. You take these medications  atazanavir/cobicistat (Evotaz)
once per day. Each person’s dosage is different. These  saquinavir (Invirase)
drugs include:  lopinavir/ritonavir (Kaletra)
 efavirenz/emtricitabine/tenofovir disoproxil  fosamprenavir (Lexiva)
fumarate (Atripla)  ritonavir (Norvir)
 emtricitabine/rilpivirine/tenofovir disoproxil  darunavir/cobicistat (Prezcobix)
fumarate (Complera)  darunavir (Prezista)
 elvitegravir/cobicistat/emtricitabine/tenofovir  atazanavir (Reyataz)
disoproxil fumarate (Stribild)  nelfinavir (Viracept)
 abacavir/dolutegravir/lamivudine (Triumeq)
Some protease inhibitors are only approved by
1. Nucleoside/nucleotide reverse transcriptase the U.S. Food and Drug Administration (FDA) to treat
inhibitors (NRTIs) hepatitis C. But there drugs are also sometimes
You may hear these drugs referred to as effective in treating HIV. This special use of these drugs
“nukes.” They work by interrupting the life cycle of HIV I called “off-label use.” Off-label drug use means that a
as it tries to copy itself. These drugs also have other drug has been approved by the FDA for one purpose
actions that prevent HIV from replicating in your body. but it is used for another purpose that the FDA has not
NRTI drugs include: approved. A doctor can still use the drug for that
purpose. This is because the FDA regulates the testing
 abacavir (Ziagen) and approval of drugs, but not how doctors use drugs to
 efavirenz/emtriacitabine/tenofovir disoproxil treat their patients. So, your doctor can prescribe a drug
fumarate (Atripla) however they think is best for your care. Doctors who
 lamivudine/zidovudine (Combivir) are experienced at treating both HIV and hepatitis may
 emtriacitabine/rilpivirine/tenofovir disoproxil choose to prescribe these drugs for people with HIV.
fumarate (Complera) These drugs include:
 emtricitabine (Emtriva) 4. Entry inhibitors (including fusion
 lamivudine (Epivir) inhibitors)
 abacavir/lamivudine (Epzicom) Entry inhibitors are another class of HIV
 zidovudine (Retrovir) medications. HIV needs a host T cell in order to make
copies of itself. These drugs block the virus from
 abacavir/lamivudine/zidovudine (Trizivir)
entering a host T cell. This prevents the virus from
 emtricitabine/tenofovire disoproxil fumarate replicating itself. These drugs also prevent the
(Truvada) destruction of targeted cells. This action helps your
 didanosine (Videx) immune system work well.
 didanosine extended release (Videx EC)
 tenofovir disoproxil fumarate (Viread) An example of an entry inhibitor includes:
 stavudine (Zerit)  enfuvirtide (Fuzeon), which comes in an
injectable form
2. Non-nucleoside reverse transcriptase
inhibitors (NNRTIs) 5. Integrase inhibitors
These drugs work in the same way as NRTIs. Integrase inhibitors are a class of drugs that
They stop the virus from replicating itself in your body. stop the action of integrase. This is a viral enzyme that
These drugs include: HIV uses to infect CD4+ T cells. These drugs include:
 rilpivirine (Edurant)  raltegravir (Isentress)
 etravirine (Intelence)  dolutegravir (Tivicay)
 delavirdine mesylate (Rescriptor)  elvitegravir (Vitekta)
 efavirenz (Sustiva)
 nevirapine (Viramune) 6. Chemokine co-receptor antagonists (CCR5
antagonists)
 nevirapine extended-release (Viramune XR)
CCR5 antagonists prevent the spread of HIV.
3. Protease inhibitors These drugs block infection in one of two molecules
Protease inhibitors work by binding to found on the surface of each body cell. Because it only
protease. This is a protein that HIV needs to affects one molecule, this drug is usually used with
replicate in the body. When protease can’t do other medications for full HIV treatment. An example of
this type of drug includes:
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  maraviroc (Selzentry) III. PHYSICAL THERAPY EXAMINATION,
EVALUATION, DIAGNOSIS
Cytochrome P4503A (CYP3A) inhibitors
CYP3A is an enzyme that protects liver and A. Points of Emphasis in Diagnosis
gastrointestinal (GI) health. HIV can destroy this
enzyme, leading to problems with your liver and GI
It is well documented that “exercise is a strategy used
tract. CYP3A inhibitors protect these enzymes to keep
to reduce the disabling effects from the chronic
you healthy. These drugs affect your liver and come
problems brought on by the HIV infection”.  Therefore, it
with the risk of jaundice. This may cause yellowing of
is important that every HIV/AIDS patient become
your skin and the whites of your eyes. An example of
involved in treatment provided by a physical therapist.
this type of drug includes:
According to the 2014 World Health Conference for
 cobicistat (Tybost) Physical Therapy, it is vitally important for individuals
living with HIV/AIDS to maintain and/or improve their
7. Immune-based therapies level of physical activity.  Due to the expertise of
Because HIV affects your immune system, researchers physical therapists in movement and exercise and the
are studying ways that drugs can help boost immunity. understanding of the effects of pathologies on bodily
Certain immune-based treatments have been systems, it is important that therapists design,
successful in some people. Like some protease prescribe, and manage the exercise for HIV/AIDS
inhibitors, these drugs are used off-label for HIV. They patients.
are used along with other HIV medications. An example
of an immune-based therapy includes:
Although the physical therapist is not involved in
 hydroxychloroquine sulfate (Plaquenil), which is treating the disease of the HIV patient, the therapist
a drug approved to treat autoimmune diseases plays an important role in treating the conditions
such as lupus and rheumatoid arthritis brought on by HIV and AIDS that limit movement and
help the HIV/AIDS patient maintain a better quality of
life.  Patients with HIV develop many of the functional
limitations that other patients may have, such as
B. Other Rehabilitative and Supportive Care arthritis or sports related type injuries.  HIV patients
Physicians: Physicians play a key role in the early have an abnormally low functional capacity which
detection of viral infection, especially human manifests itself in a decreased capacity to perform
immunodeficiency virus.They viral infection by work. In 2014 in an article in Moving Forward PT, the
evaluating patients’ symptoms, diagnosing their medical goal of the physical therapist in working with HIV/AIDS
conditions, considering whether it is genetic or patients was stated to be to “improve the quality of life
acquired, and giving appropriate treatment. of the HIV/AIDS patient and keep them active at home,
work and in the community”.
Nurses: HIV health nurses play an important role in
monitoring the trends of HIV by planning appropriate PT should develop a plan of care which will help
interventions, and evaluating prevention programs. HIV improve ability for daily activities, improve heart health,
health nursing includes: improve balance, reduce pain, and help to maintain a
healthy weight.  The physical therapist should also
 Managing and administering HIV health prescribe a home exercise program with goals for the
servicss within legal and professional patient to achieve.  Within the plan of care, the physical
parameters therapist must address the following:
 Conducting health examinations
 Assessing the work environment
 Providing primary, secondary, and tertiary 1. Quality of Life.
prevention strategies 2. Work Hardening.
 Providing health education and promotion 3. Community Management (accessing
programs transportation, socialization opportunities,
 Providing counseling interventions and ability to access and negotiate health care and
programs insurance systems).
 Managing information
 Conducting health surveillance programs Other sources also believe that the plan of care
should:

Allied health professionals. They also play a

significant role in the reduction of risk relating HIV and 1. Tailor treatments that take HIV disease into
improving their quality of life by addressing their health account
care need and strong implementation of prevention and 2. Provide customized exercise and pain
regression in the development of HIV. management programs, and
3. Help people with advanced HIV disease to
prevent, reduce, and delay movement and
function problems. 

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 The overall benefits of exercise for HIV/AIDS 5. Deep breathing exercises x 5-7 reps to
patients include: accustom patient to proper breathing
techniques.
6. Lumbar stabilization exercises x 12 reps x
 Pain relief 3 sets to improve muscle performance of
 Reduces muscle atrophy core muscle and relieve stresses on pain
 Regularity of bowels sensitive structures.
 Enhances immune function (by increasing T 7. Strengthening of major muscles of the UE
helpers and induce CD4 cells and activating (Shoulder flexors, extensors and
CD8 cells) abductors; Elbow flexors and extensors;
 Improves cardiovascular function wrist and hand flexors and extensors) and
 Improves pulmonary function LE (Hip flexors, extensors and abductors;
 Improves endurance Knee flexors and extensors; ankle
 Helps prevent pneumonia and other respiratory plantarflexors and dorsiflexors) using low
infections, and load free weights and theraband x 12 reps
 Reduces anxiety and improves the patient’s x 3 sets to improve muscle performance
mood and prevent atrophy.
8. Endurance training: treadmill exercise at 2
kmph for 15-20 minutes to improve
It is important for physical therapists to work with
cardiopulmonary endurance and exercise
HIV patients on the following activities in
tolerance.
addition to progressive resistance and aerobic
exercise:
b. HEP:

 Stretching 1. Deep breathing exercises x 5-7 reps to

 Soft tissue and joint mobilization accustom patient to proper breathing
 Gait and balance training techniques.
2. Lumbar stabilization exercises x 12 reps x
 Functional electrical stimulation/neuromuscular
3 sets to improve muscle performance of
electrical stimulation
core muscle and relieve stresses on pain
 Proprioceptive neuromuscular facilitation, and
sensitive structures.
 Desensitization techniques 3. Self-strengthening of major muscles of the
UE (Shoulder flexors, extensors and
B. Problem list abductors; Elbow flexors and extensors;
1. SOB wrist and hand flexors and extensors) and
2. Dry Cough LE (Hip flexors, extensors and abductors;
3. Fatigue Knee flexors and extensors; ankle
4. Cutaneous changes(dry skin, plantarflexors and dorsiflexors) using
telangiectasis, dermatitis) theraband x 12 reps x 3 sets to improve
5. Muscle Atrophy muscle performance and prevent atrophy.
6. LBP 4. Community ambulation for 20-30 mins to
7. Poor wound healing improve exercise tolerance and
cardiopulmonary endurance; improve
patient’s social participation.
IV. PHYSICAL THERAPY PROGNOSIS
A. Plan of Care c. Precautions:
a. Intervention
1. Avoid Valsalva maneuver.
1. Patient education of proper skin care and 2. Avoid overexertion.
wound care techniques to prevent further 3. Remember to apply proper coughing
complications, trophic irritation and hasten techniques.
wound healing if presence of wound is 4. Avoid crowded and enclosed spaces
noted. where ventilation may be difficult.
2. Application of proper wound care: 5. Wear preventive masks to avoid inhalation
cleansing through pulsatile lavage with of pathogens that may cause infection.
suction, proper wound dressing and 6. Avoid exposure to substances that can
bandaging to prevent wound infection and cause adverse effects on your overall
expedite healing. health.
3. HVPG over healing non-infected wounds 7. Avoid the spread of HIV by practicing
pulse duration of 200 ms x pulse interval of protection during sexual intercourse and
500 ms x frequency of 100 Hz for 15-20 keeping body fluids to yourself.
minutes to aid in wound healing. 8. Keep yourself healthy and hydrated and
4. Conventional TENS: frequency of 100z adapt a healthier diet.
and pulse duration of 50 ms for 15-20
minutes over bilat. low back to relieve pain.
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BURNS - Charred
- Subcutaneous tissue evident; anesthetic;
I. GENERAL MEDICAL BACKGROUND muscle damage; neurological involvement
A. DEFINITION - Tissue defects; heals with skin graft or flap;
scarring
- a type of injury to skin, or other tissues,
caused by heat, cold, electricity, chemicals, C. EPIDEMIOLOGY
friction, or radiation.
- The most common cause of burn injury in
B. CLASSIFICATION children 1 – 5 years of age is from scalds
from hot liquids
a. Epidermal Burn - The primary cause of burn injury in
- Cell damage is only up to the epidermis adolescents and adults is accidents with
- Erythematous, pink or red; irritated hot liquids.
epidermis - Men, especially those between ages 16
- No blisters, dry surface, delayed pain, and 40, have the highest incidence of injury
tender - Fires that occur in homes and other
- Minimal edema; spontaneous healing; no structural dwellings are the leading cause
scars of burn injury in other age groups
- Most of the deaths associated with home or
b. Superficial Partial - Thickness Burn structure fires are due to inhalation injury.
- Cell damage occurs through the epidermis
D. ETIOLOGY
and into the papillary layer of the dermis
- Bright pink or red, mottled red; inflamed
 Thermal
dermis; erythematous with blanching and
brisk capillary refill - Cold burn(frostbite)
- Intact blisters, moist weeping, or glistening - Hot liquids/gases
surface when blisters removed; very - Contact burn
painful, sensitive to changes in - Flame/flash
temperature, exposure to air currents, light  Chemical
touch - Strong acids/bases
- Moderate edema; spontaneous healing; - Hydrofluoric /gases
minimal scarring; discoloration - Contact burn
- Flame/flash
c. Deep Partial – Thickness Burn  Radiation
- Cell damage involves destruction of the - Exposure to UV light
epidermis and papillary dermis with - Tanning booths
damage down into the reticular dermal - X-rays
layer - Radiation therapy
- Mixed red, waxy white; blanching with slow - Sunlamps
capillary refill - Radioactive elements (Uranium, plutonium)
- Broken blisters, wet surface; sensitive to  Electrical Burn
pressure but insensitive to light touch or - Due to exposure to electrical currents
soft pinprick - Burn results from the passage of an electric
- Marked edema; slow healing; excessive current through the body after the skin has
scarring made contact with an electrical source
- Initial contact (entrance wound) = charred,
d. Full Thickness Burn depressed and smaller; skin appears yellow
- All of the epidermal and dermal layers are and ischemic
destroyed completely - Ground site (exit wound) = dry and larger
- In addition, the subcutaneous fat layer may - Injury may become necrotic and gangrenous
be damaged to some extent in a few days
- White (ischemic), charred, tan, fawn, - Arteries may undergo spasm; (+) necrosis of
mahogany, black, red (hemoglobin vascular wall
fixation); no blanching; thrombosed
vessels; poor distal circulation Types:
- Parchment – like, leathery, rigid, dry; a. Low voltage: <1000v
anesthetic; body hairs pull out easily - Usually 110v (US) or 220v (other countries), both
- Area depressed; heals with skin grafting; with AC 60 Hz current
scarring b. High Voltage: >1000v

e. Subdermal Burn  Mechanical

- Complete destruction of all tissue from the - Usually due to friction
epidermis down to and through the  Subdermal Burn
subcutaneous tissue - Complete destruction of all tissue from
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epidermis-subcutaneous infection, the loss of the cutaneous barrier facilitates
- Damaged muscles and bones entry of the patient's own flora and of organisms from
- Pathophysiology the hospital environment into the burn wound. The
wound often contains devitalized or frankly necrotic
 Regardless of the causative agent, a burn tissue that quickly becomes contaminated with bacteria.
initially undergoes the ff. physiologic Invasive infection localized and/or systemic occurs
responses: when bacteria penetrate viable tissue, usually below the
eschar.
 Burn Injury release of histamine Intense
vasoconstriction after few hours, vasodilation & F. CLINICAL MANIFESTATIONS
capillary permeability Plasma loss after 24
hours, abnormal aggregation of platelets &  A burn injury will present with the following
leukocytes thrombosis progressive vascular local effects:
obstruction area of ischemia increase 1-7 times - Lost of ability to regulate evaporative water loss
larger or greater impaired nutrient transfer more - Susceptibility to infection
damage. - Loss of massive amounts of body fluids,
especially in open wounds
 Because of the skin also serves as protection - Local burn wound sepsis secondary to bacterial
from infection, the loss of the cutaneous barrier contamination
facilitates entry of the patient’s own flora and of
organisms from the hospital environment into  Zone Of Burn Injury
the burn wound. The wound often contains a. Zone of Coagulation
devitalized or frankly necrotic tissue that quickly - Irreversible skin damage & cell death occurs
becomes contaminated with bacteria. Invasive - (+) infection
infection localized and/or systemic occurs when b. Zone of Stasis
bacteria penetrate viable tissue, usually below - Cells may die 24048 hours if not treated
the eschar. c. Zone of Hyperemia
- Minimal cell damage
 Burn wound healing occurs through separate - Cells should recover
mechanisms in the epidermis and dermis:
Degree AKA Damage Characteristics
PHASES OF WOUND HEALING 1st Superfici Epidermis Clinical Presentation:
al burn only Erythema, slight edema,
a. Epidermal healing
tenderness (e.g.
- Occurs if there are viable epithelial cells lining the sunburn)
wound. Healing Process: 3-7
days
b. Dermal Healing 2nd Superfici Epidermis & Clinical Presentation:
al partial upper layer Intact blister, moist,
- Scar formation occurs thickness of dermis moderate edema, bright
- Even if phase is described separately, they occur on a burn red, severe pain
continuum and one phase often overlaps another. 2nd Deep Epidermis & Clinical presentation:
partial most Broken blisters, wet
thickness dermis surface, marked edema,
E. Pathophysiology burn waxy white/Red, minimal
to no pain
 Destruction of vascular integrity of the skin Healing period: 21-35
days
 Formation of edema Scar formation:
 Loss of protein rich fluid into interstitial spaces Hypertrophic scar, keloid
 Fibrosis (LOM) scar
 Collagen forms adhesions 3rd Full Epidermis, Clinical presentation:
thickness Dermis, & white, gray, black or
burn subcutaneo charred
 Further LOM us tissue (+) Eschar
1. Burn Injury 4th Subderm Epidermis, Damage:
2. Release of histamine al burn dermis May cause osteomyelitis
subcutaneo eg: Electrical burn,
3. Intense vasoconstriction us tissue prolonged contact with
4. Followed by vasodilation, ↑ extending flame
permeability to muscles (+) Surgical intervention:
5. Plasma loss & bone Amputation
6. Abnormal aggregation of platelets &
leukocytes G. Complications
7. Thrombosis
 Infection. Burns can leave skin vulnerable to
8. Progressive vascular obstruction
bacterial infection and increase your risk of
9. ↑ area of ischemia (3 – 7 times)
sepsis. Sepsis is a life-threatening infection that
10. Impaired nutrient transfer
travels through the bloodstream and affects
11. More damage
your whole body. It progresses rapidly and can
cause shock and organ failure.
Because the skin also serves as protection from
8|Page
 Low blood volume. Burns can damage blood burn), and muscle, tendon, and bone
vessels and cause fluid loss. This may result in (fourth–degree burn). Injuries may have
low blood volume (hypovolemia). Severe blood a charred appearance and contain
and fluid loss prevents the heart from pumping white, brown, or black patches.
enough blood to the body. Patients may have severe pain, but the
 Dangerously low body temperature. The skin burns are often non–tender because
helps control the body's temperature, so when the nerve endings are destroyed.
a large portion of the skin is injured, you lose However, partial thickness burns often
body heat. This increases your risk of a surround full thickness burns and will
dangerously low body temperature be painful. Healing occurs only at the
(hypothermia). Hypothermia is a condition in wound edges, and scarring is
which the body loses heat faster than it can significant, unless skin grafting is done.
produce heat.  Biopsy is rarely needed to verify infection.
 Breathing problems. Breathing hot air or
smoke can burn airways and cause breathing I. Differential Diagnosis of Burn Injury
(respiratory) difficulties. Smoke inhalation
damages the lungs and can cause respiratory Depth of Burn Wound color/ Surface Swelling/Heal
failure. Vascularity appearance/Pain ing/ Scarring
Superficial Erythematous, No blisters, dry Minimal
 Scarring. Burns can cause scars and ridged pink or red, surface; delayed edema,
areas caused by an overgrowth of scar tissue irritated pain, tender spontaneous
dermis healing; no
(keloids). scars
 Bone and joint problems. Deep burns can Superficial Bright pink or Intact blisters, Moderate
partial thickness red, mottled moist surface, edema, slow
limit movement of the bones and joints. Scar red; inflamed weeping or healing,
tissue can form and cause shortening and dermis; glistening; painful; excessive
erythematous sensitive to scarring
tightening of skin, muscles or tendons with blanching changes in
(contractures). This condition may permanently and capillary temperature,
pull joints out of position. refill exposure to light
touch, air currents
Deep partial Mixed red, Broken blisters, Marked
thickness waxy white, wet surface; edema; slow
blanching with sensitive to healing;
H. Diagnosis slow capillary pressure but excessive
refill insensitive to light scarring
touch or soft pin
 A detailed history and physical examination is prick
the first step. The physician will evaluate the Full thickness White Parchment like, Area
(Ischemic),cha leathery, rigid, dry; depressed;
type, duration, and timing of the burn; the burn rred, tan, anesthetic; body heals with skin
location and severity; and associated fawn, hairs pull out grafting,
mahogany, easily scarring
dehydration, disfigurement, and infection. Fires black red
in enclosed spaces should raise the suspicion hemoglobin
for smoke–inhalation injury. fixation; no
blanching;
 Burns are classified based on the depth and thrombosed
extent of skin damage, degree of pain, and vessels; poor
distal
swelling: circulation
Subdermal Charred Subcutaneous Tissue
tissue evident; Defects; heals
 Partial Thickness Burns. First–degree anesthetic; muscle with skin
burns affect only the outer skin layer damage; grafting;
Neurological scarring
(epidermis) and are characterized by involvement
redness or discoloration, mild swelling,
and pain. Sun overexposure is a
J. Prognosis
common cause. Injuries heal in three to
six days. 
The prognosis is worse in those with larger
Second–degree burns affect the burns, those who are older, and those who are
epidermis and various portions of the females. The presence of a smoke inhalation injury,
lower skin layer (dermis), causing a red other significant injuries such as long bone fractures,
appearance and blisters. Fluid is lost and serious co-morbidities (e.g. heart disease,
through damaged skin, and the burns diabetes, psychiatric illness, and suicidal intent) also
are painful and tender. These injuries influence prognosis The Baux score has historically
require one to three weeks or more to been used to determine prognosis of major burns.
heal. Scarring is uncommon, but there However, with improved care, it is no longer very
can be long–term skin color changes, accurate. The score is determined by adding the size of
although most color changes fade over the burn (% TBSA) to the age of the person, and taking
time. that to be more or less equal to the risk of death.
 Full Thickness Burns. Burns that
penetrate beyond the epidermis and
dermis may affect fat (third–degree II. GENERAL HEALTHCARE MANAGEMENT

9|Page
A. Medical, Surgical, & Pharmacologic b. Consists of roll gauze or elastic bandages,
which hold the other layers in place but
MEDICAL MANAGEMENT allow movement.
Initial management:
1. Minor and Moderate Burns:
The goals in the initial management of a patient with a - Cleaned with soap & warm water
burn are to address critical life-threatening problems - Remove loose epithelium
and stabilize the patient through procedures designed - Ice or Cold water
to (1) establish and maintain an airway; (2) prevent - Antibacterial agents
cyanosis, shock, and hemorrhage; (3) establish - Tetanus prophylactics if full thickness
baseline data on the patient, such as extent and depth - Wound dressing
of burn injury; (4) prevent or reduce fluid losses; (5) 2. Major Burns:
clean the patient and wounds; (6) examine injuries; and - Maintenance of airway
(7) prevent pulmonary and cardiac complications. - Antibiotics
The goals of wound cleansing and debridement are to - Intravenous resuscitation
remove dead tissue, prevent infection, and promote - Sedatives
revascularization and/or epithelialization of the area. - Tetanus Prophylactics
3. Asepsis and Wound Care:
- facilitate wound healing, prevent infection,
Initial wound care: decrease pain, reduce scarring and contracture,
and prepare wound for any necessary grafting
After dressings are removed, the wound should be
a) Removal of charred clothing.
inspected carefully for:
b) Wound cleansing.
 appearance
c) Topical medications (antibacterial
 depth agents): can be applied without
 size dressings (open technique); reapplied
 exudate daily.
 odor - Silver nitrate: acts only on surface organisms;
applied with wet dressings; requires frequent
Infection is characterized by thick purulent drainage, dressing changes.
odor, fever, a brownish-black discoloration, rapid - Silver sulfadiazine: common topical agent.
separation of eschar, boils in adjacent tissue, or - Sulfamylon (mafenide acetate): penetrates
conversion of a deep partial-thickness burn to a full- through eschar.
thickness injury. - Bacitracin/Polysporin
-Collagenas, Accuzymie
A. sharp debridement d) Occlusive dressings (closed technique):
-the use of surgical scissors or scalpel and forceps dressings are applied on top of a topical agent.
to remove eschar - Prevents bacterial contamination, prevents
-sloughed epidermis and loose eschar are removed fluid loss, and protects the wound.
and pockets of pus are drained. - May additionally limit ROM.
-After the wounds have been cleaned, the patient 4. Establish and maintain airway, adequate
should be kept warm to reduce any further oxygenation, and respiratory function.
metabolic demand due to additional heat loss
5. Monitor.
B. Open technique
-The technique of applying a topical cream or - Arterial blood gases, serum electrolyte levels,
ointment without dressings urinary output, vital signs.
-Allows for ongoing inspection of the wound and - Gastrointestinal function: provide nutritional
examination of the healing process. support.
-Topical medication must be reapplied throughout  Pain relief, e.g., Morphine sulfate.
the day.  Prevention and control of infection.
- Tetanus prophylaxis.
C. Closed technique - Antibiotics.
-applying dressings over a topical agent; used to: - Isolation, sterile techniques.
a. hold topical antimicrobial agents on the  Fluid replacement therapy.
wound - Prevention and control of shock.
b. reduce fluid loss from the wound - Post shock fluid and blood
c. protect the wound replacement.
SURGICAL MANAGEMENT
Dressings consist of several layers: Primary Excision, Types of Skin Grafts, and Skin
a. First layer – non-adherent to protect the Substitutes
fragile healing surface from disruption. May Primary excision - surgical removal of eschar. The
be followed by cotton padding to absorb excision generally includes removal of peripheral layers
wound drainage of eschar until vascular, viable tissue is exposed as the
site for skin graft placement; usually within 1 week of
injury.
10 | P a g e
 the silicone layer is
1. ESCHAROTOMY - To relieve pressure on underlying removed and a very thin
arteries and veins skin. graft or CEA is
applied.
2. FASCIOTOMY - For persistent impairment of
peripheral blood flow
6. DEBRIDEMENT
3. Z-PLASTY - Surgical procedure used to lengthen
scars from burn wound injury; helps increase ROM Types:
4. GRAFTS: a. Mechanical - Usually post-hydrotherapy
ALL GRAFTED PARTS SHOULD BE IMMOBILIZED
AT LEAST 3-5 DAYS TO PREVENT DISLODGING OF b. Enzymatic - enzymatic debriding agent that
THE GRAFTS. selectively debrides necrotic tissue
Autograft tissue of the body to - Sutilains
burned area
Allograft/Homograft Skin grafts from - Travase/Elase
cadavers
Xenograft Skin graft from other c. Surgical
species (ex. Pig) d. Fascial - Rarely indicated in severe burns
Splint-thickness graft graft for epidermis
and some part of e. Tangential - Most widely used
dermis
Full-thickness graft graft from epidermis f. CO2 laser – expensive
to dermis

TOPICAL CREAM USED IN BURNS

5. SKIN SUBSTITUES
1. Silver Sulfadiazine - Most common used topical
- Skin from cadaver allowing it to grow in the antibacterial agent; effective against/Pseudomonas
laboratory then it is being graft on the burned area infections.
(susceptible to infection)
2. Mafenide acetate(Sulfamylon) – Effective against
Cultured epidermal A skin biopsy is obtained gram negative or gram positive organisms; diffuses
autografts from a patient, and only easily through eschar.
the epidermal cells are
cultured 3. Silver Nitrate - Maintains moist environment;
Cultured autologous A skin biopsy is obtained Antiseptic germicide and astringent; will penetrate only
composite grafts from a patient, and both 1-2 mm of eschar; stains black
epidermal and dermal
cells are cultured. This 4. Bacitracin/Polysporin - Bland ointment; effective
forms a bilayer structure. against gram-positive organisms.
Allogenic skin substitute The epidermal layer of 5. Collagenase, Accuzyme - Enzymatic debriding agent
skin and all immune cells selectively debrides necrotic tissue; no antibacterial
are removed from action.
cadaver skin. This tissue
is applied to the graft bed B. Other Healthcare Management
and once adhered, a thin
epidermal autograft or Physical therapy management:
CEA is applied. Rehabilitation of a patient with burns begins the
Cultured dermis Cultured dermal matrix is moment he or she arrives at the hospital and is an
(temporary) seeded with human evolving process that may need to be modified daily.
neonatal fibroblasts and
used as a temporary  Physical therapy interventions are directed toward:
covering in place of - Prevention of scar contracture
cadaver skin. This - Preservation of normal ROM
substitute eventually is - Prevention orminimization of hypertrophic scar
removed and replaced formation and cosmetic deformity
with an autograft. - Maintenance or improvement in muscular
Cultured dermis This skin substitute is strength and cardiovascular endurance
(definitive) composed of cultured - Return to pre-burn function
bovine collagen with a - Performance of activities of daily living
silicone outer layer. Pores
in the material allow for REHABILITATIVE:
controlled growth of a
neodermis. After  Respiratory therapy
approximately 14 days, - may be indicated in inhalation injury
11 | P a g e
 Speech pathologists provide: of the TBSA burned can be calculated using a tool such
- may participate if speech is affected due to an as the Lund and Browder chart. Other estimators of
inhalation injury burn size can be made by following the “rule of nines”
 Occupational therapists provide: or estimating that the palm of the patient’s hand is
- Skills retraining if affected approximately 1% of the TBSA.
- Dysphagia management if affected due to an IV. PHYSICAL THERAPY PROGNOSIS
inhalation injury
- Psychiatric counseling may be counseling
I. Plan of Care (Generalized)
may be indicated if any psychological impact to the
injury is noticed.
Acute care of burn patients will most often be geared
toward achieving the following goals:
III. Physical Therapy Examination, Evaluation, &  Allow rapid wound healing
Diagnosis  Resolve edema
 Preserve function
A. Points of Emphasis in Examination  Prevent/minimize hypertrophic scarring
After the initial examination for depth of  Prevent respiratory complications
burn and percentof TBSA involved, the physical  Achieve good cosmetic outcome
therapist then examines the patient to
determine the presence ofimpairments and Long-term (sub-acute and chronic) care of burn:
activity limitations. The therapist needs to  Evaluate the patient’s home environment and
obtain an accurate history from the patient and family support and address any necessary
family members regarding any preexisting home environment changes
limitations or previous injuries that may affect  Evaluate and address any related physical
rehabilitation potential. The therapist must also dysfunctions
anticipate the potential for development of  Evaluate and address any risk for secondary
indirect impairments as the burn wounds heal complications
and mature. For example, active or passive
ROM may be limited as a result of edema,
restrictive eschar, or pain, and an initial a. Intervention
baseline measure should be obtained.
1) Wound care
Other tests and measures discussed in this text can be a. Cleansing
included in the initial examination and reexamination of  Local wound care - For small areas and
a patient following burn injury: areas difficult to treat with hydrotherapy
 Hydrotherapy
 Cardiovascular system examination- Circulation  immersion (Whirlpool, High Boy, Low
to and from the sites of burn boy)
 Pulmonary system examination  Non-submersion (Spray technique –
 Musculoskeletal examination Suspended on a stretcher at an angle
 ROM over a hubbard tank)
 MMT  Pulsative lavage with suction
 LGM (Alternative to hydrotherapy)
 MBT b. Debridement
 Joint play  May be done during or after hydrotherapy
 Functional assessment  Physical therapist may apply any of the
debridement techniques mentioned
c. Topical agents
B. Problem List  Applied after cleansing and debridement
1.) Pain ( Deep partial thickness and full partial  Physical therapist may apply any of the
thickness sensation will be diminished) topical agents mentioned
2.) Infection secondary to compromised skin d. Dressings - Applied after cleansing,
integrity debridement, and application of topical agents
3.) Hypovolemia secondary to fluid loss
4.) Hypothermia 2) Functional activities and exercises:
5.) Loss of motion secondary to contractures  Only during healing
6.) Muscle weakness secondary to muscle  All grafted parts should be immobilized at least
disuse 3-5 days
7.) Impaired Posture secondary to  Goals of exercise:
compensation and contractures - Reduce edema
8.) Decreased Performance on basic ADLs - Maintain ROM
C. Physical Therapy Diagnosis - Prevent skin contractures
 Activities and exercises:
The initial depth of burn injury is estimated by  Range of motion and stretching
examination. Burns can be divided into superficial,
partial thickness, and full-thickness injuries. Estimations
12 | P a g e
 - AROM/AAROM exercises at bedside
2-3x/day
- PROM for critically ill, spastic, heavily
medicated patients
 Ambulation
 Strengthening
- PRE for involved & uninvolved areas
 Endurance

3) Scar management techniques:

 Positioning and splinting

Indications:
 Patient cannot voluntarily maintain
proper positioning
 Edema
 Exposed tendons
 Peripheral neuropathy
 Unresponsive patients

 Compression garment
- Hypertrophic scarring and edema
- Worn 24 hrs a day to 1 year until scar
matures
Types:
a. Elastic cloth garment
b. Silastic mask
c. Clear plastic mask
 Friction massage
- To align collagen in healing skin
- Not done after grafting for at least 5
days
- initially gentle and then more
aggressive

4) Post-healing education
 Moisturizing newly-healed skin
 Avoiding direct sunlight:
- Use of sunscreen
- Covering affected area with clothing
- Planning activities in early morning and
late evening
 Protecting fragile skin

After discharge, the patient is followed-up less

intensively in physical therapy
 Depending upon the extent of the burn, the patient
will need only 2-3 sessions/week of supervised PT
 Follow-up the severely burned patient for at least
18-24 months until the scar is completely matured
and all rehabilitation complications have been
resolved
 Some important points:
 Check pressure garments for excessive
pressure and skin breakdown
 Remind patient to avaoid prolonged exposure
to heat or cold
 Warn patient against vigorous outdoor
activities until tolerance develops
 Remind patient to avoid direct sunlight
exposure
- Sunlight exposure can begin gradually,
with caution, after about 6 months.

13 | P a g e
FRACTURE
I. GENERAL MEDICAL BACKGROUND
A. Definition Le Fort fractures
A complete or incomplete break in a bone
resulting from the application of excessive force or - fractures of the midface, which collectively
traumatic injury causing the discontinuity of bone involve separation of all or a portion of the midface
tissues or bony cartilage to be disrupted or broken. from the skull base.

Le Fort type 1
B. Classification
- horizontal maxillary fracture, separating
Salter-Harris Classification
- Involves the epiphyseal plate or growth plate of the teeth from the upper face
- fracture line passes through the alveolar ridge,
a bone. Commonly used in children.
lateral nose and inferior wall of maxillary sinus
Salter-Harris Description Le Fort type 2
Fracture - pyramidal fracture, with the teeth at the pyramid
Classificatio base, and nasofrontal suture at its apex
n - fracture arch passes through posterior alveolar
Type I fracture through the ridge, lateral walls of maxillary sinuses, inferior
physeal plate (often orbital rim and nasal bones
not detected Le Fort type 3
radiographically) - craniofacial dysjunction
Type II fracture through the - fracture line passes through nasofrontal suture,
metaphysis and maxillo-frontal suture, orbital wall, and zygomatic
physis (most arch / zygomaticofrontal suture
common; up to
75% of all physeal  ACCORDING TO COMPLETENESS
fractures) Incomplete Fx- cortex is broken in the convexity of
Type III fracture through the the curve whereas the bone on the concave is
epiphysis and bent.
physis 1. Greenstik Fx-bone is bent and broken only part of
Type IV fracture through the the way through its shaft. Occur in children at an
metaphysis, physis age when bones are soft and pliable.
and epiphysis 2. Fissured- a mere split of the bone without
Type V crush injury displacement of the fragments.
involving part or all 3. Perforating- there is a hole such as those made of
of the physis bullets.
4. Interperoisteal Fx- Fx in which the periosteum is
Gustillo-Anderson Classification (mc) not disrupted.
5. Depressed- saucer or gutter shaped in which a
fragment of bone is driven inward. Seen frequently
in fracture of the skull.
Complete Fx- there is separation in the apophysis.
1. Simple(closed fx)- it does not communicate with
the skin or . mucous membrane. The fractured
surface is protected from contamination with the
outside air.
2. Impacted- the broken bone ends are driven into
each other.
3. Comminuted- bone is broken into several pieces
of fragments.
4. Compound(open)- has communication between
the fracture surface and the skin and mucous
membrane so that air and bacteria maybe admitted
hence causing infection.
5. Complicated- there is injury to some organs or
important structures near the fracture site.
6. Compression- usually in short bones, disruption
Garden’s Classification of Hip Fx of tissues; causes collapse of involved bone.
 Garden stage I : undisplaced incomplete,
including valgus impacted fractures.  ACCORDING TO DISPLACEMENT
 Garden stage II : undisplaced complete 1. Undisplaced- fragments or ends of fracture sites
 Garden stage III : complete fracture, are not separated
incompletely displaced 2. Displaced- separation of bone fragments exists.
 Garden stage IV : complete fracture, completely
displaced
14 | P a g e
 ACCORDING TO PLANE OR FRACTURE 19.Endocrine- resulting from weakness due to
SURFACE endocrine disorder
1. Transverse Fx- the plane of the fracture surface is 20.Epiphyseal- involves epiphyseal growth plate of
perpendicular to the axis of the bones. long bone resulting separation or fragmentation
2. Oblique Fx- fracture surface forms an angle with 21.Extracapsular- occur near joint but not directly
the axis of the shaft. Break runs in slanting involving or entering joint capsule,
direction of bones. extremely common in hip
3. Spiral Fx- fracture surface is spiral and is 22.Fatigue fracture- results from excessive physical
produced by torsional stress which fracture the activity
bone. 23.Fracture dislocation- involves bony structures of
Note: The spiral and oblique fractures results from joints with associated w/ associated dislocation of
indirect violence and soft tissue damage is often same joint
slight. 24.Gunshot Fx- results from bullets or other missiles
4. Butterfly Fx- center fragment of 2 disruptions in 25.Inflammatory- fx of bone weakened from
continuity of tissue creates a triangular effect. inflammation
5. Comminution- > 2 fragments or potential 26.Infarction Fx- results in a small radiolouscent line
fragments are present commonly associated w/ metabolic dysfunction
27.Intracapsular Fx- fx within joint capsule
The displacement of the fragments may consist of: 28.Intrauterine- occurs during fetal life
a. Lateral displacement 29.Lead pipe Fx- compression at point of impact &
b. Angulation- the fragments form an angle with each linear fx at opposite side; aka; Torus Fx
other instead of being a line 30.Linear- extends parallel to long axis of bone w/ no
c. Overlapping- resulting in the shortening of the displacement
bone 31.Multiple Fx- fx of several bones fro one injury
d. Rotation-or twisting of the distal fragments 32.Neoplastic- fx in bone weakened by neoplasm or
malignancy
A fracture is undisplaced when a plane of cleavage 33.Neurogenic- results from destruction of nerve
exist in the bone without angulation or supply to specific bone
displacement. If separation of bone fragments 34.Occult Fx- accompanied by usual clinical signs
exists, the fracture is said to be displaced. 35.Periarticular- located near joint but not directly
involving joint
 ACCORDING TO PATHOLOGIC FRACTURE 36.Pressure- created by pressure resulting from
1. Agmetic- spontaneous fracture due to imperfect tumor
osteogenesis 37.Puncture- due to projectile creating loss of bone
2. Angulated- fracture in which fragments are tissue w/o disruption of continuity of involved bone
angulated 38.Sprain Fx- separation of tendon or ligament
3. Angulation- caused by angulations of spine or 39.Y Fx- intercondylar fx shaped like a “Y”
shaft of long bone
4. Apophyseal- Fx separating apophysis from bone C. Epidemiology
where there is a strong tendinous attachment - The 5th leading diagnosis in hospital
5. Articular- aka: intraarticular joint Fx; involves discharges in the US.
articular surface of a joint - Fractures occur more commonly in adults
6. Atrophic- spontaneous fx due to atrophy rather than in children.
7. Avulsion- caused by tearing away of bone - The older the person is the more fragile their
fragment; ligamentous tendinous attachment bones become.
forcibly pulls away from the rest of the bone - Greenstick Fx : children are most likely affected
8. Bending- results from bending of extremity - Pathologic Fx :  elderly 60- 70 y/o; f>m over
9. Bent Fracture- incomplete greenstick fx 90 y/o
10.Bursting fracture- fx resulting in multiple
fragments usually at near end of bone
11.Buttonhole- caused by perforation of bone by D. Etiology
bullet  Pathologic Fracture
12.Capillary- hairlike fracture Occur in bones weakened by pre-existing
13.Chip fracture- usually involves a bony process disease such as tumors, cysts, or
near a joint;presence of small fragmental fx osteomyelitis.
14.Cortical- involves cortex of bone  Traumatic Fracture
15.Dentate- results in fragmented ends being  External Causative Factors
serrated and opposing each other Violence /Trauma- the bone is normal
16.Direct Fx-- fx resulting at specific point of injury and the causative force maximal
and due to injury itself
17.Double fx- results in > 2 segments with fx in 2 o Direct Violence- Fx due to blows or falls
places to which break occurs at the point of
18.Dyscrasic Fx- caused by weakening of specific impact with the ground or object.
bone from debilitation disease

15 | P a g e
 o Indirect Violence- occurs when the 4. Bruising or Ecchymosis- presence of blood in
force is transmitted to the bone through the subcutaneous tissue and leads to
some parts of the body. discoloration in the tissue
 Bending Forces 5. Deformity- signifies a change in the position
 Torsional Forces or shaped of the limb that is due to alterations
 Compressive Forces in the bony structure. Search for the deformity
 Shear Forces should be the first step.
 Internal Causative Forces 6. Pain- at the time of injury and afterwards,
Muscular action- ex. Fx in the patella due to a both spontaneous and upon mov’t of the fixed
sudden contraction of the quadriceps; Fx of the limb is a constant accompaniment of fracture
arm in throwing a ball or Fx of the humerus of 7. Tenderness- amount of tenderness varies
women wringing clothes. greatly in different persons & also varies
directly with the amount of injury to the soft
E1. Pathophysiology tissue & w/ the elapsing after injury.
In fracture, the actual damage to the bone 8. Absence of active movement
consist of a break in the continuity which results in 9. Muscle spasm- during attempt to move the
damage to blood and lymphatic vessels. The extremity.
periosteum will be stripped off on the region of the 10. Characteristic attitude
injury and sometime it is torn but since it is a tough 11. Soft tissue edema- present in surrounding
fibrous membrane, it may remain intact. An intact structure; fx site may feel warm to touch
periosteum is essential because it traps the blood
12. Excessive motion- present especially if the
from the ruptured vessels that is essential from
site is not near a joint or is not splinted by
hematoma formation needed in the repair process.
surrounding soft tissue structure
Due to sharp edges of the broken bone or the force
13. Open wounds- may sometimes mask
impacted upon the body part, there are the damages
degree of damage
on the surrounding soft tissue like the torn muscle,
muscle tearing of the fascia and other connective 14. Neurovascular impairment-due to
tissues, ruptured blood vessels and considerable fragmentation
extravation of blood take place. Tissue debris and
blood clots as irritants and an inflammatory reaction G. Complications
occurs, neighboring small vessels dilate and 1. Neurovascular injuries- injuries involving both
hyperemia results and the area affected is invaded nerve & blood vessels
by inflammatory cells. Some salts are absorbed 2. Infection- invasion of the body by disease-
recalcification of the fracture bone ends may occur. producing organisms
3. Acute Respiratory Distress Syndrome
E2. Pathomechanics 4. Compartment Syndrome
The energy imposed on the human body by the 5.Osteomyelitis-inflammation of bone,
forces of impact must be absorbed by non-injury especially of the marrow caused by bacterial
producing methods. The principal energy absorbing infection
mechanism in the body is a lengthening contraction 6. Avascular necrosis- is a disease resulting
of muscle. from a temporary loss of the blood supply of
Therefore, strong muscles provide good the bone
protection from fracture. Energy can also be 7. Joint stiffness, Reflex Sympathetic
absorbed by protective gear such as helmets, pads, Dystrophy, Non-union or delayed union,
etc. but these along are inadequate to absorb the malunion, Post-traumatic arthritis, Growth
entire force of an impact. Load is transmitted deformity
through these protective materials and absorbed in
part by the body’s own padding in the form of H. Diagnosis
muscle bulk, fats, bone and cartilage. If the energy
at the time of impact is greater than what can be  Dysfunction
absorbed by protective gear or lengthening  Example: paralysis with spinal
contractions. Injury occurs first to the soft tissue fracture, unconsciousness with
(bruise, strain) and then to bone or ligaments cranial fracture, or masticatory
(fracture) dysfunction with mandibular
fracture.
F. Clinical Manifestations  Pain
1. Abnormal mobility- motion in a limb at a point  Common on site of fracture
in a direction in which it does not normally  Local trauma
reach.  In open fracture, examination will
2. Crepitus- one of the most reliable sign; a present with swelling, hematoma,
sound produced by the friction of one contusion, or laceration.
fragments moving into the other  Onset of swelling is immediate
3. Swelling- in the vicinity of the fx as the result after injury.
of extravasation of blood and serum in the  Abnormal posture or limb positioning
tissue.
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  There is deformity or a deviation  Patient who are not
from the normal anatomical compliant could
structure of the bone. worsen their condition
 Crepitus further.
 A gritting sensation transmitted to  Age
the palpating fingers by the contact  Children heals faster
of the broken bone ends on each than older adults.
other.  Diet
 Abnormal mobility  Vitamin D and Food
 Occurs in a complete fracture of rich in calcium hasten
the shaft of a long bone. healing process.
 There is difficulty in moving the  Proper balance diet
affected structure. also hasten healing
 Radiographic signs process.
 Shows a break in the continuity of  Overall health condition of the
a bone line. patient
 Radiolucency: fragments  Patients who are
are distracted. psychologically
 Radiopacity: fragments compromise are less likely
are compressed or to heal fast than those
superimposed. patient without them.
 Diagnostic tool
 CT scan
 MRI II. GENERAL HEALTH MANAGEMENT
 X-ray Dependent on different factors such as:
 Ultrasonography a. General condition of the patient
b. Presence of associated injuries
c. Type of fracture (open or closed)
I. Differential Diagnosis d. Location and displacement of the fracture
 Congenital A. MEDICAL, SURGICAL AND
 Osteogenesis imperfecta PHARMACOLOGIC MANAGEMENT
 Menke’s syndrome 3 basic objectives:
 Nutritional/Metabolic 1. Reduction
 Copper deficiency 2. Maintenance of reduction
 Rickets 3. Preservation and restoration of function
 Scurvy
 Renal osteodystrophy  REDUCTION
 Infectious - Replacement of the bone to near normal
 Congenital syphilis anatomic position
 Osteomyelitis - indicated for fractures with displacement
 Neoplasm - performed with general or regional anesthesia
 Leukemia due to painful procedure and of reduction and
 Langerhans cell histiocytosis may involve counteracting strong muscle pulls.
 Bony metastases 1. Reduction by manipulation (MC method):
 Normal variant involves longitudinal traction to restore length,
 Physiologic periosteal new bone angulations to allow locked fragments to
 Neuromuscular disease disengage and slide past one another and
 Cerebral palsy manual pressure to reposition bone
 Congenital insensitivity to pain
2. Traction: second method of reduction which is
applied over a period of several hours or days.
J. Prognosis Reduction by sustained traction is indicated if
traction is used to maintain reduction (MC in tx of
 Fractures may take several weeks to femoral shaft fx and cervical spine injuries)
several months to heal.
 Its healing time depends on the 3. Open surgery: indicated if fx segments are
following: caught within soft tissues; reduction by
 Extent of injury manipulation or traction is impossible or
 Internal organs might contraindicated; applied if internal fixation is
be compromise. contemplated for maintaining the reduction
 Patient’s compliance of
doctor’s advice.  MAINTENANCE OF REDUCTION
3 common methods:

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  External fixation (cast or splint) a. Transfixion screw: simplest form; oblique fx of
- MC method tibial shaft
- accomplished by means of plaster cast or by b. Bone plate: metal plate fastened to the surface
splints of plastic, metal or wood of the fragments by at least 2 screws above and
- may cause pressure sores over boney below; involves periosteal stripping which may
prominences unless applied with adequate tend to delay union
padding c. Intramedullary rod or nail: inserting a long,
- Plaster of Paris – most satisfactory material; inflexible rod down the medullary cavity;
anhydrous calcium sulfate provides excellent fixation; promotes contact
- may be enhanced by drilling pins transversely compression, eliminates immobilization,
through the bone above and below the enables pt to walk with crutches soon after
fracture site injury

 Traction  PRESERVATION AND RESTORATION OF

- indicated for fx that cannot be immobilized FUNCTION
efficiently with cast - Adequate reduction and immobilizationsolid
- Muscles act as internal splint to protect the fx bony healingjoint stiffness and mm atrophy
- Disadvantage: requires the patient to be remain - should be started early during the period of fx
in bed and usually in hospital healing
- Methods: - AROM above and below the cast should be
a. Skin Traction – applied by means of carried out at frequent intervals
adhesive or reinforced foam rubber strips - Muscle setting or isometric exercises covered
and an encircling elastic bandage; not by the plaster (start after a day or 2)
more than 5 or 6 lbs of pull is required - joints during immobilization period should be in
Bucks extension – longitudinal pull on the leg a functional position
Russell’s traction – used for children with femoral - most important: active mm exercises
shaft fx - limb may be massaged, passively exercised and
Cloth head halter – cervical spine injuries applied with heat to facilitate exercises
Canvas girdle – pelvic fx - should be done first under warm water
(hydrotherapy on therapeutic pool, Hubbard tank,
b. Skeletal traction – drilling a wire or pin whirlpool bath or ordinary tub)
transversely through a bone; advantages - joint stiffness  gentle assistive passive
include stronger traction (femoral shaft exercise
requires as much as 20 to 30 lbs of pull); - severely incapacitated  ambulation with
applied to distal areas; avoids abrasions, walker, crutches or cane; gait training;
blisters and reaction to adhesives; MC instructions in ADLs (feeding or toilet care)
applied through the proximal part of the
tibia distal to the tibial tubercle (for femoral
fx tx); strict aseptic technique is obligatory;
most frequently used in femoral shaft fx in PHARMOCOLOGICAL MANAGEMENT
adults; limb may be supported in a
Thomas splint; used frequently in the tx of Benzodiazepines used to treat sleep disorders
dislocations and fx of the cervical spine and anxiety are often associated with falls and
(MC used device: Crutchfield, Barton) subsequent trauma including hip fractures,
**applied by means of: especially in older adults
a. Steinmann pin – 1/8 inch in diameter; rigid; Calcitonin can reduce the risk of vertebral
attached by simple yoke to the rope and fractures
pulleys Analgesics for pain relief
b. Kirschner wire – smaller diameter; flexible; Anxiolytics to decrease anxiety
supported by a special spreader that
bowstrings the wire tightly to prevent B. OTHER HEALTHCARE
bending (REHABILITATIVE/SUPPORTIVE)
Pearson attachment – clamped to the splint to a. Prosthesis
allow knee flexion b. Orthosis
Balanced Traction – balancing the suspended c. Psychology
Thomas splint

 Internal Fixation (nail, plate or screws) III. PHYSICAL THERAPY EXAMINATION,

- applied by means of metal plates, rods or screws EVALUATION, AND DIAGNOSIS
- used when other methods are impractical or A. Points of emphasis in examination
unreliable i. Age
- disadvantages: converts a closed fx to open fx; ii. Gender
infection from surgical tx iii. Type of fracture
Common methods: iv. Severity
v. Complications

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 vi. prognosis  Steinmann pin – a 1/8 inch diameter pin that is
B. Problem list rigid and simple to attach
i. Pain
ii. Muscle guarding  Kirschner wire – a smaller diameter flexible
iii. LOM material that is used more often than the
iv. Muscle weakness 2° Steinmann pin
disuse/immobilization
 PROTECTION
v. Localized swelling
vi. Affected ADL’s  make sure that the blood supply to the distal
C. Physical therapy diagnosis parts of the fractured site is not compromised
i. Musculoskeletal pattern G: and must be adequate
impaired joint mobility, motor
function, muscle performance,  Circulation must be adequate for the formation
range of motion associated of callus
with fracture
 Immobilization must not be the focus of this
IV. PHYSICAL THERAPY PROGNOSIS phase; it will cause joint stiffness and muscle
weakness

A. Plan of Care (Generalized)  Mobility of the joints must be started early in the
a. INTERVENTIONS period of fracture healing

 SURGICAL  In the upper extremity fractures – patient should

 REDUCTION – undertaken to regain have a program of finger, and other distal parts
perfect realignment of the fragments (if shoulder joint is affected) exercises in the
immobilization period, like:
 closed – manipulation under anesthesia;
usually for fractured long bones  Muscle setting exercises

 open – performed by operation; it is used when  Isometric exercises of the muscle covered by
reduction by manipulation is dangerous or the cast
impossible
 as a rule joints that must be immobilized should
 TRACTION OR MAINTENANCE OF be kept in a functional position
REDUCTION
 External Fixation – by the use of cast or splint
 POST- OP REHABILITATION
 Internal Fixation – converts closed fx into an
 if bed rest is needed for the fractured site to be
open fx
stable, then it should be treated, initially with it
o transfixion screw – for oblique fx or tibial shaft
 Rest, ice and weight bearing as tolerated (an
o Bone plate: metal plate fastened to he surface example of which is an avulsion fracture)
of the fragment by at least 2 screws above and  Rehabilitation of cemented cases by full weight
2 below. The screws should be long enough to bearing
cover the sides of the convex
 Rehabilitation of uncemented cases may be
o Intramedullary rod – enables the patient to walk partial or full weight bearing
with crutches soon after the injury
 Total joint precautions must be followed to
 Traction - used for patients that cannot be prevent dislocations
immobilized by cast
o Skin traction  Sepsis is a cause of dislocation after joint
replacement and should be considered
 Bryant’s traction – most common type of
traction in the children b. Home Exercise Program

 Buck ‘ s extension traction – used for fractures 1. Muscle setting exercises for 3-5 reps and 2
in the tibial shaft; used for children sets (initially), the progress into strengthening
ex with use of manual resistance, then progress
 russel’s traction – used for fractures in the again into Thera band exercises
femoral neck; used for children
2. AROM ex for all the unaffected joints
o Skeleletal traction – a stronger type of
traction that is used in the treatment of 3. PROM ex (initially) for the affected site and
femoral fractures and fractures of the progress into AAROM ex.
cervical spine; usually applied in adults
4. Apply cryotherapy every after exercise

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5. Open chain ex (initially) the progress into
closed-chain ex
6. Initially, don not bear weight into the affected
site but progress into bearing weight as
tolerated (8-12 weeks of healing time)
C. Precautions
1. Teach the patient not to do Valsalva
maneuver.
2. Do not bear weight right away into the
affected site.
3. Avoid doing strenuous ex that would greatly
affect the joint.

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