pbl osteomyelitis

8/13/2019 PBL Osteomyelitis

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Gross Anatomy of Leg


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Cause of Bullae Formation

1. Friction and excessive heata. Rubbing shoesrubbed for long period or intense rubbing over shorter periodb. Sunburn, scaldc. Reaction to chemical substanced. Underlying medical conditione. Tear upper layer of skin. Surface of skin remains intact is pushed outwards

because serum collects in the newly created space between layers of skin

f. Form more easily on moist skin and are more likely to occur in warm conditions.2. Medical conditions

a. Chicken poxb. Cold soresc. HerpesSTI, most commonly affects the groind. Impetigocontagious bacterial skin infectione. Pompholyxeczemaf. bullous pemphigoidcauses large blisters and usually affects people over 60

years of age

g. pemphigus vulgaris serious, blisters develop if pressure is applied to the skin;the blisters burst easily, leaving raw areas that can become infected

h. dermatitis herpetiformisa skin condition that causes intensely itchy blisters,usually on the elbows, knees, back and buttocks; blisters usually develop in

patches of the same shape and size on both sides of the body

i. epidermolysis bullosaa group of rare inherited skin disorders that cause theskin to become very fragile; any trauma or friction to the skin can cause painful

blisters

j. chronic bullous dermatosis of childhooda condition that causes clusters ofblisters to develop on the face, mouth or genitals

k. secondary bacterial infection in skin lesions such asscabies,psoriasis,poison ivy,atopic dermatitis, eczema herpeticum and kerionis a common problem
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Types of Microorganisms that Cause Necrotizing Soft Tissue Infection

Clues to the anaerobic origin of these infections are putrid discharge, gas production, and

extensive tissue necrosis with a tendency to burrow through subcutaneous and fascial planes.

1. ImpetigoImpetigo is a superficial small vesicles that pustulate ruptures and dries forming a golden-

yellow crust

2. CellulitisCellulitis generally appears as local tenderness, pain and erythema. The area involved is red,

sharply demarcated, hot, swollen, with non-elevated borders. Regional lymphadenitis and

bacteremia are common and can cause thrombophlebitis.
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3. Infectious Gangrene (Gangrenous cellulitis)This is a rapidly progressive infection that involves extensive subcutaneous tissues and

overlying skin necrosis. It includes several entities:

Necrotizing fasciitis Gas gangrene (clostridium and non-clostridial anaerobic cellulitis) Progressive bacterial synergistic gangrene Synergistic necrotizing cellulitis andfasciitis, Localized skin necrosis complicating cellulitis Gangrenous cellulitis in the immunocompromised patient

Necrotizing fasciitis (NF):NF has two bacteriological entities: streptococci, and polymicrobial

(evolving at least one anaerobe). Streptococcal gangrene starts as painful erythema and edema,

followed in 24-72 hours by dusky skin, and yellowish to red-black fluid filled bullae. The area is

demarcated and covered by necrotic eschar, surrounded by erythema. A rapid progression

occurs with frank cutaneous gangrene, accompanied sometimes by myonecrosis. Penetration

along facial planes can occur, followed by thrombophlebitis in the lower extremities,

bacteremia with metastatic abscesses and rapid death. Differentiation between cellulitis and NF

is important. Cellulitis can be treated with antimicrobials alone while NF requires also surgical

debridment.
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Group A beta-hemolytic streptococcal (GABHS) infectioncan be associated with streptococcal

toxic shock like syndrome (TSLS), manifested by fever, tachycardia, hypotension, multi-organ

failure, and in 80% evidence of soft tissue involvement.

NF due to mixed anaerobic-aerobic flora is usually associated with an endogenous organism(s),

and presents in slightly different fashion. The involved area is first erythematous, swollen, hot,

tender, painful and has no sharp margin. Progression occurs within 35 days, with skin

breakdown with bullae, and cutaneous gangrene. The involved area becomes anesthetic

because of thrombosis of the small vessels that supply the superficial nerves. This can antedate

the appearance of skin necrosis, and signifies the presence of NF and not simple cellulitis. Easy

probing with a hemostat through an incision in the lesion along a plane, is diagnostic.

Subcutaneous gas and foul smell are often present, especially in diabetics. Systemic toxicity and

elevated temperature are common. NF of the face, eyelids, neck and lips2are rare but can be

life-threatening. Crepitus, severe pain and necrosis of the epidermis and superficial fascia are

evident. The infection can spread rapidly to other areas in the neck. NF was recently described

after laryngectomy.2b

Gas gangrene, anaerobic cellulitis:In clostridial and non-clostridial anaerobic cellulitis, the

onset is gradual no local pain and swelling and no systemic toxicity. A thin, dark, sometimes

foul smelling discharge and extensive tissue gas formation manifesting crepitusis seen.
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Progressive bacterial synergistic gangrene:Starts with local tenderness, swelling and erythema

that subsequently ulcerates. The painful ulcer enlarges and is surrounded by violaceous zone

that fades into pink edematous border. Left untreated, the ulcer enlarges and may burrow

through tissue emerging in distant sites (Meleney's ulcer).

Synergistic necrotizing cellulites and fasciitis:This infection starts as cellulitis, adjacent to the

entry point, and involves the deep fascia. Pain, fever and systemic toxicity occur. When it occurs

in the male genitalsit is called Fournier's gangrene. Swelling and crepitus of the scrotum

increases, and gangrene develops. Abdominal wall involvement can be especially rapid in

diabetics.

Gangrenous cellulitis in the immunocompromised host: Cellulitis can be caused by expected as

well as opportunistic pathogens and is often seen after trauma. Pseudominas aeroginosais the

most common pathogen and cause a sharply demarcated necrotic area with black eschar and

surrounding erythema.

Diabetic, decubitus and other secondary bacterial infections complicating skin lesions.

Infections in the diabetics are divided into non-limb-threatening and limb-threatening. Non-

limb-threatening infections are superficial, lack systemic toxicity, have minimal cellulitis that

extends


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infected with aerobic and anaerobic bacteria are: scabies, eczema herpeticum, psoniasis,

poision ivy, draper dermatitis, Kerion and atopic dermatitis.

Myositis

Muscular infections frequently occur in areas of the body that have been compromisedor

injured by foreign body, trauma, ischemia, injection of illicit drug, malignancy or surgery. These

infections can develop very rapidly to life-threatening systemic illness. Pyogenic myositis can be
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classified into either GABHS necrotizing myositis, clostridial myonecrosis (gas gangrene), and

nonclostridial (crepitant) myositis.

Clostridial myonecrosis

Pathogenesis

Soft tissue and muscular infections frequently occur in areas compromised or injured by foreign

body, trauma, ischemia, malignancy or surgery. Because the indigenous local microflora usually

is often responsible for these infections, anatomic sites that are subject to fecal or oral

contamination are particularly at risk. These include wounds associated with surgery of the

intestine or pelvis, human bites, decubitus ulcers in the perineal area, pilonidal cysts,

omphalitis, and cellulitis around the fetal monitoring site.

Skin and subcutaneous infection

Decubiti and nonhealing wounds usually are produced by pressure or by circulatory

dysfunction. In an area without sensation, the ulcer develops when pressure is placed on one

site for a critical period of time, causing ischemia and necrosis. Ulcers caused by circulatory

dysfunction may result from large- or small-vessel disease or from venous stasis. Bedridden

patients are prone to decubitus ulcers. Poor nutrition, low serum albumin, anemia, and

circulatory impairment add seriously to the hazard of this development. Osteomyelitis and

anaerobic bacteremia can occur in extensive or invasive ulcers.
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Infection in diabeticpatients generally follows minor trauma in individuals with neuropathy and

arterial vascular insufficiency. The infection may progress to cellulitis, soft tissue necrosis,

osteomyelitis with a draining sinus. Proximity to mucous membrane orifices (anal, vaginal, or

oral) enables the adjacent endogenous flora to invade the ulcers.

Clostridial anaerobic cellulitisfollows introduction of organisms into subcutaneous tissues

through a contaminated or inadequately debrided wound. The source can also be a pre-existing

infection of the perineum, abdominal wall, buttocks and lower extremities that are

contaminated with fecal flora. The necrotic tissue or foreign material in the wound enhances

the infection with Clostridium spp.

Gangrenous cellulitisgenerally follows introduction of pathogens to the infected site. It can alsodevelop from extension of the infection from deeper sites to the subcutaneous and skin tissues.

Spontaneous, nontraumatic gas gangrene is often due to C. septicum, that spreads by

bacteremic route. Intestinal abnormalities that include necrotizing enterocolitis, volvulus, colon

cancer, diverticulitis and bowel infarction. leukemia, neutropenia and diabetes mellitus are the

major predisposing conditions.

Diagnosis

The recovery of fastidious organisms depends on employment of proper methods for

collection, and transportation of specimen, and cultivation of organisms.

Radiological studies of soft tissuecan reveal the presence of free gas. This can assist in the

differentiation between NF due to either streptococcal or mixed polymicrobial aerobic-

anaerobic infection. A feathery lineary pattern of gas can be observed in infected muscles in

clostridial myonecrosis.

Osteomyelitis can be detected by radiological and radionuclide scanning studies.

Radionuclide (67

Ga) and CT scanning are used to diagnose pyomyositis. MRI can detect

alteration in soft tissue and can differentiating cellulitis from pus and abscess. MRI can show


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enlargement of involved muscles and fluid collection. Sonography or CT can be used to guide

diagnostic aspiration.

Antimicrobial therapy for mixed aerobic and anaerobic bacterial infections is required when

polymicrobial infection is suspected. The combination of penicillin and clindamycin is

recommended forClostridium spp.. Antimicrobials that generally provide coverage

for S. aureus as well as anaerobes include cefoxitin, clindamycin, a carbapenem , and the

combinations of a -lactamase inhibitor and a penicillin and the combination of metronidazole

plus a -lactamase-resistant penicillin. Cefoxitin, the carbapenems, and a penicillin plus a -

lactamase inhibitor also cover the Enterobacteriaceae . However, agents effective against these

organisms (i.e., aminoglycosides, fourth generation cephlosporins, and quinolones) should be

added to the other agents when treating infections that include these bacteria.

Hyperbaric oxygen therapy for clostridial myonecrosis is controversial.However, it should be

considered when the involved tissue cannot be completely excised surgically.

Necrotizing Soft Tissue Infections

Key points

Necrotizing soft tissue infection is a progressive bacterial infection of the skin, soft tissue,fascia, or muscles

Early presentation of necrotizing soft tissue infection may be deceptively innocuous, with fewskin signs; the diagnosis should be suspected in patients whose pain and toxicity appear to be

out of proportion to clinical findings

Diagnosis is based on the clinical picture and should not be delayed while waiting for testresults

Treatment involves resuscitation as necessary, aggressive surgical debridement, and empiricbroad-spectrum intravenous antibiotics
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Morbidity and mortality are high and increase with delayed diagnosis and treatment

All patients with necrotizing soft tissue infection require hospitalization for treatment

Most patients, especially those who present later in the disease course, require resuscitationwith intravenous fluids and supplemental oxygen

Most patients require intensive care support

Early surgical consultation is recommended for all patients with suspected necrotizing softtissue infection; incision can reveal diagnostic findings of necrosis of fascial and/or

subcutaneous tissue, fascia, or muscle, which can be debrided at the same time

Empiric broad-spectrum intravenous antibiotic therapy should be started as soon as possible

Background

Description

Progressive infection involving skin, soft tissue, fascia (superficial and deep), or muscles that hasbeen classified in a number of ways, including anatomically (fasciitis, myonecrosis), by etiologic

organism (streptococcal, clostridial, synergistic polymicrobial) and clinically (gas gangrene). All

are characterized by rapidly progressive soft tissue necrosis and systemic toxicity

Infections are usually polymicrobial, when a mixture of aerobic, facultatively anaerobic, andanaerobic bacteria is involved, usually in synergistic fashion, but approximately 15% are caused

by a single species, notably group A beta-hemolytic streptococci (GABHS). Methicillin-

resistantStaphylococcus aureus(MRSA) has been found with increasing frequency in the last

decade

Most infections follow a factor predisposing to bacterial inoculation; a small proportion occurwithout such a known factor. Necrotizing infections may begin at a needle puncture site in an

injecting drug user, an insect bite, a surgical wound, skin abscess, or any other trauma that

compromises skin integrity. Occasionally, such infections arise in conjunction with colon cancer.


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Patients are often already immunocompromised by chronic disease or steroids; obesity is also

thought to be a predisposing factor. In some cases there is no apparent trauma or predisposing

condition; this is especially true in cases of necrotizing infection due to group A streptococci

Many patients have a pre-existing condition (eg,diabetes mellitus, renal failure, or injectingdrug misuse) that increases their risk for necrotizing soft tissue infections, however some do

not have a comorbid condition and were previously healthy

Necrotizing soft tissue infections are associated with high morbidity and notable mortality rate,both of which increase with delay in diagnosis and initiation of treatment

Treatment involves resuscitation as necessary, empiric broad-spectrum antibiotics, andaggressive surgical debridement

Rapidly progressive soft tissue necrosis and systemic toxicity are typical features

Necrotizing soft tissue infections can affect any part of the body, but the trunk, extremities,scrotum, and perineum are most commonly involved; course can be acute and fulminate

(progressing over minutes to hours) or may progress more slowly over a period of days

Early presentation may be deceptively innocuous, with a nonspecific systemic prodrome(eg,malaise and fever) and minimal cutaneous signs

This is followed by rapidly advancing erythema, necrosis, and formation of bullae that becomehemorrhagic

As necrosis develops there is intravascular thrombosis and, in some cases, nerve destructionresulting in hypoesthesia

Soft tissue crepitus may be palpable and gas may be visible on plain radiographs; these signsare pathognomonic but their absence does not exclude necrotizing soft tissue infections

Dishwater-like fluid may be discharged from affected area(s). May be gray, brown, or otherwisediscolored, cloudy, and air bubbles may be present


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Patients may progress tosepsis and systemic shock, with reduced level of consciousness;diagnosis at this late stage can be difficult

The diagnosis often is made surgically; suspicion of the condition should prompt probing of anexisting wound or incision over an affected area with exploration of underlying tissue. A finger

or blunt instrument will easily pass through infected tissue that would normally require sharp

dissection. The tissue may be pale or visibly necrotic, with little active bleeding. Involved muscle

may fail to contract

Severe cases can progress tomultiorgan failure and death

Epidemiology

Frequency:

Necrotizing soft tissue infections arerare

In 1999, there were 600 cases of necrotizing soft tissue infections caused by GABHS in the U.S.

In 2002, necrotizing soft tissue infections accounted for 6% of cases of invasive GABHS disease(3.2 cases/100,000 population) in the U.S.

The frequency of these infections is difficult to know precisely, as reporting is not required formost causes. A study of information from insurance databases estimated the frequency of

necrotizing fasciitis to be 0.04 cases per 1000 person-years

Demographics:

There is no predilection for age or race

Male to female ratio is from 2:1 to 3:1

Causes and risk factors

Causes
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Common causes:

Monomicrobial infections are usually caused by the following:

oGABHS

o Clostridium perfringens

o MRSA is emerging as a monomicrobial cause, particularly in injecting drug users

Polymicrobial infections are caused by combinations of the following:

o Gram-positive aerobic cocci, including GABHS; group B streptococci; enterococci; and Saureus (including MRSA)

o Other aerobic bacteria, includingBacillusspecies and Gram-negative organisms,mainly Escherichia coli,Pseudomonas aeruginosa, or Proteusspecies

o Anaerobic bacteria, including Clostridiumspecies, Peptostreptococcusspecies, andBacteroidesspecies

Rare causes:

Vibrio vulnificuscan cause necrotizing soft tissue infections, often following contamination of aminor wound with salt water or ingestion of raw seafood; this is usually associated with

significant underlying liver disease

Aeromonas hydrophilamay cause infection in wounds contaminated by fresh water (lake andstream) or leeches

Clostridium septicummay cause necrotizing soft tissue infections in patients with underlyinggastrointestinal malignancy

Serious causes:

All etiologic organisms must be considered serious in these life-threatening infections


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Risk factors

Immunosuppression from any cause (eg,chronic illness, corticosteroids) is a risk factor fornecrotizing soft tissue infections

Patients with diabetes mellitus(type 1 ortype 2),renal failure,andperipheral arterialdiseaseare at increased risk for necrotizing soft tissue infections

Varicella may be a predisposing factor

Individuals with alcoholism are at increased risk for necrotizing soft tissue infections

Infection can follow childbirth (by vaginal delivery or cesarean section)

Infection can occur at the site of the umbilicus in young infants

Associated disorders

Necrotizing soft tissue infections caused by GABHS may be associated with streptococcaltoxicshock syndrome

Necrotizing infections due to C septicumare often associated with an underlyinggastrointestinal malignancy

Preventive measures

Alcoholism and intravenous drug misuse are both risk factors for necrotizing soft tissueinfections, and individuals should seek suitable programs to help them abstain

Obesity (inadults andchildren)is a risk factor for necrotizing soft tissue infections, andindividuals should seek appropriate advice for exercise in combination with a calorie-controlled

diet to reduce weight to normal parameters

Careful hygiene in persons who are at risk, including postoperative surgical care of incisions andperinatal wound care of episiotomies or lacerations and umbilical stumps
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Routine immunization of healthy children against varicella should decrease the risk ofstreptococcal necrotizing soft tissue infections as a complication of chickenpox

Recognition of pathogenic clostridial species associated with wound infection

C. novyi type A

C. novyi type A may be widely distributed in soil and, in one study, was present in 88% of

samples examined. When an anaerobic chamber is used for isolation, anaerobic cultures for C.

novyitype A should be examined after overnight incubation within the anaerobic chamber for

any small, flat, rough or rhizoidal, translucent, haemolytic colonies with a spreading edge. It is

advised that plates should not be removed from the anaerobic chamber at this stage, as

exposure to air would be toxic to any micro-colonies that have not begun sporulation. If

anaerobic jars are used, these should be left unopened for at least 48 h before the plates are

examined. After incubation for 4872 h, colonies will often coalesce to give a fine spreading

growth that may cover the entire plate, often with a marked -haemolysis so as to make the


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blood agar plate completely transparent. Gram's staining shows gram-variable rods with

occasional sub-terminal spores. A characteristic of C. novyi type A is the production of both

lecithinase C and lipase on egg-yolk agar. The indole reaction can be variable and it can be

difficult to differentiate C. novyitype A from C. botulinumtype C. It may require specific

neutralisation of the cytopathic effect of alpha toxin in bioassay, or 16S rDNA sequence analysis

to differentiate between these species. C. novyi type A is usually unreactive in commercial

anaerobe identification kits and commonly is not identified by this approach. C. novyitype B

has different phenotypic characteristics and can be distinguished by its biochemical reactions.

The C. novyitype A isolates in the IDU outbreak were variable indole producers and could not

be differentiated from C. botulinumtype C by phenotypic tests alone. Definitive identification

was obtained by 16S rDNA gene sequence analysis [14]and detection of alpha toxin in bioassay.

Cell-free culture supernates of C. novyiisolates from IDUs produced identical cytopathic effects

to the type strain of C. novyi(NCTC 538) in Vero cells and these effects were completely

neutralised by the international standard for C. novyi, i.e., Gas Gangrene(Cl. oedematiens)

Antitoxin (3rd British Standard Established 1966) (64/24). 16S rDNA gene sequence analysis

gave 100% homology with C. novyitype A accession no.X68188 (NCTC 538) listed in the EMBL

database but only 98% homology with that listed for C. botulinumtype C.

C. perfringens

Although C. perfringenswas isolated from several cases of infection in IDUs, this organism was

not believed to be of general significance in the outbreak investigation as this organism is

frequently found as a post-mortem contaminant, being part of the normal gut flora. This fast-

growing species will usually produce quite large discrete colonies after overnight incubation.

They may be flat and rough-edged or smooth and domed, and either non-haemolytic or with a

narrow zone of complete haemolysis inside a larger zone of partial haemolysis. This target

haemolysis is more pronounced on sheep blood agar than on horse blood agar. Gram's staining

shows straight-sided gram-variable rods with no spores. The classical method of identifying C.

perfringensis the Nagler plate which is a half anti-alpha toxin egg-yolk plate that is streaked at

90 diametrically with the test organism. After incubation, the lecithinase C (alpha toxin)
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produces an opaque zone on the half plate without antitoxin that is inhibited on the half plate

with the antitoxin. It has been difficult recently in the UK to obtain good quality anti-alpha toxin

to C. perfringens. Poorer quality antisera may give a partial inhibition of lecithinase that is not

species specific and may lead to mis-identification of C. bifermentansas C. perfringens, for

example. However, colony morphologies are distinct and Gram's stain will aid differentiation of

these two species, as C. bifermentansis usually a prolific producer of sub-terminal spores

whereas C. perfringensdoes not sporulate in vitroon normal agar media. Also, the result of the

indole test differentiates between the two species (Table 1).

C. septicum

This organism is another rapidly growing Clostridiumspecies that usually produces a thickswarming growth that is quite haemolytic. In culture, it has no characteristic odour, and

Gram's staining reveals gram-variable rods with numerous sub-terminal spores. It should be

recognised by use of commercially available identification kits. The most common source of C.

septicumisolates seen in recent years has been from blood cultures from patients with

malignancies of the colon or caecum for which this organism is a marker [15]. It can also be

isolated from cases of spontaneous gas gangrene of the abdomen that are usually fatal.

C. botulinum

The proteolytic types A, B and F initially produce discrete rhizoidal colonies that spread and

coalesce. Haemolysis is variable, but the odour is strong and redolent of rotten eggs due to

production of H2S. Gram's staining shows profuse sub-terminal and free spores and gram-

variable bacilli. Phenotypically, they are identical to C. sporogenesand differentiation requires

demonstration and specific neutralisation of botulinum toxin in a mouse assay. The non-

proteolytic types of C. botulinum vary in their phenotypic characteristics but require similar

toxin assays. In addition to food-borne illness, C. botulinummay be implicated in cases of

wound botulism and such cases have occurred in IDUs [16].
http://jmm.sgmjournals.org/content/51/11/985.full#T1http://jmm.sgmjournals.org/content/51/11/985.full#ref-15http://jmm.sgmjournals.org/content/51/11/985.full#ref-16http://jmm.sgmjournals.org/content/51/11/985.full#ref-16http://jmm.sgmjournals.org/content/51/11/985.full#ref-15http://jmm.sgmjournals.org/content/51/11/985.full#T1


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C. tetani

No cases of tetanus associated with IDU have been reported recently, probably as a result of

the success of the immunisation programme. Colonies of C. tetanimay produce a fine swarming

growth that can be easily missed on cursory examination. Gram's staining of overnight cultures

often reveals readily over- decolorised long bacilli without spores. Further incubation yields the

classical drum stick appearance of cells with terminal, round spores. Phenotypically it is quite

unreactive although some strains produce indole, and attempts at identification by commercial

kits often require supplementation to confirm its identification. However, not all strains of C.

tetaniare toxigenic and referral for toxin bioassay may be required.

C. sordellii

This organism has been reported in other IDU-associated infections [17]and recently has been

implicated in a fatal post-knee transplant infection the USA [18]. Colonies are large, grey-white

and irregular, sometimes with a fern-leaf edge. They produce indole and lecithinase but are

urease negative, which differentiates them from C. bifermentans, generally regarded as a non-

pathogen.
http://jmm.sgmjournals.org/content/51/11/985.full#ref-17http://jmm.sgmjournals.org/content/51/11/985.full#ref-18http://jmm.sgmjournals.org/content/51/11/985.full#ref-18http://jmm.sgmjournals.org/content/51/11/985.full#ref-17


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II. ANAEROBIC BACTERIA

A. Gram-positive cocci

1. Streptococcus species Penicillin G Clindamycin

B. Gram-positive bacilli

1. Clostridium species

a. C. perfringens Penicillin G Clindamycin Doxycycline

b. C. novyi Penicillin G Clindamycin Doxycycline

c. C. histolyticum Penicillin G Clindamycin Doxycycline

d. C. septicum Penicillin G Clindamycin Doxycycline

e. C. sordellii Penicillin G Clindamycin Doxycycline

f. C. sporogenes Penicillin G Clindamycin Doxycycline

g. C. tetani Metronidazole orPenicillin

G

Doxycycline

C. Bacteroides species Metronidazole Clindamycin, Trovafloxacin


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Autonomy vs. Beneficence

Autonomy:

Definition: Autonomy is the personal rule of the self that is free from both controllinginterferences by others and from personal limitations that prevent meaningful choice.

Autonomous individuals act intentionally, with understanding, and without controlling

influences.

Clinical Applications: Respect for autonomy is one of the fundamental guidelines of clinical

ethics. Autonomy in medicine is not simply allowing patients to make their own decisions.

Physicians have an obligation to create the conditions necessary for autonomous choice in

others. For a physician, respect for autonomy includes respecting an individuals right to self-

determination as well as creating the conditions necessary for autonomous choice.

Individuals come to doctors for guidance in making choices because they do not have the

necessary background or information for making informed choices. Physicians educate patients

so that they understand the situation adequately. They calm emotions and address fears that

interfere with a patients ability to make decisions. They counsel patients when their choices

seem to be disruptive to health and well-being. Respect for autonomy also includes

confidentiality, seeking consent for medical treatment and procedures, disclosing information

about their medical condition to patients, and maintaining privacy.

Examples of promoting autonomous behavior: Presenting all treatment options to a patient,

explaining risks in terms that a patient understands, ensuring that a patient understands the

risks and agrees to all procedures before going into surgery.

Beneficence:

Definition: Beneficence is action that is done for the benefit of others. Beneficent actions can

be taken to help prevent or remove harms or to simply improve the situation of others.


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Clinical Applications: Physicians are expected to refrain from causing harm, but they also have

an obligation to help their patients. Ethicists often distinguish between obligatory and ideal

beneficence. Ideal beneficence comprises extreme acts of generosity or attempts to benefit

others on all possible occasions. Physicians are not necessarily expected to live up to this broad

definition of beneficence. However, the goal of medicine is to promote the welfare of patients,

and physicians possess skills and knowledge that enable them to assist others. Due to the

nature of the relationship between physicians and patients, doctors do have an obligation to 1)

prevent and remove harms, and 2) weigh and balance possible benefits against possible risks of

an action. Beneficence can also include protecting and defending the rights of others, rescuing

persons who are in danger, and helping individuals with disabilities.

Examples of beneficent actions: resuscitating a drowning victim, providing vaccinations for the

general population, encouraging a patient to quit smoking and start an exercise program,

talking to the community about STD prevention.

Balancing Autonomy and Beneficence:

Some of the most common and difficult ethical issues to navigate arise when the patients

autonomous decision conflicts with the physicians beneficent duty to look out for the patients

best interests. For example, a patient who has had bypass surgery may want to continue to

smoke or a patient with pneumonia may refuse antibiotics. In these situations the autonomous

choice of the patient conflicts with the physicians duty of beneficence and following each

ethical principle would lead to different actions. As long as the patient meets the criteria for

making an autonomous choice (the patient understands the decision at hand and is not basing

the decision on delusional ideas), then the physician should respect the patients decisions even

while trying to convince the patient otherwise.

pbl osteomyelitis

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