Case Discussion
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<Case
Presentation:>
An 80-year-old man came to the
emergency department (ER) with a two-day history of
generalized malaise, fever and drowsiness. He had cut his
right leg by the wheel of his bicycle five days ago and the
leg began to develop local erythema and swelling two days
later. His medical history is significant for poor control
diabetes, hypertension and coronary artery disease and had
social history for alcohol abuse for more than 50 years. He
also took some black pills in recent years for gouty
arthritis. He was admitted because of increasing pain and
swelling of right leg and scrotum. His physical examination
revealed an oral temperature of 38.8°C, pulse of 120
beats/min, respirations of 33/min, and blood pressure of
100/60 mm Hg. Extensive tender erythema, small blisters are
noted at the inferior aspect of leg with air crepitus and
gangrenous change of his perineum (
Figure 1
). Blood cultures are obtained along with complete blood
count with differential, chemistries,prothrombin(PT), and arterial blood gas as
shown in Table 1. Intravenous clindamycin and ceftriaxone was
given and inotropic agents for hypotension. Six hours later,
the patient's leg was observed to be dusky and rapidly
progressed. A creatinine kinase (CK) elevated to 6983 U/L with
CK-MB 5 U/L. Acute respiratory distress developed and
intubation was performed. He was immediately taken to the
operating room (OR) where an incision was made in the scrotum
and leg. The pathological findings were shown in
Figure 2
. All cultures of blood and necrotic tissues yielded Group A
streptococci. The patient's condition continued to worsen
despite maximal medical therapy and he died on the next
day.
Table 1. Blood biochemistry
obtained on admission
Hemogram |
RBC (M/uL) |
Hb (g/dL) |
Platelet (K/uL) |
WBC (K/uL) |
seg (%) |
lym (%) |
band (%) |
|
4.78 |
14.8 |
97 |
15.32 |
89 |
6 |
5 |
Biochemistry |
Sugar (mg/dL) |
GPT (U/L) |
BUN (mg/dL) |
Creatinine (mg/dL) |
Na (U/L) |
K (U/L) |
PT (sec) |
|
76 |
78 |
76 |
1.8 |
137 |
5.5 |
16.8 |
Blood gas |
pH |
PCO2 |
PO2 |
HCO3 |
BE |
|
|
O2 mask 60% |
7.13 |
28 |
158 |
9 |
-10 |
|
|
<Case
Analysis>
Necrotizing
fasciitis (NF) is a severe soft-tissue infection caused by
toxin-producing virulent bacteria, which is characterized by
widespread fascial necrosis. It is often associated with
severe systemic toxicity and is usually rapidly fatal unless
promptly recognized and aggressively treated. The histology of
NF revealed microbial invasion of the subepithelial soft
tissues (including fascia), resulting in perivascular
leukocytic infiltrate, vascular thrombosis, tissue edema, and
necrosis. The perineal region is a common site of infection
followed by foot ulcerations and traumatic wounds. Mortality
(30-70%) can be influenced by predisposing patient
characteristics (such as diabetes, liver cirrhosis, steroid
use and other immunocompromised conditions) as well as the
site and pathogen of infection, with perineal sources carrying
the highest mortality rate in most studies.
Necrotizing
fasciitis present a unique and demanding diagnostic challenge
to clinicians. Soft tissue infections often begin as a result
of a trauma and may no longer apparent once the infection has
set in. The most common signs of NF are nonspecific local
pain, edema out of proportion to erythema, development of
blistering, crepitus, and radiological evidence of soft tissue
gas. Diagnosis of NF must be considered in cases of cellulitis
with crepitus, local cutaneous anesthesia, or when progression
is rapid or associated with necrosis. Radiological studies,
including plain radiographs, CT, ultrasonography, and MRI have
been used to aid in diagnosing NF. With evidence of NF,
immediate surgical evaluation is crucial. Necrotizing
fasciitis of scrotal gangrene (Fournier's gangrene) could
occur with fever and scrotal edema which progresses quickly to
gangrene and shock, often accompanied with anaerobic
streptococci. Other common pathogens causing NF including
Staphylococcus aureus, Clostridium perfringens (classic gas
gangrene), gram-negative bacilli (Aeromonas hydrophilia,
Vibrio vulnificus), group A streptococci. The identification
of the causative pathogen is performed by Gram's stain and
culture of debrided tissues. Most NF is polymicrobial and
aggressive surgical debridement of lesions involved should be
initiated. Patient survival is highly dependent on
resuscitation from shock, early and repeated surgical
debridements, broad-spectrum antibiotic coverage
(third-generation cephalosporin and anaerobic coverage), and
early hyperalimentation. Complications of NF include acute
renal failure, adult respiratory distress syndrome,
disseminated intravascular coagulation, multi-organ system
dysfunction, surgical wound infections, and bacteremia and
many patients receiving skin grafting later.
Another disease entity of this patient is
toxic shock syndrome (TSS), which was usually caused by
Staphylococcus aureus and group A streptococcus. Nearly every
clinical setting where infection or colonization with S.
aureus and group A streptococcus can occur, such as
post-surgical procedures, traumatic injuries, focal tissue
infections and post-influenza pneumonia. The clinical picture
associated with TSS includes high fever, a diffuse
erythroderma involving the palms of the hands and soles of the
feet that can desquamate over the course of 1-2 weeks, and
hypotension. Multiple organ system involvement may also be
present and can include vomiting, diarrhea, renal or hepatic
dysfunction, thrombocytopenia, mucous membrane hyperemia,
myalgias, and disorientation. The onset of symptoms is acute
and symptoms may vary in intensity. Diagnosis is based on
criteria include fever of >38.8°C, a diffuse macular
erythrodermal rash, palmar and sole desquamation, hypotension
(systolic <90 or orthostatic), multiple organ systems
involvement, and negative results for other diseases such as
Rocky Mountain Spot Fever, leptospirosis, and measles. A
marked leukocytosis may be present and a transient
lymphocytopenia may occur. The mortality rate in TSS is near
3% and is generally attributable to refractory hypotension or
associated comorbidity with adult respiratory distress
syndrome and/or disseminated intravascular coagulation.
Treatment of toxic shock syndrome focused on correcting shock
and the treatment of comorbid conditions. Choice of
antibiotics should both cover S. aureus and streptococci, and
if the diagnosis is unclear, a broad-spectrum third generation
cephalosporin may be
given.
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繼續教育考題
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|
1.
(E) |
Necrotizing fasciitis occurs frequently in which following condition: |
A | Diabetes |
B | Alcoholics |
C | Immunosuppressed patients |
D | Liver cirrhosis |
E | All of above |
2.
(D) |
Which region of the
body is less common of developing necrotizing fasciitis: |
A | Extremities |
B | Perineum |
C | Abdominal wall |
D | Head and neck |
E | Post-surgical wound |
3.
(C) |
Which of the following
statement is wrong: |
A | Pain out of proportion to
physical findings in a patient who appears to have a systemically
toxic condition should raise the clinical suspicion of necrotizing
fasciitis. |
B | Typical skin manifestations of
necrotizing fasciitis usually presented as dusky blisters and
(hemorrhagic) bullaes, necrosis of the superficial fascia and fat
and subcutaneous air crepitation. |
C | Perivascular leukocytic
infiltrate, vascular thrombosis, fascia and fat necrosis and tissue
edema contribute to the necrosis of necrotizing fasciitis.
Hypercalcemia can develop from extensive fat necrosis. |
D | Subcutaneous nerves can be
irritated or destroyed by necrotizing fasciitis and the previously
tender skin could become hypersthetic or anesthetic. |
E | Necrotizing fasciitis
occasionally to have metastatic abscess formation in liver, lungs,
spleen, brain, and other organs. |
4.
(A) |
Which pathogen is the
least likely to causing necrotizing fasciitis of extremities: |
A | Streptococcus pneumoniae |
B | Staphylococcus aureus |
C | Streptococcus pyogenes |
D | Clostridium perfrigens |
E | Aeromonas and Vibrio species |
5.
(E) |
Which of the following
clinical manifestations indicate necrotizing fasciitis rather than
cellulites: |
A | Hemorrhagic bullae formation |
B | Necrosis or gangrenous changes
of full thickeness of involved skin |
C | Systemic toxic signs such as
septic shock |
D | Subcutaneous air crepitaions |
E | All of above |
6.
(B) |
Which one of the
following is the most important management to control the
progression of necrotizing fasciitis: |
A | Resuscitation from shock by
using albumin to keep oncotic pressure |
B | Early and repeated
surgical debridements and fasciotomy to decrease bacterial loads |
C | Broaden antibiotic coverage
for gram-positive and gram-negative bacteria |
D | Hyperalimentation for
nutritional support |
E | Transfusion and steroid given |
7.
(E) |
Which statement about
the outcome of necrotizing fasciitis is wrong: |
A | Mortality rates of necrotizing
fasciitis ranged from 30 to 70%. |
B | Delays in diagnosis and
treatment (particularly adequate surgical debridement and
fasciotomy) correlated with poor outcome. |
C | Old age, diabetes mellitus,
peripheral vascular disease and other systemic disorders, poor
nutritional status, and infection involving the trunk and perineum
had worse prognosis. |
D | Patient survival is highly
dependent on resuscitation from shock, early and repeated surgical
debridements, broad-spectrum antibiotic coverage (third-generation
cephalosporin and anaerobic coverage), and early hyperalimentation. |
E | Patients had necrotizing
fasciitis usually had rapidly recovery of wound and seldom needed
skin grafting. |
8.
(E) |
Which complications
could be occurred in patients with necrotizing fasciitis: |
A | Overwhelming sepsis |
B | Multiple organ system failure |
C | Acute respiratory distress
syndrome (ARDS) |
D | Disseminated intravascular
coagulation (DIC) |
E | All of above |
9.
(E) |
Which manifestations
is common of patients with toxic shock syndrome: |
A | High fever (>38.8°C) with
leukocytosis |
B | Diffuse erythroderma involving
the palms of the hands and soles of the feet and desquamation |
C | Hypotension (systolic
<90 mmHg or orthostatic hypotension) |
D | Multiple organ systems
involvement included vomiting, diarrhea, renal or hepatic
dysfunction, thrombocytopenia and disorientation. |
E | All of above |
10.
(C) |
Which following
statement about toxic shock syndrome is wrong: |
A | Both Staphylococcus aureus and
group A streptococcus could develop toxic shock syndrome |
B | Colonization of S. aureus and
group A streptococcus could participate development of toxic shock
syndrome |
C | Mortality rate of toxic shock
syndrome is near necrotizing fasciitis |
D | Treatment of toxic shock
syndrome focused on correcting shock and the treatment of comorbid
conditions. |
E | Broad-spectrum antibiotic for
toxic shock syndrome if the etiology is not clear |
References
|
- Weinbren MJ, Perinpanayagam RM. Streptococcal
necrotising fasciitis. J Infect 1992; 25:299-302.
- Donaldson PMW, et al. Rapidly fatal necrotising
fasciitis caused by Streptococcus pyogenes.J Clin Pathol
1993; 46:617-20.
- Voros D, et al. Role of early and extensive surgery in
the treatment of severe necrotizing soft tissue infections.
Br J Surg 1993; 80:1190-91.
- McHenry CR, et al. Determinants of mortality for
necrotizing soft-tissue infections. Ann Surg 1995;
221:558-65.
- Stevens DL. Invasive group A streptococcal infections.
Clin Infect Dis 1992; 14:2-13.
- Green RJ, et al. Necrotizing fasciitis. Chest
1996;110:219-29.
|
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<答案解說 >
- Ans: E
There is no age or sex
predilection for necrotizing fasciitis. The disease occurs
more frequently in diabetics, alcoholics, patients with
chronic renal and liver diseases, immunosuppressed patients,
IV drug users, and patients with peripheral vascular
disease. Occasionally, necrotizing fasciitis may also occurs
in young, previously healthy individuals because of the pathogenic organism is
virulent (such as group A streptococcus).
- Ans: D
Although it can occur in
any region of the body, necrotizing fasciitis most commonly
occurs in the extremities. Introduction of the pathogen into
the subcutaneous space can occur via any disruption of the
overlying skin, such as a cut, abrasion, burn, laceration,
contusion, bite, injection, or surgical incision, blunt or
penetrating trauma, postoperative complications, cutaneous
infections or ulcers, intravenous drug injections,
perirectal abscesses and animal or insect bites. It may even
develop at the site of a trivial scratch or wound or even in seemingly intact skin.
Necrotizing fasciitis of the head and neck
is rare.
- Ans: C
Erythematous, tender,
swollen, hot area of cellulitis, accompanied by local pain
and fever, is commonly the first sign of necrotizing
fasciitis. Leukocytosis with a left shift and systemic toxic
signs are usually present at the time of hospital admission.
Pain out of proportion to physical findings in a patient who
appears to have a systemically toxic condition should raise
the clinical suspicion of necrotizing fasciitis. Dusky blue
as blisters and bullae develop later accompanied with
necrosis of the superficial fascia and fat caused by
bacterial enzymes, including hyaluronidase and lipases. The
subcutaneous nerves are then destroyed by the infectious
process and the previously tender skin becomes hypersthetic
or anesthetic. Hypocalcemia can develop from extensive fat necrosis. Metastatic abscess
formation in liver, lungs, spleen, brain, and pericardium
from necrotizing fasciitis is common.
- Ans: A
Many pathogens could
lead to necrotizing fasciitis in certain conditions.
Virulent bacteria, such as Staphylococcus aureus,
Clostridium perfringens, gram-negative bacilli (Aeromonas
hydrophilia, Vibrio vulnificus), group A streptococci is
common causes of necrotizing fasciitis. Of patients with
diabetes and post-surgical wounds related necrotizing fasciitis, anaerobes
and fungi could also be contributed,
too.
- Ans: E
The most common signs of
necrotizing fasciitis are nonspecific local pain, edema out
of proportion to erythema, development of blistering,
crepitus, and radiologic evidence of soft tissue gas.
Systemic toxic signs, such as septic shock, ARDS, DIC or
acute organ failure indicate necrotizing fasciitis rather
than cellulitis. Diagnosis of necrotizing fasciitis must be
considered in patients of cellulitis with crepitus, local
cutaneous anesthesia, or when progression is rapid or
associated with necrosis. Radiologic studies, including
plain radiographs, CT, ultrasonography, and MRI have been used to
aid in diagnosing necrotizing fasciitis.
- Ans: B
Treatment of necrotizing fasciitis is
first and foremost surgical. Adequate surgery includes early
debridement of all necrotic tissue and drainage of involved
fascial planes via extensive fasciotomy until healthy fascia
is encountered. Early and adequate surgical debridement and
fasciotomy have been associated with improved survival.
Postoperatively, because of the potential for rapid
progression, the surgical wound must be reevaluated
frequently for evidence of disease extension. In many
instances, two or more major debridements, carried out in
the operating room under general anesthesia, are indicated.
In cases of extremity involvement, amputation is often
warranted to control infection, particularly in patients
with peripheral vascular disease and/or diabetes.
- Ans: E
The mortality rates of necrotizing fasciitis
is estimated from 29 to 76% in most larger studies. Delays
in diagnosis and treatment (particularly adequate surgical
debridement and fasciotomy) correlated with poor outcome.
Other risk factors such as old age (more than 50 years),
diabetes mellitus, peripheral vascular disease and other
systemic disorders, poor nutritional status and infection
involving the trunk and perineum had higher mortality.
Patient survival is highly dependent on resuscitation from
shock, early and repeated surgical debridements,
broad-spectrum antibiotic coverage (third-generation
cephalosporin and anaerobic coverage), and early
hyperalimentation. Complications of NF include acute renal
failure, adult respiratory distress syndrome, disseminated
intravascular coagulation, multi-organ system dysfunction,
surgical wound infections, and bacteremia and many patients
receiving skin grafting later.
- Ans: E
Complications of NF include acute renal
failure, adult respiratory distress syndrome, disseminated
intravascular coagulation, multi-organ system dysfunction,
surgical wound infections, and bacteremia and many patients
receiving skin grafting later. The proximate cause of death
in patients with necrotizing fasciitis is usually either
overwhelming sepsis or multiple organ system failure with or
without the ARDS. Early deaths (defined as within the first
10 days after initial debridement) were due to the
consequences of sepsis syndrome, whereas late deaths were
attributable to multiple organ system failure.
- Ans: E
The clinical picture associated with TSS
includes high fever, a diffuse erythroderma involving the
palms of the hands and soles of the feet that can desquamate
over the course of 1-2 weeks, and hypotension. Multiple
organ system involvement may also be present and can include
vomiting, diarrhea, renal or hepatic dysfunction,
thrombocytopenia, mucous membrane hyperemia, myalgias, and
disorientation. The onset of symptoms is acute and symptoms
may vary in intensity. Diagnosis is based on criteria
include fever of >38.8°C, a diffuse macular erythrodermal
rash, palmar and sole desquamation, hypotension (systolic
<90 or orthostatic), multisystem involvement, and
negative results for other diseases such as Rocky Mountain
Spot Fever, leptospirosis, and measles. A marked
leukocytosis may be present and a transient lymphocytopenia
may occur.
- Ans: C
The mortality rate in TSS is near 3% and is
generally attributable to refractory hypotension or
associated comorbidity with adult respiratory distress
syndrome and/or disseminated intravascular coagulation.
Treatment of toxic shock syndrome focused on correcting
shock and the treatment of comorbid conditions. Choice of
antibiotics should both cover S. aureus and streptococci,
and if the diagnosis is unclear, a broad-spectrum third
generation cephalosporin may be
given. | | |