|
Chief
complain:
Fever
and abdominal discomfort for one day
Brief
History:
This 50-year- old man
was a victim of chronic hepatitis B virus infection with
abnormal liver function for more than ten years, but he did
not get regular medical follow-ups. He has suffered from
general malaise two days before admission and only took some
medicine for common cold from local hospital. Fever flared up
one day later and he took antipyretics during the febrile
periods. However, his general malaise became more severe, and
was accompanied with insomnia and abdominal discomfort. There
was no other associated symptom such as nausea, vomiting,
diarrhea or constipation. He was sent to our emergency room at
4: 00 AM in the morning.
At emergency room, the pulse
rate was 82/min, the respiratory rate was 21/min, and the
blood pressure was 94/59 mmHg. He had a mild fever of 37.5
degrees Celsius. His consciousness was clear and oriented. The
sclera was icteric and pupils were 3mm/3mm in size with prompt
light reflex. The throat was not injected. The neck was supple
and the breath sounds were clear. The heart sounds were
regular without audible murmur. The abdomen was soft but
distended. Mild tenderness in the epigastric area was noted
without peritoneal signs or Murphy's sign. The four limbs were
freely movable without edema. No infectious skin lesion was
found. The initial laboratory examination revealed
thrombocytopenia, mild jaundice, azotemia and severe metabolic
acidosis (Table 1).
Abdominal sonography revealed liver cirrhosis, splenomegaly,
and mild thickening of the gall bladder. There was no
pneumonic patch in the chest X-ray film (Figure
1
). Under the impression of sepsis that was possibly
related to spontaneous bacterial peritonitis cefoxitin was
given. However, abdominal pain aggravated, and a subcutaneous
shot of Keto was given around at 3:00 PM. A sudden onset of
conscious change and apnea developed at 3:20 PM. After
cardiopulmonary resuscitation spontaneous circulation was
restored 3 minutes later. Then he was sent to intensive care
unit.
In the
intensive care unit, he remained in a state of deep coma with
rigidity of four limbs. Bediseds, acute renal failure,
hyperkalemia, hypernatremia, rhabdomyolysis, hyperammonemia,
elevated transaminases, hyperbilirubinemia, and prolonged
PT/PTT were found. Computer tomography of the head showed a
subdural hematoma on the left side. Neurosurgeon suggested
that surgical intervention was unfeasible due to poor general
condition of the patient. Antibiotics were shifted to imipenam
+ penicillin G under the impression of sepsis with multiple
organ failure. Fluid supplement, bicarbonaste infusion,
calcium gluconate, insulin + glucose and cation exchange resin
were given to correct the metabolic acidosis and hyperkalemia.
Transfusion of fresh frozen plasma was given to correct the
bleeding tendency. Pulseless ventricular tarchycardia
developed 30minutes after arrival at the intensive care unit
and was successfully converted to sinus rhythm by electrical
cardioversion. However, refractory hyperkalemia with marked
EKG change (Figure 2
) was ensued despite of aggressive medical
treatment and administration of large amount of bicarbonate.
Profound shock and anuria also developed. The patient's family
refused to receive emergent renal replacement therapy and
further resuscitation for the patient. The patient passed away
at 6:12 PM on the day of admission.
The blood culture grew Group
G Streptococcus two days after admission.
Final diagnosis:
- Group G Streptococcal bacteremia with
streptococcal toxic shock syndrome and multiple
organ failure.
- Liver cirrhosis, HBV related
- Subdura hematoma, left frontoparietal area
Discussion:
This
is a case of severe presentation of group
G streptococcal infection with toxic shock syndrome.
The severe metabolic catabolism by DIC and
metabolic acidosis with renal failure caused intractable
hyperkalemia. These factors resulted in the cardiovascular
collapse and led to death of this patient.
Group G streptococcus is
beta-hemolytic bacteria that occasional cause human infection
similar to those caused by Group A streptococcus, including
pharyngitis, pneumonia, cellulites and soft tissue infection,
arthritis, septic arthritis and endocarditis. A case
definition of streptococcal toxic shock syndrome was
formulated in 1993 (Table 2). The syndrome is often
associated with underlying disease such as malignancy, DM,
cirrhosis, alcohol/drug abuse, ESRD, steroid use, heart
disease, postpartum status, degenerative joint and child/old
age. The bacteria usually colonize at pharynx, skin, genitals
and GI tract. Skin is the most common port of entry, followed
by respiratory tract and GU tract. The most common associated
infection is soft tissue infection including necrotizing
fasiitis, myocitis, or cellulites. But, up to 50% patients did
not reveal any portal of entry. In this patient no prominent
infection focus was found. Exactly why patients develop
streptococcal toxic shock syndrome is unknown. Studies of
these patients demonstrated strong association of certain
streptococcal strains producing streptococcal exotoxin A, B or
C was associated this syndrome. The exotoxin could act as
superantigen, bind to both MHC complex of antigen-presenting
cells and Vβregion of T-cell receptors. T-cell proliferate,
then produce IL-1, TNFα, TNFβ, IL-6, γ-INF, bradykinin. The
general features are usually presented with various prodromes
such as fever, nausea, malaise and mental confusion, which
rapidly deteriorate to hypotension, renal impairment,
respiratory distress syndrome and shock. Laboratory
abnormalities include a marked shift to the left in the white
blood cell differential with many immature granulocytes;
hypocalcemia; hypoalbuminemia; and thrombocytopenia, which
usually becomes more pronounced on the secondary or third day
of illness. Streptococcal toxic syndrome is associated with a
mortality rat of 30~70 percent, with most death secondary to
shock or respiratory failure. Because of the high mortality of
this syndrome, once the syndrome is suspected patients should
be given aggressive therapy. These include fluid
resuscitation, pressors, and mechanical ventilation in
addition to antimicrobial therapy. The underlying infection
should be managed, such as necrotizing fasciitis should be
managed with surgical debridement. Penicillin is the choice of
antimicrobial therapy. Some authors advocated that treatment
with clindamycin should be considered, which through its
direct action on protein synthesis, clindamycin is more
effective in rapidly terminating toxin production than
penicillin. Intravenous immunoglobulin has been suggested as
adjunctive therapy for streptococcal toxic syndrome; pooled
immunoglobulin preparation is likely to contain antibodies
capable of neutralizing the effects of streptococcal toxin.
Table 1
< Laboratory
Examination >
1. Hemogram
| |
WBC
K/μL |
RBC
M/μL |
Hb
g/dL |
Hct
% |
MCV
FL |
PLT
K/μL |
Myelo
% |
Meta
% |
Band
% |
Seg
% |
Eos
% |
Lym
% |
| 8:30AM |
3.63 |
4.39 |
16.4 |
45.1 |
102.7 |
26 |
0 |
4 |
52 |
7 |
0 |
22 |
| 3:30PM |
5.4 |
3.97 |
14.9 |
40.7 |
102.5 |
34 |
2 |
9 |
50 |
16 |
0 |
14 |
2.
Biochemistry
| |
Albumin
g/dL |
T-Bil
mg/dL |
D-Bil
mg/dL |
AST
U/L |
ALT
U/L |
Lipase
U/L |
ALP
U/L |
CK/MB
U/L |
Tn-I
ng/mL |
| 8:30AM |
3.16 |
3.99 |
2.35 |
212 |
120 |
15 |
190 |
|
|
| 3:30PM |
|
11.04 |
|
317 |
127 |
|
313 |
5230/125.8 |
0.495 |
| 6:00PM |
2.28 |
11.17 |
8.83 |
622 |
300 |
|
|
9567/252 |
3.41 |
| |
BUN
Mg/dL |
Cre
Mg/dL |
Na
mmol/L |
K(H)
mmol/L |
Ca
mmol/L |
P
Mg/dL |
Mg
mmole/L |
NH3
Umol/L |
Lactate
Mmol/L |
|
8:30AM |
27.3 |
2.1 |
139 |
4.7 |
2.25 |
|
|
36 |
|
|
3:30PM |
32.2 |
2.4 |
161 |
5.2(2+) |
1.90 |
|
|
230 |
>12 |
|
6:00PM |
|
|
142 |
10.6(4+) |
3.21 |
22.9 |
1.73 |
|
|
3. ABG:
| |
PH |
PCO2 |
PO2 |
HCO3 |
BE |
FiO2 |
| 8:30AM |
7.18 |
35.6 |
53.7 |
12.8 |
-14. |
Room Air |
| 3:30PM |
7.06 |
19.8 |
94.0 |
5.4 |
-25.4 |
100% |
| 6:00PM |
7.42 |
41.6 |
78.1 |
27.7 |
+3.0 |
100% |
4. Coagulation
profile
| |
PT (sec) |
PTCont. (sec) |
PT INR |
PTT(sec) |
PTTCont. |
| 4:30PM |
36.6 |
13.0 |
3.0 |
127.0 |
37.4 |
| 6:00PM |
56.3 |
12.4 |
4.3 |
216 |
35.2 |
5PM,
Fibrinogen: 201(mg/dl), 3P: 4+, FDP>1280(mcg/dl), D-Dimer:
50.42(mcg/dl)
Final blood culture report: Group G
Streptococcus
(II/II)
Table 2
| Proposed Case Definition of the Streptococcal
Toxic Shock Syndrome |
- Isolation of Streptococcus
A. From a normally sterile site
B. From a
nonsterile site
- Clinically signs of severity
-
Hypotension (systolic
pressure < =
90 mmHg in adults
or in the 5th
percentile for age in children.
and
- Two or more of the
following signs:
- Renal impairment
-
Coagulopathy or disseminated intravascular
coagulation
- Liver dysfunction
(elevated GOT/GPT, bilirubin)
- ARDS
- A generalized
erythematous macular rash, may desquamate
- Soft tissue necrosis
(necrotizing fascitis, myositis,
gangrene) |
An illness fulfilling criteria IA, IIA,
and IIB is defined as a definite case. An illness
fulfilling criteria IB, IIA, and IIB is defined as
probable
case if no other etiology is
identified.
|
Case Discussion
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