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 Presentation of a
Case
This 31-year-old man, a taxi
driver, was admitted because of flu-like symptoms one week
earlier and watery diarrhea, chills, and shortness of breath
in the night prior to admission. Several bouts of watery
diarrhea, chills, and non-projectile vomiting with dark and
bily vomitus developed after eating some barbecue in the
dinner one day before hospitalization. Progressive shortness
of breath and oliguria ensued.
He had been otherwise well in the
past except splenectomy after a traffic accident 3 years earlier.
The post-splenectomy course was otherwise smooth. Pneumococcal
vaccination was not administered when he was followed as an
outpatient. He smoked half a pack of cigarettes per day and
drank 1 bottle of beer every other day for several years. He
also denied recent travel and a history of drug or food
allergy.
At emergency room, his temperature was 38.8℃,
respiratory rate 24 per minute and O2 saturation 90%, heart
rate 140 beat per minute and blood pressure 105/70 mmHg. His
conjunctiva was not pale, sclera was not icteric, and pupils
were isocoric with prompt light reflex. There was no ulcer in
the oral cavity and the neck was supple without
lymphadenopathy or jugular vein engorgement. Chest wall
expansion was symmetric and the breath sounds were clear
without rales or crackles. Heart sounds were regular without
murmurs. The abdomen was soft and mildly distended without
tenderness or rebound tenderness. A median operation scar was
noted. Liver was not palpable. The bowel sound was hypoactive.
His extremities were cyanotic but freely movable without
edema. The laboratory data showed white blood cell count
38,540 /μL, with band form of 21%, and segment 73%, blood urea
nitrogen 21 mg/dL and creatinine 6.0 mg/dL; creatine
phosphokinase (CPK) 5,331 U/L, lactate dehydrogenase 1,733
U/L, aspartate transaminase 149 IU/L. Examination of arterial
blood gas showed pH 7.37, paO2 143 mmHg, pCO2 21 mmHg, HCO3-
12.5 mmol/L, with
a base excess of -9.7 mmol/L. Urinalysis showed
pH 6.0, protein 1+, occult blood 3+ and
WBC 4-5, RBC 5-8, and epithelial
cell 2-3 per high power field in the
sediment. There was no pneumonic infiltrate on chest radiograph.
After hospitalization, ceftriaxone, oxacillin, and metronidazole were initiated. He
was intubated because impending respiratory failure on
the second hospital day. Antibiotics were
switched to ampicillin-sulbactam and ciprofloxacin on the third
hospital day when preliminary blood cultures yielded gram-positive cocci
and fever subsided thereafter. Abdominal sonogram showed probably
parenchymal liver disease without ascites or a
distended gallbladder. Because of no evident infection foci, computed tomography
(CT) of the head was
performed and revealed fluid collection in
the left maxillary and sphenoid sinuses with
mucosal thickening in the left ethmoid sinuses. Rhabdomyolysis with
acute renal failure was diagnosed
and hemodialysis was started because renal function didn't improve
after hydration and alkalization of urine. The
peak value of CPK was 28,635 U/L on
the fifth hospital day which declined rapidly after
initiation of hemodialysis. The frequency of hemodialysis decreased gradually and
no dialysis was further needed on the tenth hospital
day. Therefore, he was discharged on the twenty-seventh
hospital day. There was no more fluid accumulation or mucosal
thickening on Water’s view of skull radiographs just before
discharge. The serum creatinine level declined to 2.3 mg/dL
on discharge and later 1.3 mg/dL while he was followed
on an outpatient basis.
Blood culture showed growth of
penicillin-resistance Streptococcus pneumoniae
(serotype F23) subsequently, which was sensitive to
vancomycin, cefotaxime and levofloxacin.
案例分析
This case report demonstrates that pneumococcal bacteremia
and paranasal sinusitis can be potentially fatal in patients
who had undergone splenectomy and had not received pneumococcal vaccination
or appropriate antibiotic therapy.
Although only about 0.5 percent of
sinusitis was complicated with clinically evident acute
bacterial sinusitis, S. pneumoniae is the most common
pathogen in adults. Splenectomy may put patients at risk for
overwhelming infections especially by encapsulated organisms,
such as S. pneumoniae, in about sixty to seventy
percent of cases. About 2.5 percent of the splenectomized
patients died later from fulminant bacterial infections
because of deficient clearance of bacteria, resulting from
reduced phagocytosis, decreased IgM production, disturbances
of the complement system, and lack of tuftsin. Advisory
Committee on Immunization Practices (ACIP) recommends that
pneumococcal vaccination should be administered at least 2
weeks before elective splenectomy or as soon as this condition
is identified, repeated every three to five years, depending
on age and medical condition. Amoxicillin-clavulanic acid,
trimethoprim-sulfamethoxazole, or cefuroxime axetil
prophylaxis should be taken at the first sign of infection.
This patient had neither vaccination early after splenectomy
nor antibiotic prophylaxis at the first sign of minor illness.
This was probable the reason why our patient developed such a
fulminant course.
The treatment of invasive
pneumococcal infections in Taiwan and worldwide as well is
complicated by the emergence of pneumococci with intermediate
or high resistance to penicillins. Such isolates are often
resistant to macrolides (azithromycin, clarithromycin, or
erythromycin), and trimethoprim-sulfamethoxazole as well. In
the treatment of pneumonia with or without bacteremia due to
non-susceptible S. pneumoniae, penicillins at higher
doses (such as 24 MU/day) may be sufficient. Other
alternatives are third-generation cephalosporins, newer
fluoroquinolones with good activity against pneumocci and
vancomycin. In patients with meningitis or other infection
involving the central nervous system (CNS) due to S.
pneumoniae intermediately resistant to penicillins,
third-generation cephalosporins with or without vancomycin are
needed. In patients with CNS infection due to S.
pneumoniae highly resistant to penicillins,
third-generation cephalosporins plus vancomycin are needed,
although appropriate antibacterial therapy remains to be
investigated by carefully designed clinical studies.
The exact mechanism of
rhabdomyolysis associated with invasive pneumococcal
infections is unclear. A number of other bacterial infections
have occasionally been reported in association with
rhabdomyolysis, although their role is not clear. Animal
studies have shown that streptolysin S and extracellular
products of streptococci are toxic to the skeletal muscle, but
a direct role of pneumococci in the causation of
rhabdomyolysis has not been demonstrated. There is evidence
that skeletal muscle metabolism is altered in the presence of
pneumococcal infections in rat. Therefore, it is possible that
products of the pneumococci and disruptions of the energy
production pathways in skeletal muscle may be important in the
development of muscle injury.
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Case Discussion
繼續教育考題