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Case
Report -
A 67-Year-Old Man with Fever, Chills and Shoulder Pain
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Michael
Li, MD, MBA
A 67-year-old man, with a
history of rotator cuff tendonitis, status post physical
therapy in the recent past, presented to the emergency room
with complaints of sudden onset of chills and worsening
left shoulder pain for three days.
In the emergency room (ER), his temperature was 101.3°
F, white blood cell count was 9600/mm3, and chest
x-ray was normal. He was discharged home on acetaminophen
and advised to come back if the fever persisted.
He returned to the emergency room a few days later
because of persistent fevers (102.9° F at home) and
shoulder pain. His
shoulder pain was described as 10/10, sharp, intermittent,
exacerbated by motion, with radiation to the left arm, left
lateral chest wall, and left scapula.
He denied recent exertion or injury to his left shoulder
and stated that his shoulder pain from rotator cuff tendonitis
had significantly improved after he received physical therapy. His wife also mentioned that she had noticed
a rash on his left shoulder in the past 48 hours. The patient, however, did not recall any recent tick bites.
Review of systems was significant for fever,
chills, generalized malaise, intermittent mild headache,
and left shoulder pain as described above.
He denied dizziness, shortness of breath or cough,
chest pain, nausea, vomiting, diarrhea, or burning on urination.
Past medical history was significant for
left rotator cuff tendonitis status post physical therapy, hyperlipidemia, benign prostate hypertrophy,
kidney infection, and meningitis over 30 years ago. His only medications were fish oil and some herbal supplements.
The patient works in construction and lives
in a wooded area. He
does not smoke cigarettes,
drinks alcohol socially, and denies other substance
use. Family history is positive only for heart problems
on his maternal side.
On physical examination, his temperature
was 100.1° F, pulse 74, blood pressure 123/70,
respiratory rate 16, and oxygen saturation 95% on room air.
The remainder of his exam was unremarkable except for local
findings around his left shoulder: 1. Guarding of his left
shoulder – movement of his left arm produced pain, however,
there was no effusion, swelling or crepitus in or around
the left shoulder joint; 2. a 7x11 cm uniformly erythematous,
non-tender macule on the posterior-lateral aspect of his
left shoulder. Neurologically,
there was no sensory/motor deficits noted and deep tendon
reflexes were intact throughout.
Initial laboratory studies showed a normal
white count (7400/mm3), and mildly elevated liver
function tests (LFTs) (Alkaline Phosphatase 233, AST 152,
ALT 137). Erythrocyte
sedimentation rate (ESR) was 11. The electrocardiogram (ECG) showed normal sinus rhythm at 78 BPM
and left bundle branch block unchanged from previous ECG. Chest x-ray (CXR) again did not reveal any
acute intrathoracic disease.
HOSPITAL COURSE
Given the acute onset of fever and chills,
rash, concurrent worsening shoulder pain, and elevated LFTs,
the initial differential diagnoses considered included Lyme
disease, soft tissue infection (cellulitis versus necrotizing
fascitis versus myositis), viral infection (varicella zoster),
worsening tendonitis and septic arthritis. The latter three were deemed less likely based
on the physical exam findings.
The patient was treated with ampicillin/sulbactam,
which covered for both Streptococcal/Staphylococcal (soft
tissue infection) as well as Borrelia burgdorferi. Lyme Enzyme Linked Immunosorbent Assay (ELISA)
screen and hepatitis panel were also sent to confirm Lyme
disease and to rule out infectious hepatitis. In the ensuing
days, the patient became afebrile and his shoulder pain
significantly decreased. In addition, the rash ceased to expand, the
shoulder x-ray obtained was normal, and blood cultures were
negative. Infectious hepatitis was ruled out by serology,
and Lyme ELISA screen was negative.
The patient was discharged home three days after
admission on amoxicillin/clavulanate to finish a three week
treatment for presumptive Lyme disease.
A few days after discharge, the patient again
presented to the ER complaining of fever and left shoulder
pain which migrated around his chest, abdomen and back.
Neurological exam revealed weak left triceps, absent
left triceps reflex, and weak left pectoral muscles.
Cervical MRI was obtained which did not show any
spinal cord disease. The
Neurology consult team suspected myeloradiculitis and involvement
of the brachial plexus, likely due to B.
burgdorferi. A lumbar puncture was recommended and cerebrospinal
fluid (CSF) studies revealed an elevated protein level and
normal glucose level and cell counts.
CSF specimen was also sent for multiple virus PCR
testing and serologic testing for B. burgdorferi.
The Infectious Disease consult team deemed the elevated
protein in the CSF as evidence of CNS involvement and recommended
initiation of treatment with ceftriaxone.
In the next few days, the patient remained afebrile
and pain free. He was discharged home a week after intravenous
antibiotics to finish a total of a four-week-course treatment
with ceftriaxone per the PICC line.
Western blot of the patient's CSF specimen eventually
returned positive for IgM reactivity to B.
burgdorferi.
DISCUSSION
This was an interesting case about Lyme disease
because of its unusual presentation and somewhat complicated
course. There was
certainly some convincing evidence to support the diagnosis
of Lyme disease in this case: the erythema migrans (EM)
like rash, viral like syndrome, possible exposure to ticks,
and even hepatitis, were all consistent with Lyme disease. However, the lack of history of a tick bite,
negative Lyme ELISA screen, unusual early neurologic findings,
as well as initial failed treatment with amoxicillin/clavulanate
all challenged the diagnosis until final confirmation by
serologic tests of the CSF were obtained.
Some of the major learning points of this case are
as follows:
A.
HISTORY OF TICK BITE
Lyme disease is a multisystem inflammatory
disease caused by Borrelia
burgdorferi, which are spread by the bite of infected
Ixodes ticks.
However, only about 30 percent of patients with confirmed
Lyme disease recall the tick bite1. Therefore, lack of history of tick bites certainly
does not rule out Lyme disease.
B.
NEGATIVE LYME ELISA SCREEN
There are two caveats in using this most
commonly applied initial test to confirm the diagnosis of
Lyme disease2: lack of sensitivity in early disease
and false positives. In Lyme disease, antibodies may not be detectable
for up to six to eight weeks.
IgM typically appears two to four weeks after EM;
IgG appears after six to eight weeks.
Therefore, it is not uncommon to have a negative
Lyme ELISA screen initially among later confirmed Lyme cases.
In addition, some patients with other Borrelial diseases
(relapsing fever), spirochetal diseases (syphilis), viral
illnesses, and autoimmune diseases can generate cross-reacting
antibodies to B. burgdorferi,
which would produce a false positive test with ELISA. Therefore, a positive ELISA should be confirmed
by Western blot analysis.
C.
UNUSUAL EARLY NEUROLOGIC FINDINGS
The clinical manifestations of Lyme disease
can generally be divided into three phases1:
early localized, early disseminated, and late or chronic
disease. Early localized disease includes erythema migrans
and viral like syndrome and usually occurs less than one
month after the tick bite.
Early disseminated disease occurs weeks to months
after the tick bite, but can occur days after B. burgdorferi infection, with or without
preceding EM. Neurologic
features occur in about 10 percent of untreated patients
during this phase and can include lymphocytic meningitis,
cranial nerve palsies, and radiculoneuritis.
Late disease occurs months to years after the onset
of infection and is characterized by musculoskeletal complaints,
such as arthralgias and arthritis. What made the current case unusual was the
very early and severe neurologic involvement - only days
after the EM appeared, which was consistent with early disseminated
disease.
D.
FAILED INITIAL TREATMENT
Finally, while early localized Lyme disease
can be treated with doxycycline or amoxicillin in an outpatient
setting, disseminated and late Lyme disease require intravenous
antibiotics that have excellent central nervous system barrier
penetrating properties, such as ceftriaxone and penicillin3.
In this case, it was clear that oral agents were
not effective in treating the central nervous system involvement
by B. burgdorferi, and that in fact, ceftriaxone was the best antibiotic
for the treatment of this patient.
REFERENCES
- Sigal
LH. Epidemiology and clinical manifestations
of Lyme disease. UpToDate Online v11.2 2003.
- Sigal
LH. Laboratory confirmation of the diagnosis
of Lyme disease. UpToDate Online v11.2 2003.
- Sigal
LH. Treatment of Lyme disease. UpToDate
Online v11.2 2003.
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