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Clinical Practice

Living with Lyme Disease

By Mary VanOyen Force, R.N. (Reprinted from MEDSURG NURSING: The Journal of Adult Health
Official Journal of the Academy of Medical-Surgical Nurses - A Jannetti Publications Inc. Journal Volume 8 Number 3 - June 1999 pp 184-190)

The occurrence of Lyme disease is rising steadily in the United States. The majority of health care providers are unfamiliar with this complex syndrome. Nurses lack accurate clinical information to provide comprehensive nursing care to these patients. The progression of Lyme disease is addressed through three stages. Untreated or poorly managed, Lyme disease may become a chronic, debilitating illness. The author's personal story is interwoven and serves to highlight the patho-physiology of the disease and the emotional and physical costs to the patient.

(Mary VanOyen Force, BSN, RN, is Clinical Supervisor, Medical/Surgical Department, University Hospitals of Cleveland, Cleveland, OH.)

In 1996, the Centers for Disease Control and Prevention (CDC) reported a record high number of 16,461 cases of Lyme disease (LD) in 45 states�an increase of 41% from the 11,700 cases reported in 1995 (CDC, 1996). Lyme disease is becoming more prevalent in communities, yet many nurse practitioners and physicians are unfamiliar with the syndrome.

Personal Case Study

On a Saturday night in February 1995, I reported to an urgent care facility with complaints of severe jaw pain, left-sided Bell's palsy, occipital headaches, fatigue, low-grade fever of 99.4 F, and spontaneous bruising around my left eye. The triage nurse assessed my presentation and began to question my relationship with my spouse. "Has your husband ever struck you before? How did you get the black eye? Why did you come here alone? Do you have any other bruises?"

The physician ordered a full skull series to rule out present and past fractures. I kept insisting that I was not a battered wife and that I was ill, but the staff continued to look for bruising and question my social history. Finally the staff listened to the fact that I had completed a dental preparation for a crown molar 5 days prior; and suspected that was the culprit. The physician gave me a prescription for amoxicillin and Tylenol with Codeine�, and told me to see my physician.

I saw my physician on the following Monday, and that was the beginning of a long list of appointments. The antibiotics "cured" the symptoms, but I relapsed within 5 to 7 days after completing the course. My doctor continued to say my clinical presentation was not typical of a regular infection of the jaw. Bell's palsy does not usually resolve with antibiotic therapy. He ordered an MRI to rule out a brain lesion.

I was sent to consult a cranial nerve specialist, where more tests were done to evaluate for brain tumors - all negative. My symptoms worsened every time I stopped antibiotics. The jaw pain increased, and I could not tolerate chewing solid food. I lost 10 pounds, and my family questioned me about anorexia nervosa. I slept 18 hours a day, my neck felt stiff and the occipital headaches were so severe that I dreaded holding up my head. A lumbar puncture was performed to evaluate neurologic involvement with further negative results. I was unable to care for my three young children and had to stop working as an ICU nurse.

In late March, after another relapse upon stopping antibiotics, my doctor said, "Lyme disease can cause Bell's palsy...maybe you have Lyme disease?" I laughed and said, "How could I get a tick bite in the dead of winter?" We discussed the possibility of a 'bulls-eye" rash, but I did not recall a skin rash. Although my physician admitted he knew very little about Lyme disease, we sent blood for a Lyme ELISA - an immune response study. The ELISA indicated that I had probably been exposed to Lyme disease.

Epidemiology

Lyme disease is a relatively new infection in the United States. In 1975, an unusual clustering of children with juvenile arthritis was reported in Old Lyme, Connecticut. It was determined that the illness was caused by the bite of a tick. In 1982, Dr. Willy Burgdorfer discovered that the infectious agent in the tick was a bacterial spirochete, now called Borrelia burgdorferi (Bb). The illness was recognized in Europe as early as 1909, but given different names. The entire disease syndrome is now referred to as Lyme Borreliosis or Lyme disease (Fallon et al., 1992).

Statistics report that 1:100,000 persons will be infected with Lyme disease nationally. Approximately 90% of the cases have been reported from Connecticut, New Jersey, New York, Pennsylvania, and Rhode Island. Population groups most at risk for LD are children 5 to 16 years old and adults 35 to 50 years old. There is a 1:1 male-female ratio. Risk factors include hobbies (hunting, bird watching, taxidermy, gardening, etc.), summer camps, scouting weekends, and other outdoor activities. A seasonal trend is typical, with the onset of the illness generally seen between April and November. LD may incubate for months before symptoms become obvious.

Bb lives in the midgut of the Ixodes scapularis and Ixodes dammini (black-legged or deer tick) and is found in the eastern, midwestern, and southern parts of the United States. This spirochete is also found in another unrelated tick, Amblyomma americanum, or Lone Star tick in the southeastern United States. These are not the ticks commonly seen on pets; dog ticks, Dermacentor variabilis, do not transmit LD. Ticks cannot fly or jump; they can only crawl in search of their next blood meal. Transmission of the disease occurs after 12 to 24 hours of feeding on the skin. Bb migrates out-ward in the skin and is spread into the lymph, blood, and tissues. The incubation period from the time of exposure to onset of symptoms ranges from 3 to 30 days. There is no natural transmission from person to person. There is no natural immunity once exposed to LD and re-infection with further exposure is possible (Ostfeld, 1997).

Pathogenic spirochetes are a unique group of bacteria. Spirochetes are motile, gram-negative, corkscrew shaped organisms. They have an affinity for collagen and connective tissues. The interplay between the invading spirochetes and the subsequent host immune response plays an important part in the disease process. Borrelila burgdorferi do not destroy tissue directly. They nonspecifically activate monocytes, macrophages, synovial lining cells, B cells, and complement. This results in an elaborate protective host response which, paradoxically, leads to arthritis and neuropathies (Pavia, 1994).

My tick bite probably occurred in Michigan where we spend weekends at our family's cottage by a lake, surrounded by wood's. Deer and small animals roam freely across the property and we have never used environmental tick control measures.

Clinical Manifestations

As with other spirochetal infections, such as syphilis, LD causes stage-related disease. LD is characterized by remissions and exacerbations, and may manifest different symptoms at each stage. Lyme disease is classified into three stages:

Clinical studies now show that the disease progresses without respect to a time frame of weeks or months, but is particular to the individual patient's response. The disease may begin in any system and disseminate quickly throughout the body within 1 week. In other cases, individuals may experience vague flu-like symptoms for months before seeking treatment for subjective numbness and tingling of an extremity. The spectrum of disease ranges from migratory painful joints without swelling to erosion of cartilage and permanent joint disability.

Early Infection

A rash may develop from the entry of spirochetes in the skin. The hallmark sign of LD is the "bulls-eye rash" or erythema migrans (EM) which may develop with each tick bite. This rash may appear 4 days to several weeks after a tick bite and presents as an expanding circular lesion. It may have a necrotic center, but is usually painless. A characteristic EM has alternating red and pale concentric rings forming on the skin. A wide variety of sizes and appearances of skin inflammation from LD has been documented. It is important to remember that fewer than 50% of all LD patients will develop a rash (Burrascano, 1997). A patient may present with an atypical skin rash and any skin lesion should be documented, including a picture for the chart. EM generally resolves spontaneously, with or without treatment, after 2 days to several weeks. Obtaining a specimen, prepared from the reddened outer edge of the EM, may grow Bb in culture. The recovery rate of spirochetes in culture or slide preparation from an EM is very low.

Early symptoms of LD are low-grade fever (99-100 degrees F), chills, muscle and joint soreness, headaches, stiff neck, and fatigue. Symptoms may fluctuate in severity, be intermittent, and change from neurologic to musculoskeltal all within a week. This is very confusing to the patient, who may be embarrassed to admit that the symptoms change day to day.

Early Diagnosis

There is a window of opportunity in treatment to stop the progression from early LD to disseminated and chronic infection. The "wait and see" approach can be very detrimental to the patient's prognosis. Early confirmation of a diagnosis of LD and an effective antibiotic protocol is essential to prevent persistent infection. The key to recognizing early LD is clinical presentation and patient history. A complete review of tick exposure risk factors will provide information on a possible unnoticed tick attachment. The decision to treat a tick bite or early viral symptoms of a high-risk tick exposure/tick bite patient with 4 to 6 weeks of amoxicillin (or doxycycline) orally could prevent that patient from progressing to a stage of chronic disease.

Disseminated Disease:

Clinical Manifestations

I did not experience an early stage of LD. It was as if I woke up one day with disseminated LD. Weeks after my initial course of antibiotics, I began to have recent memory loss, such as listening to the answering machine and then being unable to recall what I had just heard. One afternoon, I drove six children to the local roller-skating rink and I became disoriented. The street signs and buildings were totally unfamiliar to me. I had no sense of direction. (I know how Dorothy felt when she woke up in Oz). My 11-year-old daughter noticed that the drive was taking too long, and asked me where we were going. Embarrassed and frightened, I quietly asked her to help me find a familiar landmark We drove for 45 minutes, and I did not recognize a single street or building. My daughter said, 'Mom, both sides of your smile are drooping now!" Fortunately, my daughter recognized a building behind the rink, and I took the children in to skate. I called my physician and told him that the Bell's palsy had extended bilaterally and I was experiencing memory loss and disorientation.

I was referred to a neurologist. We discussed the subtle mental problems that were an embarrassment to me. My inability to concentrate made it difficult to read, and I was unable to retain what I had just read. The most frustrating symptom was the extreme fatigue: I slept all day. I was moody tearful, irritable, and depressed. I became hypersensitive to light. Ironically I was thankful for the physical manifestation of Bell's palsy; it confirmed that my illness was physical and not psychological

A rheumatologist became my primary physician. He ordered home IV therapy with ceftriaxone 2 gm every day for 6 weeks. The home health care nurse placed a midline catheter in my left basilic vein. I infused the antibiotic myself, but nurses visited once a week for dressing changes to the insertion site and physical assessments.

Neurologic Manifestations

Neurologic abnormalities of disseminated LD include motor and sensory neuropathies, headaches (frontal or occipital), stiff neck, profound fatigue, photophobia, and mild-to-severe encephalopathy. The encephalopathy can cause subtle changes in mood, memory; sleep patterns, and concentration. Patients may complain of word-finding difficulties, inability to perform calculations, or short-term memory problems. Behavioral changes, especially in children, and emotional irritability may also occur.

Bell's palsy (nerve VII) Is the most common cranial neuropathy and accounts for 70% to 80% of all cranial nerve palsies that develop, and 10% of all Lyme patients will develop this symptom. The weakness usually is acute and may extend to both sides of the face within days to weeks. The degree of facial paralysis varies with the individual. Other cranial neuropathies occur, including the optic nerve (II), which results in optic disc edema and inflammation along the meninges of the optic nerve. Patients may complain of a blind spot and loss of vision. Involvement of III, IV, and VI, the nerves controlling the intraocular muscles, may also occur, leading to an acute onset of double vision, which may last for hours or days. Trigeminal neuralgia (V) involvement is seen and causes facial numbness, weakness, and pain (Fallon & Nields, 1994; Reik, 1991).

Laboratory and imaging tests may not disclose any objective neurologic involvement. EEGs and other laboratory studies are frequently normal. Spinal fluid analysis may reveal a pleocytosis (elevated WBC count) and/or elevated IgG or IgM for Bb. In patients with severe neurologic involvement, MRI irregularities may resemble those seen with multiple sclerosis.

After10 days, the IV therapy was successful in completely resolving the Bell's palsy and trigeminal neuralgia. The other symptoms resolved more slowly. After completing the ceftriaxone, I started doxycycline 100 mg TID orally.

Ten months after the initial diagnosis of LD, I developed costochondritis. The cartilage at the costochondral junctions enlarged to form bony nodules on my chest wall. The pain progressed from mild to severe with movement, deep breathing, and coughing. My doctor was not confident that this was a manifestation of LD. We treated it as an inflammatory process. We could not find any medical documentation of LD causing inflammation of the rib cage. A serum Lyme polymerase chain reaction test and bone scan were negative. In desperation, I wrote a physician in New York who is considered a national authority on LD. I requested a consult with my rheumatologist on the possibility that LD can cause costochondritis. He called my physician, and that was the beginning of the next 12 weeks of intravenous antibiotics.

From September to December 1996, I infused cefotaxime into a midline catheter every 8 hours. Three days after starting IV therapy I experienced a Jarish-Herxheimer (JH) reaction consisting of the return of previous symptoms. The Bell's palsy, trigeminal neuralgia, headaches, stiff neck, and profound fatigue remained for 3 weeks. It took 10 weeks before all the symptoms resolved. After the IV course, I started Ceftin� orally to continue the treatment protocol.

Musculoskeletal Considerations

The JH reaction occurs when treating any spirochetal infection. As the spirochete is destroyed, a toxin is given off that either directly or indirectly stimulates the immune system. Symptoms can include a low-grade fever, headache, chills, arthralgia, and a worsening or return of other LD symptoms (McEvoy et al., 1996). Patients should be cautioned about this reaction. It does not indicate a failure of the treatment, but rather is an indicator of a correct diagnosis of LD.

About 60% of all LD patients develop joint involvement within 2 to 24 weeks after the tick bite. Upon examination, you may not find typical swelling of arthritis. These painful attacks may last weeks to years before developing swelling and chronic synovitis. Because the Bb spirochete has an affinity for connective tissues and collagen, involvement can occur in any joint. Attacks of arthritis may last from a few weeks to months and be followed by periods of remission. The most common joint involved is the knee. Bb is a potent stimulator of the inflammatory response. The attacks may continue to be intermittent and migratory, or may develop to a chronic inflammatory process with permanent degeneration of cartilage and bone (Malawista, 1997).

The following April 1997, 1 began experiencing chest pain and dizziness for brief periods of time. During these few minutes, my pulse rate would be 40 to 50 beats per minute. It would always spontaneously resolve. Over the next 3 weeks, the episodes increased in duration and became more frequent. While at a baseball game, I had a prolonged episode of bradycardia. I became symptomatic with chest pain, dizziness, nausea, and lightheadedness. It was 11:00 PM and we were 10 minutes from the hospital. I called the nurses with whom I work and asked if I could come in for an ECG to document this bradyarrhythmia.

Upon arrival to the ICU, my pulse was 48 beats per minute and I was hypotensive. I was having chest pain, pale, and so diaphoretic that the ECG leads would not adhere to my skin. The ECG showed a first-degree atrioventricular block. I paged my attending physician from the ICU I don't think he has ever received a call like that before: nurses helping a nurse cope with a difficult situation. After 2 years of working through LD together my doctor and I have a trusting relationship which allows us to speak frankly. We discussed options to get through this episode. As we talked, the chest pain began to fade and the other symptoms resolved. I went home. I had several more episodes of symptomatic bradycardia, which led to changing the oral antibiotic to Bicillin� IM injections twice weekly. Within 10 days, the cardiac manifestations completely resolved. I maintained the injections for the next 6 months.

Cardiac Manifestations

Patients may not notice any symptoms for weeks or months after a tick bite. Untreated, the spirochetal infection can become disseminated and affect the heart. LD may cause inflammation along the AV nodal conduction pathways leading to sinus bradycardia or junctional bradycardia. Approximately 8% of LD patients demonstrate cardiac involvement.

The most common abnormality is a fluctuating atrioventricular block. First-degree, second-degree (Wenckebach and Mobitz II), and third-degree (complete) block have been documented with LD. The cardiac involvement may be brief, lasting only a few days, and resolve spontaneously. Occasionally, patients will become symptomatic with the episodes of bradycardia and complain of chest pain, dizziness, headaches, nausea, diaphoresis, and anxiety. Blood pressure and cardiac output are decreased. Patients may also develop more diffuse involvement such as myopericarditis and cardiomegaly.

Severe cardiac manifestations may require inserting a pacemaker to provide immediate stabilization. Pharmacologic therapy is usually reserved for acute situations. Atropine and isoproterenol are useful in increasing the heart rate and decreasing symptoms in AV block. LD-induced bradyarrhythmias respond to intravenous antibiotic infusions. Endomyocardial biopsies have documented spirochetal infections in the myocardium. During this time of discovery and correction of the cause of the cardiac involvement, it is important to provide patients with reassurance and comfort (Josephson, Marchlinski, & Buxton, 1991).

Chronic Infection

The existence of chronic persistent infection in patients with seemingly adequate antibiotics continues to mystify LD experts. Many patients experience repeated relapses despite very aggressive antibiotic regimes. Immune mediated mechanism of injury to tissues and joints may complicate persistent active infection. Clinical studies show a higher incidence of chronic infection in patients with a longer duration of clinical symptoms before initiating effective treatment (Burrascano, 1997). This theory suggests that aggressive antibiotic therapy during early Lyme manifestations may prevent chronic infection.

Nursing Care of Patients with Lyme Disease

Lyme disease is a very difficult disorder to diagnose. Currently, there is no test to confirm LD or that the patient is cured after treatment. Some LD patients will never have a positive Lyme study. Lyme disease is a clinical diagnosis, based on a thorough history and evaluation of risk for tick exposure and tick bites. Together with the clinical picture, history and laboratory data, nurses can help patients toward a diagnosis. Patients require a great deal of support, careful listening, and reassurance through this phase.

After a probable diagnosis of LD, patients must be monitored closely for signs that the antibiotic regimen is or is not effective. The presentation of LD is quite varied and treatment must be individualized. Nurses must document new symptoms and follow the changing clinical presentation. If the patient is not responding, the treatment and diagnosis should be reassessed. After starting antibiotics, patients must be prepared for a JH reaction. Patients should be encouraged to continue the antibiotic therapy as planned, even though the pain, fever, and symptoms appear to be worsening. The JH reaction may begin approximately 3 days after starting antibiotics and last 2 to 3 weeks.

Patients with LD require comprehensive education about both the disease itself and the treatment (see Tables 1-5). Teach patients about super infections, and methods to avoid this complication of prolonged antimicrobial therapy. Patients will require education on proper nutrition to promote healing. Patients may need counseling on changes in lifestyle to promote their general health, such as avoiding alcohol, nicotine, and stress. Encourage patients to advance their activity levels as they regain their strength. Help them incorporate a healthy pattern of sleep, exercise, and proper diet into their life. Encourage them to find support groups to share their feelings and concerns.

Identify the patient's individual problems and evaluate coping strategies and priorities. Recommend appropriate consults with physical therapy, pain management, and relaxation therapy. Patients with cognitive impairments may need to learn ways to adapt to overcome mental deficits; such as writing reminder notes, allowing more time for learning by using visual aides and recordings, and taking naps in the afternoon to improve concentration later. Frequently evaluate the care plan and institute changes as indicated by changing symptoms.

People at high risk in endemic areas, should consider Lymerix�, the Lyme disease vaccine now available from SmithKline Beacham PLC. This vaccine is offered in a series of two injections given 1 month apart followed by a third injection 1 year later. Controlled studies found that Lymerix was 80% effective in preventing LD in people ages 15 to 70 who had completed the series of three injections. The cost for the series is $210 plus physician fees (Crake, 1999). The vaccine stimulates the production of antibodies against Borrelia burgdorferi. When a tick attaches and begins to feed, it ingests these antibodies which neutralizes the bacteria in the midgut of the tick, before it can enter the victim (Chase, 1998).

Lymerix is not a substitute for strict adherence to preventative tick control measures and self-inspection and proper removal of attached ticks. Educate your patients that this vaccine is not 100% effective. It must be combined with environmental and personal tick precautions. Lymerix is not approved for pregnant women or children under the age of 15.


Summary

Presently, I am in remission and have discontinued antibiotic treatment for the past 5 months. Mild symptoms remind me that I still harbor a persistent Bb infection. I have resumed all my previous activities, but I require more sleep. Living with chronic Lyme disease has taught me the importance of having consistent, compassionate, supportive clinicians through all phases of illness.

Many questions remain. Does chronic infection require chronic treatment? Are the risks of prolonged antibiotic therapy worth the prophylactic treatment of chronic LD? How is it possible for a bacterial pathogen to hide within a body and cause debilitating damage for decades? LD research continues to seek answers on this unusual disorder. Presently, there is no cure for chronic Lyme disease, but comprehensive nursing care can do much to help patients face the challenges of this puzzling disease.


Table 1.
Personal Protection Against Tick Bites



Table 4.
    Indirect Serology: Testing for the Antibody-Antigen Reaction

Indirect Fluorescent Antibody (IFA)
Within the laboratory, whole cells of the specific bacteria are fixed to a glass slide. Dilutions of the patient's sera are added. Staining detects the patients who have formed antibodies to the bacteria. Limitations of the method are the subjective interpretation of the technician and the lack of specificity to the Bb antibody-antigen complexes.

Enzyme-Linked Immunosorbent Assay (ELISA)
The ELISA has been the backbone of laboratory tests for Lyme disease. It provides the quantitative determination of lgG and IgM antibodies directed against the Bb bacteria. It is recommended 4 weeks after tick-bite exposure. The presence of antibodies indicates exposure, not disease. Results are posted as separate IgG and IgM titers. The normal progression of the immune response is reflected in the ELISA.

  • IgM begins to increase 2 weeks after exposure and peaks at 4 to 6 weeks. IgM is the "primary response" after the first exposure to an antigen. It gradually tapers to low levels after 24 to 36 weeks. lgM has a half-life of 5 days. A continual detection of IgM reflects the persistence of antigen. The response may be aborted or inhibited by antibiotic treatment.
  • IgG (secondary response) begins to increase 4 to 6 weeks after exposure and peaks 12 to 18 weeks and remains elevated.
    Results are expressed as "negative," " equivocal" or possible exposure and "reactive" or a positive response. Limitations of ELISA are the cross reactivity with similar proteins. It is technically demanding and time consuming (requires 4 hours), and the sensitivity and specificity varies with different labs. Variations of results from the same specimen occurs frequently when sent to different laboratories.



    • Table 5.
    Direct Serology - Antigen Detection
    Source: Tilton, R.C. (1994)

    Direct detection of a micro-organism is a more reliant indicator than observation of the immune response. Traditional culture methods have proven unreliable due to the small numbers of organisms present and the ability of Bb to hide deep in tissues.

    Polymerase Chain Reaction (PCR)
    PCR is the molecular amplification/duplication of DNA. Ideally, the final steps of PCR allow the production of millions of copies of a DNA sequence, then the subsequent identification of the bacteria by Western immunoblot. Potential body fluid specimens are serum, plasma, CSF, synovial fluid, and urine.

    Laboratory studies show that the best time to recover antigen is 3 to 6 days after the initial start of antibiotic and when the patient is febrile. At this time, the patient should be shedding dead spirochetes and a specimen should have the highest yield for detection. But in Lyme disease, unlike other diseases, organisms are sparse and difficult to isolate. A negative result only implies that the specimen was negative for recovery of partial Bb DNA. Limitations of this test are the high costs ($150 to $330 per specimen), DNA contamination, and lack of specificity and sensitivity toward Bb antigen-antibody complexes. Laboratory controls vary greatly between labs, and caution should be used in choosing a laboratory for a PCR study.

    Culture of Borrelia Burgdorferi (Bb)
    Obtaining a culture of Bb from a skin lesion is definite evidence of disease. Preparing a nonsterile specimen from the inflamed edge of an erythema migrans lesion requires the addition of rifampin or kanamycin to the medium. Bb will grow in a stationary culture but the recovery rate is low (6% to 45%) Limitations are the low number of organisms present in the skin and the difficulty in stimulating growth of Bb.

    Lyme Urine Antigen Test (LUAT)
    This test requires antigen to be captured by unique antibodies which have reactivity only to specific proteins of Bb The affinity of the antibody allows for detecting very low levels of antigen. Clinical data shows that antigen is not shed daily, so multiple samples must be sent over several days to increase reactivity. Samples taken during the acute symptoms and 3 to 6 days after the onset of antibiotic therapy and during the Jarish Herxheimer reaction increase chances of antigen detection. Limitations of this test are the low numbers of organisms present and the lack of sensitivity and specificity to Bb.



    Treatment Categories
    Source: Burrascano, 1997

    There is no gold standard of treatment for LD Each patient's regime should be individualized to treat the particular clinical manifestations and history. Optimal duration of treatment and dosages have not been published in clinical studies These regimes are provided as general guidelines for treatment.

    Tick bites: Patient recalls an embedded tick Before deciding to treat, you need to explore the circumstances of the tick bite. How long was the tick attached? Was the tick engorged with blood? Was the tick removed properly? What did the tick look like'? Was it a Ixodes tick? Did the tick bite occur in an. endemic area?

    Chronic or Late Disseminated: Severely ill patients with clinical manifestations involving one or more body system.
    Note: A complication from prolonged, high dose IV therapy 12g/d) of ceftriaxone is the formation of biliary pseudolithiasis. This drug complexes with calcium in bile salts to form precipitates which resemble sludge and gallstones upon sonography. When ceftriaxone is stopped, these stones resolve spontaneously within weeks to months. Patients may present with severe upper quadrant pain, nausea, and vomiting (Kirejczyk, 1992). Conservative observation, pulsing the drug with intermittent 24 hour breaks, or changing the drug to cefotaxime may prevent needless surgical intervention.
    (References available on request.)



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