Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2664_Библиотеки_им_академика_М_И_Перельмана
.pdf
USMLE Step 2 CK
l Internal Medicine
Diagnosis. Clinical appearance. Differentiation must be made between flat warts and condylomata lata of secondary syphilis.
Treatment
• Destruction (curettage, sclerotherapy, trichloroacetic acid)
• Cryotherapy
• Podophyllin
• Imiquimod (an immune stimulant)
• Laser removal
URINARY TRACT INFECTIONS
Cystitis
A 32-year-old woman is in your office because of dysuria. For the last several days,
she has burning on urination with increased frequency and urgency to urinate.
Definition. Infection of the urinary bladder.
Epidemiology
• Very common; 6 million office visits per year in the United States
• Majority in women
Etiology
• Roughly the same as for pyelonephritis
• Any cause of urinary stasis or any foreign body predisposes
• Tumors/stones/strictures/prostatic hypertrophy/neurogenic bladder
• Sexual intercourse in women (“honeymoon cystitis”)
• Catheters are a major cause, and the risk is directly related to the length of catheterization (3–5% per day).
• Microbiology: E. coli in >80%; second are other coliforms (Gram-negative bacilli)
such as Proteus, Klebsiella, Enterobacter, etc.; enterococci occasionally, and Staph. sapro-
phyticus in young women.
Presentation
• Dysuria, frequency, urgency, and suprapubic pain are common.
• Hematuria, low-grade fever; foul-smelling and cloudy urine are less common.
• On exam, suprapubic tenderness but no flank tenderness.
Diagnosis
• Best initial test is the urinalysis looking for WBCs, RBCs, protein, and bacteria; WBCs
is the most important.
• Nitrites are indicative of Gram-negative infection.
• A count of <5 WBCs is normal.
240
• Urine culture with >100,000 colonies of bacteria per mL of urine confirmatory but
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
not always necessary with characteristic symptoms and a positive urinalysis.
Treatment
• For uncomplicated cystitis, 3 days of trimethoprim/sulfamethoxazole, nitrofurantoin,
or any quinolone is adequate.
• Seven days of therapy for cystitis in diabetes
• Quinolones should not be used in pregnancy.
• Fosfomycin is a single-dose oral therapy for cystitis only
Acute Bacterial Pyelonephritis
Definition. An acute patchy, most often unilateral, pyogenic infection of the kidney.
Etiology
• Infection usually occurs by ascension after entering the urethral meatus.
• Predisposing factors: obstruction due to strictures, tumors, calculi, prostatic hypertrophy, or neurogenic bladder, vesicoureteral reflux
• More common in women, in childhood, during pregnancy, or after urethral catheterization or instrumentation
• E. coli is the most common pathogen; others include: Klebsiella, Proteus, and
Enterococcus. Patients who are immunosuppressed and subjected to indwelling cath-
eters are more prone to Candida.
Chapter 7
l Infectious Diseases
Pathology. Polymorphonuclear neutrophils, leukocytes (in interstitial tissue and lumina of
tubules).
Clinical Findings. Chills, fever, flank pain, nausea, vomiting, costovertebral angle tenderness,
increased frequency in urination, and dysuria.
Diagnosis. Dysuria, flank pain and confirmation with:
• Clean-catch urine for urinalysis, culture, and sensitivity
• >100,000 bacteria/mL of urine in the majority of cases.
Routine imaging is not required. However, if the patient does not improve in 48–72 hours or
complications are suspected (obstruction, renal, or perinephric abscess), U/S or CT scan can
be done.
Treatment. Antibiotics for 10–14 days (fluoroquinolone), or ampicillin and gentamicin, or a
third-generation cephalosporin are all acceptable. Essentially, any of the antibiotics for Gramnegative bacilli are effective.
Most patients can be treated as outpatients, though pregnant women who appear very ill and
those unable to tolerate oral medication due to nausea or vomiting should initially be hospitalized. Because of increasing resistance to TMP/SMZ, which has approached almost 20% in some
parts of the United States, this agent is no longer recommended for empiric therapy until culture results and antibiotic sensitivity results are available.
241
USMLE Step 2 CK
l Internal Medicine
Perinephric Abscess
Definition. A collection of infected material surrounding the kidney and generally contained
within the surrounding Gerota fascia. Very uncommon.
Etiology. Although any factor predisposing to pyelonephritis is contributory, stones are the
most important and are present in 20–60%. Other structural abnormalities, recent surgery,
trauma, and diabetes are also important.
Pathophysiology
• Arises from contiguous pyelonephritis that has formed a renal abscess
• Rupture occurs through the cortex into the perinephric space
• Microbiology: 1) The same coliforms as in cystitis and pyelonephritis; 2) E. coli most
common, then Klebsiella, Proteus; 3) Staph. aureus sometimes accounts for hematog-
enous cases
Signs and Symptoms
• Often insidious; 2–3 weeks of symptoms prior to first physician visit
• Fever is the most common symptom
• Flank pain/palpable abdominal mass/abdominal pain
• Persistence of pyelonephritis-like symptoms despite treatment for pyelonephritis
Diagnosis. Urinalysis (normal 30%) and urine culture (normal 40%) are the best initial tests.
Fever and pyuria with a negative urine culture or a polymicrobial urine culture are suggestive.
• Imaging is essential; U/S is the best initial scan but CT or MRI scan offers better imaging.
• Aspiration of the abscess is necessary for definitive bacteriologic diagnosis.
Treatment
• Antibiotics for Gram-negative rods
• Third-generation cephalosporins, antipseudomonal penicillin, or ticarcillin/clavulanate, often in combination with an aminoglycoside, for example
• Antibiotics alone are unlikely to be successful. Drainage (usually percutaneous) is
necessary.
BONE AND JOINT INFECTIONS
Osteomyelitis
A 59-year-old man was admitted last night because of a painful leg for 2 weeks.
Over the last 4 days, he developed an ulcer over the proximal portion of his tibia
just below the knee. He has a history of peripheral vascular disease and diabetes.
He is afebrile. He has a sinus tract in the center of the red, inflamed ulcer that is
draining purulent material.
242
Definition. Infection of any portion of the bone including marrow, cortex, and periosteum.
Chapter 7
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
Etiology. There are 3 types:
• Acute hematogenous: Occurs mostly in children in the long bones of the lower extremi-
ties and is secondary to a single organism 95% of the time. The most common organism
is Staphylococcus aureus. The most commonly involved bones are the tibia and femur, and
the location is usually metaphyseal due to the anatomy of the blood vessels and endothelial lining at the metaphysis. In adults, hematogenous osteomyelitis accounts for about
20% of all cases and the most common site is the vertebral bodies (lumbar vertebrae
are most frequently involved). The infection can extend posteriorly to form an epidural
abscess. A patient with this diagnosis would present with fever and back tenderness.
• Secondary to contiguous infection: Can occur in anyone with recent trauma to an
area or placement of a prosthetic joint. Although this is secondary to a single organism most of the time, a higher percentage is polymicrobial in origin. S. aureus is the
most common organism.
• Vascular insufficiency: Majority are age >50, with diabetes or peripheral vascular disease, resulting in repeated minor trauma, which is not noticed because of neuropathy
and decreased sensation. It is most common in small bones of the lower extremities. The
majority is polymicrobial, but the single most common organism is still S. aureus.
Presentation. Pain, erythema, swelling, and tenderness over the infected bone. With vascular
insufficiency, there is often an obvious overlying or nearby ulceration or wound. Occasionally,
a draining sinus tract is present.
l Infectious Diseases
Note
Injection drug use is a
significant risk factor for
vertebral osteomyelitis
in adults.
Diagnosis. The earliest tests to detect osteomyelitis are the technetium bone scan and the
MRI. Both have equal sensitivity for early pick-up, but the MRI can allow better differentiation between the overlying soft-tissue infection and bone. The MRI can be less readily available, however.
• Plain x-ray: Usually the initial test because it is more easily obtained, easily read, and
inexpensive. Periosteal elevation is the first abnormality visible. The disadvantage is
that 50–75% of bone calcification must be lost before the bone itself appears abnormal,
which usually takes at least two weeks to develop.
• Erythrocyte sedimentation rate (ESR): Nonspecific. It is useful to follow during treatment. A normal value strongly points away from osteomyelitis.
• Bone biopsy and culture: This is the best diagnostic test but also the most invasive.
• CT scan, indium, and gallium: All 3 can be abnormal in osteomyelitis, but none are as
specific or sensitive as the tests listed above.
Treatment. Acute hematogenous osteomyelitis in children can usually be treated with antibiotics
alone; however, osteomyelitis in adults requires a combination of surgical (wound drainage and
debridement, removal of infected hardware) and antibiotic therapy. Antibiotic therapy depends
on the specific isolate obtained, which must be as precise as possible because empiric treatment
for 6–12 weeks would be undesirable. A semisynthetic penicillin (oxacillin, nafcillin) or vancomycin (if MRSA is suspected) plus an aminoglycoside or a third-generation cephalosporin would be
adequate until a specific diagnosis is obtained. Chronic osteomyelitis must be treated for as long
as 12 weeks of antibiotic therapy, and in some cases, even longer periods of antibiotics may be
required. The other MRSA drugs are daptomycin, linezolid, ceftaroline, and tigecycline.
243
USMLE Step 2 CK
l Internal Medicine
Septic Arthritis
A 73-year-old woman was admitted to your service today with a swollen right
knee for the last several days. The knee has an obvious effusion and decreased
mobility. There is also redness and tenderness of the knee.
Definition. Infection of a joint due to virtually any agent. The most common etiology is bacterial; specifically, Neisseria gonorrhoeae, staphylococci or streptococci, but Rickettsia, viruses,
spirochetes, etc., may also cause it. Generally, bacterial arthritis is divided into gonococcal and
nongonococcal types.
Etiology
Pathogenesis. Sexual activity is the only significant risk factor for gonococcal septic arthritis.
A total of 1–5% of people with gonorrhea will develop disseminated disease, and 25% will
have a history of recent symptomatic gonorrhea. Nongonococcal bacterial arthritis is usually
spread by the hematogenous route. Additional routes may include bites (animal or human),
direct inoculation of bacteria into the joint through surgery or trauma, or spread of infection
from surrounding structures such as bone. Even though both normal or damaged joints can
get infected, any previous damage to a joint, such as from rheumatoid arthritis or osteoarthritis, previous surgery, prothesis placement, gout, sickle cell disease, or the presence of certain
risk factors such as IV drug abuse, diabetes mellitus, or HIV infection can predispose a joint
to infection. Any cause of bacteremia can seed the joint because the synovium does not have a
basement membrane.
Microbiology. Nongonococcal:
• Gram-positive (>85); (S. aureus [60%], Streptococcus [15%], Pneumococcus [5%])
• Gram-negative (10−15%)
• Polymicrobial (5%)
Presentation
Nongonococcal. Monoarticular in >85%, with a swollen, tender, erythematous joint with a
decreased range of motion. Knee is the most common. Skin manifestations are rare.
Gonococcal. Polyarticular in 50%; a tenosynovitis is much more common. Effusions are less
common. Migratory polyarthralgia are common. Skin manifestations with petechiae or purpura are common.
Diagnosis
Nongonococcal. Culture of joint aspirate fluid is positive in 90–95% and Gram stain is posi-
tive in 40–70%. The cell count of the synovial fluid is high (>50,000) and is predominantly
PMNs with a low glucose. Blood culture is positive in 50%.
Gonococcal. Much harder to culture. Only 50% of joint aspirates have positive synovial fluid
culture; <10% of blood cultures are positive. Other sites such as cervix, pharynx, rectum, and
urethra may also be positive. In the aggregate, culture of the other sites has a greater yield
than culturing the joint itself.
Treatment. Bacterial arthritis is usually treated by a combination of joint aspiration and antimicrobial therapy.
244
Chapter 7
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
Nongonococcal. In the absence of a specific organism seen on a stain or obtained from culture, good empiric coverage is nafcillin or oxacillin (or vancomycin) combined with an aminoglycoside or a third-generation cephalosporin. Combine an antistaphylococcal/antistreptococcal drug with a Gram-negative drug.
Gonococcal. Ceftriaxone is the drug of choice.
Gas Gangrene (Clostridial Myonecrosis)
Definition. The necrotizing destruction of muscle by gas-producing organisms, associated
with signs of sepsis.
Epidemiology. Gas gangrene is uncommon; a large referral center may admit 10 cases per
year; there are 1,000–3,000 cases per year in the United States, though incidence markedly
increases during times of war.
Etiology. Gas gangrene is largely due (80%) to the spread of infection from wounds contaminated by Clostridium perfringens (the toxins produced by clostridia play a significant role in tissue damage). It is strongly associated with traumatic injury (50%), shrapnel in war, and motor
vehicles in peacetime. The trauma may be as minor as an intramuscular injection; however, the
wound must be deep, necrotic, and without exit to the surface. Postoperative (30%), nontraumatic (20%). Uterine gangrene was formerly a major complication of improper abortion.
l Infectious Diseases
Signs and symptoms. Symptoms usually begin <1–4 days of incubation after the wound and
include pain, swelling, and edema at the site of the wound. Later hypotension, tachycardia,
and fever can occur. Crepitation over the site and renal failure are late developments, usually
prior to death.
Diagnosis. A Gram stain of the wound shows Gram-positive rods, but no white cells. A culture may be positive for C. perfringens as early as 1 day; however, this is not necessarily diagnostic because up to 30% of wounds can be colonized by Clostridia. Gas bubbles on x-ray are
suggestive but may be caused by streptococci as well. Direct visualization (usually at surgery)
of pale, dead muscle with a brownish, sweet-smelling discharge is ultimately diagnostic.
Treatment. High-dose penicillin (24 million/day) or clindamycin (if penicillin allergic)
is necessary, but surgical debridement or amputation is the absolute center of treatment.
Hyperbaric oxygen is of possible benefit, but this is still controversial.
CARDITIS
Infective Endocarditis
A 40-year-old man is brought to the hospital because of fever. He has a history of
IV drug use. On physical examination, there is a systolic murmur at the lower left
sternal border.
Definition. Colonization of heart valves with microbial organisms causing friable infected
vegetations and valve injury. Bacterial endocarditis produces large vegetations and may affect
any value in the heart, although left-sided lesions of the aortic and mitral valves are more
common.
245
USMLE Step 2 CK
l Internal Medicine
Epidemiology and etiology. There are several important invasive and other predisposing factors to bacterial endocarditis:
• Dental procedures that cause bleeding
• Oral and upper respiratory tract surgery
• Genitourinary surgery
• Prosthetic heart valves
• Catheters in the right heart
• Pressure-monitoring catheters
• IV drug use
Table 7-4. Relative Risk of Various Predisposing Conditions for Infective Endocarditis
High Risk Intermediate Risk Low/Negligible Risk
Prosthetic valves* Mitral valve prolapse with regurgitation Mitral prolapse without regurgitation
Aortic valve disease Mitral stenosis Atrial septal defect
Mitral regurgitation Tricuspid valve disease Luetic aortitis
Patent ductus arteriosus Hypertrophic obstructive cardiomyopathy Transvenous pacemakers
Arteriovenous fistula Calcific aortic sclerosis
Tetralogy of Fallot
Coarctation of the aorta
Indwelling right heart catheters
Indwelling right heart and pulmonary
artery catheters
Surgically corrected congenital lesions
(no prosthesis) >6 mo after surgery
Aortocoronary bypass surgery
Cardiac pacemakers
(hyperalimentation)
Previous infective endocarditis Nonvalvular intracardiac prosthesis
Marfan syndrome
*Indication for endocarditis prophylaxis.
246
Table 7-5. Microorganisms Responsible for Infective Endocarditis
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
Organism Incidence, %
Chapter 7
l Infectious Diseases
Native valves
Streptococcus viridans
Enterococci 5−15
Other streptococci:
Staphylococcus aureus
Staphylococcus epidermidis
Gram-negative bacilli <5
Fungi (Candida, Aspergillus, Histoplasma) <3
Culture negative <5
In narcotic addicts
Staphylococcus aureus
Staphylococcus epidermidis
Streptococci 10−20
Enterococci 8−10
Gram-negative bacilli 4−8
Fungi 4−5
Diphtheroids 1−2
50−60
15−20
20−30
1−3
60−95
5−10
Prosthetic valves
Staphylococcus epidermidis
Streptococcus viridans
Staphylococcus aureus
Enterococci 5−10
Other streptococci 1−5
Culture negative <5
Pathogenesis. Acute infective endocarditis is caused by bacteremia.
• S. aureus is the most common cause of acute endocarditis
• Seed previously normal valves, producing necrotizing, ulcerative, invasive infection
• Produces large, bulky vegetations (2 mm to 2 cm) on the atrial side
• IV drug use a major risk factor
• Rapid onset with fever and sometimes sepsis
• Splenomegaly
• Associated with invasion of myocardium (abscess cavities) and rapid valve destruction
• Embolic complications, particularly to the lungs with right-sided lesions
Acutely: first 2 months after surgery
40−50 acutely; 10−20 later
5−20 acutely; 40−60 later
15−20 acutely; 20−30 later
247
USMLE Step 2 CK
l Internal Medicine
With subacute infective endocarditis, viridans group streptococci is the most common
organism and is associated with low virulence.
• Seed previously abnormal valves
• Produce smaller vegetations composed of fibrin, platelets, debris, and bacteria
• Risk factors: 1) Ventricular septal defect with shunt, 2) stenosis of any valve, 3) pros-
thetic valves, 4) indwelling catheters, 5) bicuspid aortic valve, 6) mitral valve prolapse,
and 7) Marfan syndrome
• Clinical course: 1) Slow onset with vague symptoms; 2) malaise, low-grade fever,
weight loss, flulike symptoms; 3) destruction of valves is also present; and 4) less fatal
than acute, with 5-year survival 80–90% with treatment
Clinical manifestations
Table 7-6. Incidence of Clinical Findings in Infective Endocarditis
Symptoms, % Signs, %
Chills, 41 Heart murmur or changing murmur, 80−90
Weakness, 38 Fever, 90
Dyspnea, 36 Embolic events, 50
Sweats, 24 Skin manifestations, 50
Anorexia, weight loss, 24 Splenomegaly, 28
Malaise, 24 Septic complications, 19
Cough, 24 Mycotic aneurysms, 18
Skin lesions, 21 Glomerulonephritis, 10
Stroke, 18 Digital clubbing, 12
Nausea, vomiting, 17 Retinal lesions, 5
Chest pain, 16
Table 7-7. Peripheral Manifestations of Infective Endocarditis
Physical Findings (Frequency) Pathogenesis Most Common
Organisms
Petechiae (20−30%): red, nonblanching lesions in crops on conjunctivae,
buccal mucosa, palate, extremities
Splinter hemorrhages (15%): linear, red-brown streaks most
suggestive of IE when proximal in nailbeds
Osler’s nodes (5−10%): 2−5 mm painful nodules on pads of
fingers or toes
Vasculitis or
emboli
Vasculitis or
emboli
Vasculitis Streptococcus
Streptococcus,
Staphylococcus
Staphylococcus,
Streptococcus
Janeway lesions (10–15%): macular, red, or hemorrhagic, painless
patches on palms or soles
Roth’s spots (<5%): oval, pale, retinal lesions surrounded
by hemorrhage
248
Emboli Staphylococcus
Vasculitis Streptococcus
Chapter 7
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
Complications of infective endocarditis are as follows:
• CHF (most common cause of death)
• Septic embolization (related to infarctions and metastatic infections): brain (“mycotic”
aneurysm); spleen (greater with subacute); kidneys; coronary arteries
• Glomerulonephritis with nephrotic syndrome or renal failure (immune complex)
Diagnosis. The major criteria for the diagnosis of endocarditis are a combination of positive
blood cultures and an abnormal echocardiogram. The sensitivity of transthoracic echo is <60%,
but its specificity is excellent. Transesophageal echo is >90% sensitive and >95% specific.
If 1 of the major criteria is absent, a combination of 1 major and 3 minor criteria will constitute a diagnosis. The minor criteria are:
• Fever
• Predisposing cardiac lesion
• IV drug use
• Vascular phenomena (arterial embolic, septic pulmonary infarcts, Janeway lesions),
immunologic phenomena (such as Osler nodes, Roth spots, glomerulonephritis, or a
positive rheumatoid factor)
• Microbiologic evidence (positive blood cultures not meeting major criteria or evidence of active infection with an organism consistent with infective endocarditis)
l Infectious Diseases
Treatment. Treatment decisions for infective endocarditis should be based on the identification
of the specific organism found in blood culture and its specific antimicrobial sensitivities. Prior
to the results of blood cultures, therapy can be started if the patient is very ill or there is very
clear evidence of endocarditis such as fever, a clearly new or changing murmur, and embolic
phenomena. Acceptable empiric therapy would be a combination of an antistaphylococcal drug
such as nafcillin (or oxacillin), a streptococcal drug such as penicillin (or ampicillin), and gentamicin. You must alter therapy as soon as a specific microbiologic agent is known. Vancomycin
and gentamicin are the standard empiric treatment of infective endocarditis.
Table 7-8. Therapy of Specific Microorganisms Causing Endocarditis
Organism Medication Duration
Strep. viridans Penicillin
Penicillin-allergic: ceftriaxone or
vancomycin
Penicillin or ceftriaxone + 2 weeks of
gentamicin
Staph. aureus, native valve
(Methicillin-sensitive)
(Methicillin-resistant)
Nafcillin (+ 5 days of gentamicin)
Penicillin-allergic: cefazolin or
vancomycin + gentamicin for first 5 days
Vancomycin
4 weeks
4 weeks
4 weeks
4−6 weeks
4−6 weeks
4−6 weeks
Enterococcal Penicillin (or ampicillin) and
gentamicin (vancomycin if penicillinallergic)
Penicillin-allergic or resistant:
vancomycin and gentamicin
4−6 weeks
4−6 weeks
249
Соседние файлы в папке Библиотека им академика М.И. Перельмана