Download 01 NON-SPECIFIC AND SPECIFIC INFLAMMATORY DISEASES OF

NON-SPECIFIC AND SPECIFIC
INFLAMMATORY DISEASES OF ORGANS
OF THE URINO-GENITAL SYSTEM
Etiology
Acute pyelonephritis is an infectious inflammatory disease that involves both
the parenchyma and the pelvis of the kidney; it may affect one or, on occasion,
both kidneys.
Aerobic gram-negative bacteria are the principal causative agents; common
strains of E coli are the predominant pathogens. All species of Proteus are
especially important because they are potent producers of urease, an enzyme that
splits urea and produces highly alkaline urine that favors the precipitation of
phosphates to form magnesium ammonium phosphate (struvite) and calcium
phosphate (apatite) stones. Klebsiella species are less potent producers of urease
but elaborate other substances that favor urinary stone formation.
Gram-positive bacteria other than the enterococ-cus Streptococcus faecalis
seldom cause pyelonephritis. Staphylococci may infect the kidney by the
hematogenous route and cause bacteriuria and renal abscesses. Obligate anaerobic
bacteria rarely cause pyelonephritis.
Pathogenesis
Renal infection usually ascends from the urethra and lower genitourinary
tract. Hematogenous infection of the kidney occurs infrequently; lymphatic spread
occurs rarely, if ever.
The short urethra in girls and women and its close proximity to the anus allow
periurethral pathogenic bacteria easy access to the bladder during sexual intercourse or urethral manipulation. Girls and women with breached local defenses
due to biologic, anatomic, or other abnormalities frequently experience introital
and periurethral colonization by pathogenic enteric bacteria and are especially
prone to infection that ascends from the urethra.
Males are less susceptible to ascending urethral infection because the male
urethra is much longer than the female urethra and the meatus is not so near the
anus and because the prostate normally secretes antibacterial factors that give some
protection against invading pathogens.
Once pathogenic bacteria reach the bladder via the urethra, whether infection
becomes established is influenced by the quality of the bladder defenses: the
efficacy of voiding and muscle coordination, the antimicrobial properties of the
urine, and factors that allow or inhibit bacterial adherence to surface cells.
Once bladder infection is established, whether infection ascends via the
ureters and involves the kidneys is influenced by microbial virulence factors, the
presence or absence of vesicoureteral reflux, the quality of ureteral peristalsis, and
the susceptibility of the renal medulla to infection.
Classification
The primary and secondary pyelonephritis are distinguished.
There is no dysfunction of the urine outflow during the primary
pyelonephritis.
The secondary pyelonephritis goes with urostasis.
The secondary pyelonephritis goes with urostasis
1/ The unilateral and bilateral.
a/ Acute /purulent, serous/
b/ Chronic;
c/ Relapsing course.
2/ By the mode of bacteria pathway there are differed
3/ a/ hematogenous /ascending/;
b/ urogenic /ascending/;
c/ urolithiasis /infected urinary stones/;
d/ tuberculosis of the kidneys;
e/ the other renal diseases.
By the course, age, stage of the organism there are differed:
1/ the pyelonephritis of newborn;
2/ the pyelonephritis of the aged patients;
3/ the pyelonephritis of the pregnant women;
4/ the pyelonephritis in diabetes mellitus patients.
The acute pyelonephritis may be complicated with purulent nephritis,
carbuncle of the kidney, the renal abscess, renal insufficiency.
Clinical Findings
A. Symptoms: The usual symptoms of acute_py-elonephritis include abrupt
onset of shaking chills, moderate to high fever, a constant ache in the loin
(unilateral or bilateral), and symptoms of cystitis: frequency, nocturia, urgency,
and dysuria. Significant malaise and prostration are the rule; nausea, vomiting, and
even diarrhea are common. Young children most often complain of poorly
localized abdominal discomfort and seldom localize the discomfort specifically to
the flank.
B. Signs: The patient generally appears quite ill. Intermittent chills are
associated with fever ranging from 38.5 to 40 °C (101-104 °F) and tachycardia (the
pulse rate may range from 90/min to 140/min or faster). Fist percussion over the
costovertebral angle overlying the affected kidney usually causes pain. The kidney
often cannot be palpated, because of tenderness and overlying muscle spasm.
Abdominal distention may be marked, and rebound tenderness may suggest an
intraperitoneal lesion. Auscultation usually reveals a quiet intestine.
C. Laboratory Findings: The hemogram typically shows significant
leukocytosis (polymorphonu-clear neutrophils and band cells); the erythrocyte
sedimentation rate is increased. Urinalysis usually shows cloudy fluid with heavy
pyuria, bacteriuria, mild proteinuria, and often microscopic or gross hematuria.
Leukocyte casts and glitter cells (large polymorphonuclear neutrophils containing
cytoplas-mic particles that exhibit dramatic brownian movement) are occasionally
seen. Quantitative urine culture generally grows the responsible pathogen in heavy
density (≥100,000 colonies/mL); sensitivity tests are helpful in therapy and of vital
importance in the management of complicating bacteremia. Serial blood cultures
are indicated, because bacteremia commonly accompanies acute pyelonephritis. In
uncomplicated acute pyelonephritis, total renal function generally remains normal,
and the serum creatinine level is not elevated.
D. X-Ray Findings:
A plain film of the abdomen may show some degree of obliteration of the
renal outline owing to edema of the kidney and perinephric fat. Suspicious
calcifications, must be carefully evaluated, because infected renal stones and
calculous obstruction complicating pyelonephritis require special management.
Excretory urograms
Excretory urograms performed during the acute stage of uncomplicated
pyelonephritis usually show few abnormalities but are important in surveying for
possible complicating factors. The severely infected kidney may appear enlarged,
show a decreased nephrogram effect on the initial film, and reveal little or no
caliceal radiopaque material. Following appropriate therapy, the urograms return to
normal.
Voiding cystograms are best delayed until several weeks after the infection is
cleared; otherwise, transient vesicoureteral reflux, often associated with the
accompanying cystitis, may be confused with more serious permanent reflux.
E. Radionuclide Imaging: At times, imaging ' the kidneys with gallium-67
helps to determine the site of infection and distinguish between acute pyelonephritis and renal abscess. Despite some false-positive and false-negative images,
Hurwitz et al (1976) claim 86% accuracy in confirming acute pyelonephritis by
this method.
Instrumental Examination
There can be seen the bullous edema of the urethral orifice because of
calculus at the intravesical portion, ureterocele, tumor compression.
Chromocystoscopia shows the range even sometimes the cause of the
functional loss of the urine outflow.
Differential Diagnosis
Because of the location and nature of the pain, pancreatitis at times may be
confused with acute pyelonephritis. Elevated serum amylase and normal results of
urinalysis help to confirm a diagnosis of pancreatitis and rule out pyelonephritis.
Basal pneumonia is a febrile illness that causes pain in the subcostal area. The
pleuritic nature of the pain and the chest x-ray usually allow differentiation.
Acute intraabdominal disease, including such conditions as acute appendicitis,
cholecystitis, and di-verticulitis, must at times be distinguished from acute
pyelonephritis. Although the signs and symptoms may be confusing initially, the
normal urinalysis associated with primary gastrointestinal disease and other
laboratory tests should make the differential diagnosis uncomplicated.
In women, the onset of acute pelvic inflammatory disease (PID) at times must
be distinguished from acute pyelonephritis. Characteristic physical findings and
negative urine cultures should make differentiation fairly easy.
In male patients with febrile genitourinary tract infection, the main
differential diagnosis consists of acute pyelonephritis, acute prostatitis, and acute
epididymoorchitis. Characteristic physical findings and symptoms in prostatitis
and epididymitis should make this differentiation easy.
Acute pyelonephritis must be distinguished from renal abscess and
perinephric abscess. Radiographic studies often are necessary to confirm the
specific diagnosis.
Treatment
A. Specific Measures: When the infection is severe or complicating factors
are present, hospitaliza-tion may be required. Urine and blood specimens must be
obtained immediately for culture; recognized pathogens must be tested for
antimicrobial sensitivity. Until the results of these tests are known, antimicrobial
drugs should be given empirically. Although clinicians differ in their choice of
antimicrobial agents, our preference is to administer an aminoglycoside (amikacin,
gentamicin, or tobramycin) plus ampicillin intravenously in full dosage. If the
pathogen is sensitive and the clinical response is favorable, this treatment is
continued for about 1 week and then replaced with an appropriate oral
antimicrobial drug for an additional 2 weeks. Complicating factors, eg, obstructive
uropathy or infected stones, must be recognized early and dealt with effectively if
complications are to be avoided.
B. General Measures: Complete bed rest is advised until symptoms subside.
Medication should be given for pain, fever, and nausea. It is important to give
fluids intravenously and orally to ensure adequate hydration and maintenance of
adequate urinary output.
C. Failure of Response: If the clinical response remains poor after 48-72
hours of therapy, reevalua-tion is necessary to assess for possible complicating
factors (eg, obstructive uropathy) or the use of inappropriate drugs. Excretory
urography is required; if this is contraindicated, retrograde urography must be
done. Unless treated quickly and effectively, obstructive uropathy complicating
acute pyelonephritis can lead to bacteremia and irreversible renal damage.
D. Follow-Up Care: Clinical improvement does not always imply cure of the
infection. In about one-third of patients, symptoms improve despite persistence of
the bacterial pathogen. Therefore, repeat urine cultures are important during and
after therapy for a follow-up period of at least 6 months.
PrognosisWhen identified promptly and treated appropriately in a patient
who has no underlying complicating factors, acute pyelonephritis carries a good
prognosis for cure without sequels. The likelihood of serious sequels and a less
favorable prognosis varies with the severity of complicating factors and the
patient's age at the onset.
Gestation pyelonephritis.
(Pyelonephritis of pregnancy).
The inflammatory process develops while pregnancy, delivery and puerperal
period. Most frequently it is observed in pregnant (48%) more rare in puerperal
(35%) women. It develops while 1 pregnancy 2 trimester often. There are women
18-25 years old. That is explained by a not complete adaptation to immunologic,
hormone changes of the pregnancy. It is supposed not to be a primary disease but
activation of latent pyelonephritis.
Urinoculture finds out E.Coli, Staphylococcus albicans, Clebsiella in pregnant
women. Association of the Proteus and Blue pus bacilli is observed in puerperal
women. The primary source of the infection may be any purulent inflammatory
place (furunculosis, dental caries, inflammatory diseases of the genital organs).
The pathogenetic sign is bacteriuria. It is observed in 7% only. Urodynamic
dysfunction favors the pyelonephritis development. Pathogenesis may be explained
with mechanical, neurohumoral and endocrine factors. The enlarged uterus
compresses the pelvic portion of the ureters causing ureteropyeloectasia while
pregnancy. Urostasis at the upper portion develops because of decreasing of the
ureteral muscles and pelvises of the kidney tension.
The moderate hypotonia and hypokinesia of the calicopelvic of the both kidneys
and ureters are observed on 8th week.
Changes of the upper portion of the urinary tract may be explained by weakening
of the sympathetic nervous system tonus. Dysfunction of the urinary output
because of the urinary pathway atonia is a condition for pathogen activation.
Vesicoureteral and pelvicorenal refluxes favor spreading of the infection into the
interstitial tissue of the renal parenchyma (medulla of the kidney).
Acute pyelonephritis of pregnancy. Primary acute process acute rarely. This is an
active phase of the chronic process frequently. The prepueral women have attacks
of the acute pyelonephritis at the 4-, 6-, 12- day of the puerperal period (these are
days of the postpartum complications: endometritis, metrophlebitis).
Clinical findings.
Clinical findings have the own peculiarities according to the different terms of
pregnancy. They also depend on the range of the urinary output damage. A sharp
pain in loin that irradiates to the lower portions of the abdomen, genitals are at the
1 trimester. 2nd and 3rd trimesters are characterized with a moderate pain because of
the dilatation of the upper urinary tract and intrarenal pressure decreasing.
An acute purulent pyelonephritis develops more frequently in pregnant and
postpueral women. There is a high lethality rate caused by an acute purulent
pyelonephritis.
Diagnosis is rather difficult. The enlarged uterine hinders the palpation. The right
kidney damage should be differed from the acute appendicitis and cholecystitis.
Ultrasonography (shows dilatation of the calyces and renal pelvis, dysfunction
of the urine passages, edema of the adipose capsule looks as rarefaction about the
kidney)
X-ray imaging is inadmissible exclusive rare occasions.
Chromocystoscopia
The endoscopy investigation isn’t recommended too. In case of the suspicion of
purulent process the complete clinical research is required including
Chromocystoscopia, radionuclide renography, scanning, excretory urography,
ultrasonography. The delayed excretion of the indigocarmine while
Chromocystoscopia is attended to peculiar urodynamic due to pregnant uterus.
Treatment.
Caesar’s incision by retroperitoneal access is performed because of an acute
inflammation at the last days of pregnancy.
Antibiotics shouldn’t be harmful to fetus. The natural and semisynthetic
penicillines are recommended at the 1st trimester. Wider choice of antibiotics is at
the 2nd and 3rd trimesters because placenta has its barrier function then.
The puerperal women may transfer drugs to child with milk.
Treatment should be continuous. Nitrofuranes are admissible after 2nd month in
dosage 50-100mg per day. Nalidixone acid is admissible after the 4 th month of
pregnancy (2g per day for 2-3 weeks). But its administration must be stopped
before delivery.
Ureteral catheterization
The acute purulent pyelonephritis in pregnant women requires the obligate
surgical measures. Its scope depends on form of the disease. It is necessary anyway
until the delivery.
RENAL ABSCESS (Renal Carbuncle)
Etiology
Renal cortical abscesses develop primarily as a result of hematogenous spread
of Staphylococcus aureus infections at distant sites (most often the skin). At times,
foci of primary renal infections caused mainly by gram-negative bacteria (coliform
organisms) coalesce in the renal medulla to form abscesses. In the past, most renal
abscesses were caused by staphylococci; recently, coliform bacteria have become
the predominant pathogens in renal abscesses. Renal abscesses caused by obligate
anaerobic bacteria are rare.
An abscess (carbuncle) caused by S aureus develops from hematogenous
spread of the organism from a primary skin lesion. Intravenous drug abusers are
especially prone to develop staphylococcal renal abscesses. Multiple focal
abscesses evolve and eventually coalesce to form a multilocular abscess. Untreated
cortical abscesses may rupture into the pyelocaliceal system or into the perinephric
space (perinephric abscess). Urinary tract infection occurs only if the abscess
communicates with the pyelocaliceal system.
The more common type, renal medullary abscess, evolves from acute or
chronic foci of pyelonephritis, often associated with ureteral obstruction or
calculous disease (calculous pyonephrosis). The infecting pathogens usually are
gram-negative rods. Timmons and Perlmutter (1976) believe that gram-negative
bacillary abscesses in children may be a complication of vesicoureteral reflux, with
the pathogens invading the collecting tubules. In adults, the kidney usually is
damaged by chronic suppurative pyelonephritis that may culminate in one or more
abscesses. Medullary abscesses may also rupture into the perinephric space. Onethird of affected patients are diabetics.
Clinical Findings
A. Symptoms: Staphylococcal renal abscess is typified by an abrupt onset of
chills, fever, and localized costovertebral pain. In the early stages, when the
abscess does not communicate with the collecting system, symptoms of vesical
irritability are absent and urinalysis is normal, although the patient may appear
quite septic. The clinical picture often mimics that of acute pyelonephritis.
In most patients with medullary abscesses due to gram-negative rods, there is
a history of persistent or recurrent bouts of urinary tract infection, often associated
with urolithiasis, obstructive uropathy, or renal surgery.
B. Signs: In acute cases, localizing signs are flank tenderness, possibly a
palpable mass, and erythema and edema of the skin of the overlying loin. At times,
however, abscesses associated with both acute and chronic infections present as
febrile illnesses with few localizing signs.
C. Laboratory Findings: The hemogram usually shows marked leukocytosis
with a shift to the left. With cortical abscesses that do not communicate with the
collecting system, urinalysis shows no pyuria or bacteriuria, and urine culture is
negative. Medullary abscesses generally are associated with heavy pyuria,
bacteriuria, and positive urine cultures. The sudden appearance of heavy pyuria
and bacteriuria may herald the rupture of a previously noncommunicating abscess
into the collecting system. Blood cultures may be positive.
Depending upon the extent of renal involvement and associated renal
abnormalities, the serum creatinine and urea nitrogen values may be normal or
elevated. Since patients with renal abscesses often are diabetic, glycosuria and
hyperglycemia may be found.
D. X-Ray Findings: If the renal outline is visible, the plain film may show an
enlarged kidney or a bulge of the external renal contour. With perinephric edema,
however, often the renal outline is obliterated and the psoas shadow indistinct.
Unless the abscess has ruptured into the perinephric space or is quite large,
scoliosis generally is not observed. Renal stones may be noted. When cortical
abscesses are small, the excretory urogram may appear normal; most often,
however, a space-occupying lesion (the abscess) is delineated. Pyelonephritic
changes, hydronephrosis, and urolithiasis also may be observed. Delayed
opacification or even a nonfunctioning kidney may be found.
Renal angiography usually makes the diagnosis. The abscess fails to opacify;
its walls are irregular. Surrounding vessels are displaced, and hypervascularity is
common. The most important sign is excessive capsular vessels overlying the
abscess.
E. Ultrasonography:
Renal echograms generally distinguish simple cysts (no internal echoes) from
solid masses (many internal echoes) but often fail to distinguish renal abscesses
from malignant lesions, particularly necrotic, cystic renal cell carcinomas.
Percutaneous needle aspiration of the mass under ultrasonic guidance may confirm
the diagnosis.
CT Scans
F. CT Scans: Experience has been limited in the utilization of CT scans for
the diagnosis of renal abscess. The attenuation coefficient value (CT number)
varies considerably with the amount of liquid pus or solid debris within the
abscess, and abscesses cannot be differentiated from hemorrhagic cysts or solid
neoplasms with certainty. Percutaneous needle aspiration of the mass under CT
control may confirm the diagnosis.
G. Isotope Scanning: The rectilinear scan will depict a space-occupying
lesion. With the use of technetium and iodine compounds, the Anger camera will
show an avascular mass lesion. These findings also are compatible with simple
cyst. Gallium-67 localizes in inflammatory tissue; an abscess will therefore "light
up" on dynamic scanning.
Gallium scanning may demonstrate an abscess even when excretory urograms
are normal.
Differential Diagnosis
In acute pyelonephritis, symptoms and signs may be similar to those of
abscess; however, no space-occupying lesion is shown on the urogram, and a
gallium scan will not show an abscess.
When symptoms of vesical irritability are absent and urinalysis is normal,
renal abscess may be confused with acute cholecystitis. The presence of a palpable
and tender gallbladder may make the diagnosis. Radiographic visualization of the
gallbladder and kidneys should be definitive.
Acute appendicitis may be confused with renal abscess, because renal pain
often radiates to the lower abdominal quadrant. The findings on physical examination, laboratory studies, and radiographic studies should allow differentiation.
At times, renal cell carcinoma may be confused with renal abscess, especially
when there is fever related to tumor necrosis. Radiographic studies and scans
usually will allow differentiation; however, percutaneous needle aspiration may be
required in some cases.
Complications
Complications of renal abscess include both bacteremia with generalized
sepsis and rupture of the abscess into the perinephrium.
Treatment
Staphylococcal abscesses should be treated with a penicillin resistant to 3lactamase. In the early stages, antibiotics alone may cure the abscess. When the
abscess is caused by gram-negative rod infection, therapy should consist of an
aminoglycoside alone or in combination with a cephalosporin or other agent.
Aminoglycosides are important in therapy because they are concentrated in renal
parenchyma and thus may obviate the need for surgical drainage.
NEPHROSTOMY
Drainage by percutaneous means or surgical incision may be necessary.
Relief of complicating urinary obstruction is mandatory. Nephrectomy and partial
nephrectomy are required less often today than in the past.
Prognosis
The outlook is good provided the diagnosis is made promptly and effective
therapy is instituted immediately.
PERINEPHRIC ABSCESS
Etiology
Perinephric abscesses lie between the renal capsule and the perirenal
(Gerota's) fascia. Most result from rupture of an intrarenal abscess into the
perinephric space; the causative organisms are usually coliform bacteria and
Pseudomonas, less often staphylococci and obligate anaerobes.
Pathogenesis & Pathology
Staphylococcal perinephric abscesses probably originate from rupture of a
small renal cortical abscess or, less commonly, from a renal carbuncle. The primary renal lesion may heal, although the perinephric abscess progresses.
Usually, however, perinephric cellulitis and abscess complicate severe renal
parenchymal infection caused by gram-negative bacteria in association with
calcufous pyonephrosis or infected hydronephrosis. It is presumed that
spontaneous extravasation of infected material occurs. In this instance, pus and
bacteria usually are found in the urine.
Perinephric abscesses may become quite large. When advanced, they tend to
point over the iliac crest (Petifs triangle) posterolaterally.
Clinical Findings
A. Symptoms: The most common symptoms of perinephric abscess include
chills, fever, unilateral flank pain, and abdominal pain. Malaise and prostration
occur variably. Only about one-third of patients complain of dysuria.
B. Signs: Fever tends to be low-grade unless generalized sepsis evolves.
There is usually marked tenderness over the affected kidney and costovertebral
angle. A large mass may be felt or percussed in the flank. Abdominal tenderness
accompanied by variable rebound tenderness may be elicited. The diaphragm on
the affected side may be elevated and fixed. Ipsilateral pleural effusion is common.
Scoliosis with the concavity to the affected side usually is seen; this results from
spasm of the psoas muscle, which also causes the patient to lie with the ipsilateral
leg flexed on the abdomen. Erythema and edeina of the overlying skin may be
evident. Minimal edema is best demonstrated by having the patient lie on a rough
toweLfor a few minutes.
C. Laboratory Findings: Leukocytosis is usual but may be mild; a shift to
the left is commonly seen. The erythrocyte sedimentation rate usually is elevated;
anemia may be present. Pyuria and bacteriuria are found commonly but not
routinely. Blood cultures may be positive. Unless bilateral renal disease is present,
the serum creatinine and blood urea nitrogen values generally are normal.
Plain film (stoun in the left kidney)
D. X-Ray Findings: A plain film of the abdomen typically shows evidence of
a flank mass. Surrounding edema often results in obliteration of the renal and psoas
shadows on the affected side. Scoliosis with the concavity to the affected side is
common. The presence of a calcified body in this area suggests an abscess
resulting from calculous pyonephrosis. Occasionally, a localized collection of gas
caused by infection with gas-forming (coliform) organisms may be observed in the
perirenal area.
Excretory urogram
Excretory urograms may show delayed visualization or nonfunction related to
obstructive uropathy or parenchymal disease. Changes suggesting a spaceoccupying lesion (eg, carbuncle) may be noted; however, evidence of advanced
hydronephrosis or calculous pyonephrosis is seen most commonly. Lack of
mobility of the kidney with change in position of the patient or with respiration
strongly suggests acute or chronic perinephritis. The entire kidney or only one pole
may be displaced laterally by the abscess.
A barium enema may show displacement of the bowel anteriorly, laterally, or
medially. Paralytic ileus may be observed on plain films of the abdomen or on
upper gastrointestinal series. Chest films may demonstrate an elevated diaphragm
on the ipsilateral side; fluoroscopy often shows fixation on respiration. Some free
pleural fluid and platelike atelectasis may be observed.
When the findings of excretory urography are equivocal, the performance of
retrograde urograms may be helpful.
Gallium-67 localizes in inflammatory tissue; hence, the diagnosis often may
be confirmed by use of the scintillation camera.
Echograms, CT scans, and renal angiograms may assist in diagnosis,
especially when combined with percutaneous needle aspiration.
Differential Diagnosis
Acute renal infections cause many of the symptoms that accompany
perinephric abscess: fever, localized pain, and tenderness. In acute pyelonephritis,
the urine uniformly shows evidence of infection; in perinephric abscess, the urine
may or may not show evidence of infection. X-ray studies and scans, however,
should facilitate differentiation of these 2 conditions.
Infected hydronephrosis may cause fever and localized pain and tenderness
and may account for the presence of a flank mass. Again, x-ray studies and scans
should make the differentiation.
Paranephric abscess is a collection of pus external to the perirenal fascia and
often is secondary to inflammatory disease of the spine (eg, tuberculosis). Many of
the signs of perinephric abscess may be seen on a plain x-ray film, but the finding
of a lesion in bone in the low thoracic area should suggest the correct diagnosis.
Urograms are normal.
Complications
Unless the correct diagnosis is made promptly and effective therapy is
initiated early, the mortality rate from generalized sepsis is quite high. Rarely, the
perinephric abscess may point just above the iliac crest posterolaterally or extend
downward into the iliac fossa and inguinal region. It is most unusual for the
phlegmon to extend within the perirenal fascia across the midline to involve the
opposite side of the body.
The abscess may produce considerable ureteral compression, giving rise to
hydronephrosis. Even after drainage of the abscess, ureteral stenosis from
periureteritis may evolve during the healing process.
Prevention
Early, effective treatment of urinary tract disease is the only means of
preventing perinephric abscess. Appropriate therapy of urinary tract infection and
removal of calculi and other obstructive conditions are of highest priority.
Treatment
Generally, treatment is similar to treatment for renal abscesses, except that
surgical drainage usually is required for perinephric abscesses but may not be
required for intrarenal abscesses. Intensive antimicrobial therapy, based upon
culture and sensitivity testing of the pathogen isolated from urine, blood, or pus
obtained by needle aspiration of the lesion, is mandatory. Unless adequate
percutaneous drainage can be established, surgical drainage usually is needed.
Because of underlying renal disease, nephrectomy may be required, either acutely
or subsequent to initial control of the abscess. When nephrectomy is not required—
indeed, even if the kidney itself is normal—excretory urography should be
performed about 3 montns after therapy is completed to make certain that late
complications (eg, ureteral stenosis) are not missed.
Prognosis
Perinephric abscess often is fatal when diagnosis and appropriate therapy are
delayed. A high index of suspicion and improved methods of diagnosis and
treatment should offer a better prognosis than the 44% mortality rate observed by
Thorley, Jones, and San-ford (1974).