Renal carbuncle N15.10

A renal carbuncle is the confluence of multiple abscesses in the area of the cortex renalis (Herold 2021). The term "renal carbuncle" also represents the historical expression of a renal abscess (Manski 2019).

Abscesses in the kidney are divided into:

• Renal carbuncle:
  • solitary confluent abscess located in the cortex
  • predominantly haematogenous (Keller 2010)
• medullary abscess:
  • intrarenal (Hegele 2015)
  • predominantly caused by an ascending infection of the urinary tract, in which germs of a primary urinary tract infection ascend into the kidney (Kasper 2015)
• perinephritic abscess:
  • located in the perinephritic space within the Gerota's fascia
  • primarily the result of an abscess rupture (Risler 2008)
• paranephritic abscess:
  • located outside the Gerota's fascia
  • consequence of an abscess rupture through Gerota's fascia (Vahlensieck 2015)

Before the antibiotic era, the majority of renal abscesses were of hematogenous origin, whereas nowadays > 75% of abscesses are of ascension origin (Kasper 2015).

Renal abscesses account for approximately 2% of all renal space-occupying lesions and are thus rather rare (Schaefer- Prokop 2007).

All forms of renal abscesses (see "Classification") occur significantly more frequently in women than in men (ratio of 5: 1 [Vahlensieck 2015]). The average age of onset of the disease is between 53 - 57 years (Hegele 2015).

In the case of an ascending infection, anatomical anomalies are not infrequently detectable (in 2 out of 3 affected patients) (Keller 2010).

Renal abscesses are caused by hematogenous spread or abscessing infections, with the latter playing a greater role numerically (Keller 2010).

• Abscessing infection:

Abscessing infection may involve the following pathogens in descending order:

• gram-negative pathogens
• Gram-positive pathogens
• Anaerobes
• Candida spp.

(Hegele 2015)

The following risk factors can play a role here:

• Nephrolithiasis (found in 20 % - 60 % of all patients with perinephritic abscesses).
• structural changes of the urinary tract
• history of urological surgery
• trauma
• diabetes mellitus

(Kasper 2015)

• Hematogenous spread:

In most cases of hematogenous spread, the primary cause is a skin infection (preferably by Staphylococcus aureus), which then spreads hematogenously.

However, hematogenous spread is also possible through Candida spp. - in addition to the above-mentioned cause of an abscessing infection (Kasper 2015).

Particular risk factors here are pre-existing conditions such as:

• Diabetes mellitus
• Immunosuppression
• Hemodialysis
• i. v. drug abuse

(Risler 2008)

• In very rare cases also an infection with Pyoderma gangraenosum

(Reynolds 2016)

• Abscessing infection

In this type of infection, there is primarily a urinary tract infection from which the pathogens enter the kidney through ascension and initially cause pyelonephritis here.

In this case, the renal parenchyma can be affected by the pathogens, starting from the medulla and extending to the cortex, whereby the local vascular channels of the kidney are often involved in the transport of the pathogens.

The abscesses, which initially form in the parenchyma, spread perinephritically and may rupture into the paranephritic space after rupture of the Gerota's fascia. This may result in an abscess route extending to the psoas muscle, transversus abdominis muscle, and anterior peritoneal cavity, downward into the pelvis, and upward into the subdiaphragmatic space.

(Kasper 2015)

The symptoms are sometimes unspecific or may be absent altogether (especially in diabetics [Vahlensieck 2015]). The appearance of the primary focus in a hematogenous spread is anamnestically 1 - 8 weeks ago (Hegele 2015).

Otherwise, the following symptoms are possible:

• Fever (occurs in ≥ 50% of patients and may persist for > 5 d despite adequate antibiosis).
• Depending on the localization, the following protective postures or changes are possible:
  • Abscess inferior pole: hip flexion forward to relieve posture of the m psoas.
  • Abscess dorsal: posture of the WS in lordosis
  • cranial abscess: diaphragmatic elevation
  • medio- ventral abscess: irritation of the peritoneum possible
• redness of the corresponding dermatome with paresthesias

(Keller 2010)

• pain in the region of the groin or extremities
• Hematuria

(Kasper 2015)

• reduced general condition
• Nausea
• occasional palpable tumor in the flank area
• symptoms of a urinary bladder infection (see d.)
• Signs of septic metastasis such as secondary endophthalmitis (blurred vision)

(Vahlensieck 2015)

Because of the sometimes unspecific symptoms, the diagnosis of a kidney abscess can often be made only after a delay. A renal abscess should therefore be considered in the following clinical pictures:

• persistent symptoms of pyelonephritis
• persistent fever
• urine culture shows a mixed form
• Known nephrolithiasis and concurrent fever and pyuria in sterile urine culture.

(Kasper 2015)

Sonography

• a renal abscess may be detectable as an anechoic or anechoic zone in approx. 60 % of cases
• enlargement of the kidney
• contour may be altered
• surrounding kidney tissue is often thickened with edema
• not infrequently there is evidence of nephrolithiasis

(Vahlensieck 2015)

In case of sonographic abnormalities, it is recommended to perform a CT (Manski 2019).

Doppler sonography

Doppler sonography usually shows increased blood flow at the edge of the abscess, while no blood flow is detectable in the center (Manski 2019).

Computed tomography / MRI

CT and MRI are considered the best frahling methods in terms of abscess visualization, although rupture is usually better seen on MRI.

There are:

• initial renal enlargement
• focal foci with absent contrast uptake
• in the further course around the abscess fibrotic wall
• Within the abscess:
  • fluid level
  • septa
• thickening of the Gerota fascia

(Vahlensieck 2015)

Typical after contrast administration is an accumulation of the contrast medium in the marginal area as a so-called "ring sign" (Manski 2019).

i. v. pyelogram

If CT or MRI are not accessible, the diagnosis can also be made by an i. v. pyelogram. This will show:

• enlargement of the kidney
• irregular contour
• missing respiratory displacement of the kidney
• missing psoas edge shadow
• concave scoliosis towards the abscess
• silent kidney in case of diffuse involvement

If the abscess is on the anterior or posterior surface of the kidney without access to the renal pelvic caliceal system, the IVP may be completely unremarkable.

(Vahlensieck 2015)

• Leukocytosis (which persists for > 5 d despite adequate antibiotic treatment)

(Keller 2010)

• BSG acceleration
• CRP increase
• Quick- decrease
• Drop in thrombocytes
• Derailment of electrolytes
• Increase of the retention parameters

(Vahlensieck 2015)

In addition, the determination of the following parameters in particular is recommended in cases of suspected sepsis:

• Blood cultures (are positive in about 20% [Vahlensieck 2015)].
• Blood gas analysis
• Procalcitonin
• AT III
• Fibrinogen

[Manski 2019)

Urine findings:

The urine findings may be unremarkable - especially in the case of hematogenous spread (Kuhlmann 2015).

If there is a connection to the draining urinary tract one finds:

• Pyuria
• Bacteriuria

Regarding the identification of the germ, it should be taken into account that anaerobes (cause in about 12%) and fungi (occurs in 1%) are not part of routine bacteriology.

(Vahlensieck 2015)

• Kidney tumor (especially Wilms tumor in children [Freisen 2010])
• infected cyst
• abscess within a cyst
• Tuberculosis

[Vahlensieck 2015)

- sepsis

Treatment of renal abscess usually includes:

• immediate antibiotic treatment
• abscess drainage
• Removal of any obstructions or other causal factors that may be present.

(Hegele 2015)

In exceptional cases, e.g. in diabetics who show obstruction or a large tissue breakdown, a nephrectomy may also be necessary (Hegele 2010).

Pretreated patients:

Patients who have already received monotherapy (for pyelonephritis) before diagnosis and who have since shown partial success should be continued.

Non-pretreated patients:

In previously unpretreated patients, the 1st choice agent recommended is a fluoroquinolone such as:

• Ciprofloxacin (recommended dosage: 2 x 0.4 g / d)
• Levofloxacin (recommended dosage: 1 x 0.5 - 0.75 g / d)

or

a group 3 and 4 cephalosporin such as:

• Cefotaxime (recommended dosage: 3 x 2 g / d)
• Cefepim (dosage recommendation: 2 x 1 - 2 g / d)

(Hegele 2015)

Particularly in large abscesses, different pathogens can sometimes be detected in the abscess fluid than in the urine culture. In these cases, an adjustment of the antibiosis is necessary (Keller 2010).

The duration of treatment is between 4 - 6 weeks (Hegele 2015) and should in any case be continued beyond 10 d after normalisation of the laboratory parameters (Keller 2010).

Abscess drainage

If the abscess size is < 3 cm and there are no other risk factors, antibiotic treatment alone may be sufficient.

If the abscess size is between 3 cm - 5 cm and the immune system is compromised or does not improve with antibiotics, percutaneous drainage with culture may improve the situation(Hegele 2015).

Abscesses that are > 5 cm should always be drained open-surgically, laparoscopically, or percutaneously(Hegele 2015).

Percutaneous drainage predominates with 56 % compared to open surgical drainage with 29 %.

Immediate or delayed nephrectomy is required in an average of 13 % of patients.

(Vahlensieck 2015)

At the beginning of the 20th century, a renal abscess represented a life-threatening disease with a mortality rate of up to 50 %, not least because of the limited diagnostic and therapeutic options (El-Khadra 2004), but even today the average mortality rate of a renal abscess or renal carbuncle is still between 8 % - 23 % (Vahlensieck 2015).

Only in cases where subcapsular spread is still absent are the prognostic prospects good if appropriate treatment is initiated immediately (Keller 2010).

After cessation of antibiotics, laboratory controls with special regard to leukocytes, ESR, urine culture and urine sediment should initially be carried out at 2-week intervals for 3 months (Keller 2010).

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