causes [6, 12, 13]. In a recent blunt renal trauma series, 80% of injuries were found to be grade I–II renal injuries, 9.5% grade III, 8.1% grade IV, and 2.7% grade IV [5]. Thus, imaging all renal injuries is unnecessary, and criteria have been developed (see below). Table 1.1 summarizes the large (n > 100) series with emphasis on blunt injuries.
Table 1.1 Demographics of renal trauma.
| SERIES a | [6] | [14] | [15] | [1] b | [4] | [16] | [5] b | [17] | [18] | [19] |
|---|---|---|---|---|---|---|---|---|---|---|
| Year published | 1984 | 1986 | 1995 | 2001 | 2003 | 2012 | 2012 | 2013 | 2013 | 2014 |
| Renal injury (N) | 154 | 132 | 2254 | 227 | 6231 | 1505 | 221 | 338 | 9002 | 105 |
| Renal injury (%) | 2.9 | 3.25 | n/a | 1.4 | 1.2 | n/a | n/a | n/a | n/a | n/a |
| Blunt (%) | 93.5 | 95.4 | 89.8 | 93.4 | 81.6 | 95.0 | 100 | 96.2 | 82.0 | 96.1 |
| Penetrating (%) | 6.5 | 4.6 | 10.2 | 6.6 | 18.4 | 5.0 | 0 | 3.9 | 17.8 | 3.9 |
| Grade IV–V (%) | n/a | 14.6 | 10.9 | 29.3 | 21.1 | 23.5 | ||||
| Initial non‐operative management among all trauma (%) | 92.6 | 92.6 | n/a | 88.6 | 94.5 | n/a | 92.6 | 86.8 | 98.0 | |
| Initial non‐operative management among blunt trauma (%) | 98.3 | 89.5/92.9? | 96.3 | 92.3 | 92.6 | 94.4 | ||||
| Nephrectomy (%) among all trauma | 3.8 | 3.2 | 7.9 | 3.1 | n/a | 7.1 | 8.6 | 1.9 | ||
| Nephrectomy (%) among blunt trauma | 0 | 7.2 | 3.3 | 5.4 | 7.4 | 4.7 |
Blank cells indicate missing data.
a Series with N < 100 not included.
b Data showing grade and management of blunt renal injuries only.
Pathophysiology
Blunt trauma injury to the kidney is thought to occur as a result of kinetic energy transmission, often as a consequence of rapid deceleration forces or direct interaction of structures in the environment with the soft tissues and bones of the flank and then the kidney. Studies using animal models have shown that the kidney has viscoelastic properties and that damage occurs as a result of stresses that cause tissue deformations exceeding an impact energy threshold of 4 J [20, 21]. A three‐dimensional animal model also demonstrated that the primary site of load‐bearing, where injuries result from, is the junction between the renal pelvis and the renal cortex [21]. Research has also demonstrated that the kidney with a fluid‐filled structure (i.e. ureteropelvic junction obstruction, hydronephrosis, or renal cyst) may be more prone to rupture due to the hydrostatic pressure and resulting distribution of forces within the kidney [20, 22].
Children may have a higher risk of significant renal injury from blunt trauma and this is thought to be related to the proportionately larger kidney for their body size as compared to that of adults, the possibility of children retaining fetal lobulations that may predispose to parenchymal disruption, and the pediatric kidney having less protection due to lower perirenal fat content, weaker abdominal muscles, and less ossification of the rib cage [23, 24].
The proportion of patients with renal trauma found to have congenital anomalies varies, depending on different series, ranging from 1 to 23% [23]. One series that reviewed 193 pediatric renal trauma patients found that just over 8% of patients had a congenital anomaly [25]. Data regarding renal trauma and congenital anomalies is somewhat mixed, with most studies suggesting that congenital anomalies increase the risk of significant renal injury and decrease the possibility of renal salvage, while other series suggest that there is no effect on morbidity or mortality [25-30]. Overall consensus is that pre‐existing renal anomalies likely increase the vulnerability of kidneys in blunt renal trauma [4, 30]. They may also complicate the management of a renal laceration involving the collecting system or parenchyma (e.g. horseshoe kidney with complex arterial
