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2 Penetrating Renal Trauma: A Civilian and Military Perspective
Jonathan Wingate
Madigan Army Medical Center, Tacoma, WA, USA
Introduction
The World Health Organization (WHO) defines traumatic injuries as either intentional (interpersonal violence related, war‐related, or self‐inflicted injuries) or unintentional injuries (motor vehicle collisions, falls, etc.). Traumatic injuries are the leading cause of death in the United States for people aged 1–44 years [1]. Worldwide, traumatic injuries are the ninth leading cause of death and disproportionately affects males and those in low and middle‐ income countries (LMIC) [2]. By 2030, the WHO projects a 28% increase in global deaths due to trauma and injury [3].
Civilian Versus Military Trauma
In civilian trauma, the kidneys are the most commonly injured genitourinary (GU) organ. The kidneys are injured in 1–5% of trauma patients and comprise up to 24% of traumatic solid abdominal organ injuries [4–6]. Stratifying by mechanism, there is wide geographical variation for penetrating renal injury (PRI) versus blunt renal injury (BRI) and the reported range for PRI is between 10.9 and 43.9% of all renal injuries [7–9].
Historically, in wartime trauma, the kidneys were the predominant GU organ injured during conflicts in the early and mid‐twentieth century. Hugh Hampton Young described the GU injury patterns for Allied Forces in World War I and noted a 7.3% incidence of renal trauma at time of laparotomy with a 50% mortality rate [10]. These were almost all penetrating injuries, with 93.9% of soldiers having a concomitant hollow viscous injury. Surprisingly, the nephrectomy rate was only 18.1% [10]. There has been a paradigm shift in GU injuries due to advancements in technology – specifically the use of Kevlar body armor – resulting in a significant decline of PRIs and an increase in complex lower tract blast injuries, the signature GU injury of the recent conflicts in the Middle East [11–14].
Although penetrating trauma is seen in both civilian and military trauma, mechanistically they vastly differ. Civilian penetrating trauma has an equal distribution between stab and gunshot wounds (GSW) and the majority of GSW are low‐velocity handguns [15]. Military penetrating trauma is usually due to high kinetic weapons such as rifles or due to blast injury (BI). However, due to the global increase of terror attacks and mass shootings, managing patients with injuries from these high kinetic weapons among civilian surgeons is increasing, so understanding how to manage these injuries is paramount.
Pathophysiology of Penetrating Trauma
Low‐velocity weapons, such as knives, lead to local tissue damage and effects along the tract of penetration. High‐velocity projectiles, such as bullets and shrapnel, result in wider tissue injury. This is governed by the formula KE = ½ MV2, where KE is kinetic energy, M is the bullet mass, and V is the velocity. On average, a rifle (such as the AK‐47 or M‐16A1) has a bullet velocity 2–3 times greater than a standard handgun. This translates into 4–9 times greater kinetic energy (holding mass constant), thus causing greater damage. There are two areas of projectile‐tissue interaction in missile wounds – the permanent and temporary cavity. The permanent cavity is due to local tissue damage and necrosis due to the projectile, whereas the temporary cavity is caused by the transient lateral displacement of tissue [16]. Due to varying bullet characteristics, such as fragmentation, weight, and yaw patterns, bullets can cause variable and significant damage in the temporary cavity that may seem out of proportion to the entry or exit wound.
Injury from explosions are classified into: (i) primary BI due to the interaction of the blast wave with gas‐filled structures; (ii) secondary BI due to ballistic trauma resulting from fragmentation wounds from the explosive device or the environment; (iii) tertiary BI due to displacement of the victim or environmental structures, which are largely blunt injuries; and (iv) quaternary BI or burns, toxins, and radiation contamination [17]. Most primary BI do not result in surviving causalities because these patients would have been so close to the blast epicenter that they likely sustained lethal injuries. The pressure wave caused by blasts cause damage primarily to gas‐containing organs, such as the lung; the kidneys are remarkably resilient to the pressure effects of blasts, although renal pelvis injuries have been documented [18]. The kidneys are mainly injured by the secondary and tertiary mechanisms. The PRI from blasts have pathophysiology similar to more common injury patterns, such as GSW. Although these fragments are often much smaller than bullets, they may cause more tissue damage due to the sheer number of fragments and because the velocity of these fragments can be over twice that of a rifle.
Anatomy
It is imperative to have a sound understanding of renal anatomy, as it is foundational for understanding associated injury patterns, surgical approach/reconstruction, and comprises the basis of non‐operative management (NOM). The kidneys are paired retroperitoneal organs extending from vertebral levels T12 to L3. From deep to superficial, the layers surrounding the kidney are as follows: renal capsule, peri‐renal fat, renal fascia (Gerota's fascia), and para‐renal fat. Both Gerota's fascia and the renal capsule are responsible for tamponade of renal hematomas and they are both critical layers for renorrhaphy. The vascular supply consists of one main renal artery and vein, although about 25% of kidneys have accessory vessels. The internal structure can grossly be divided into the renal parenchyma and collecting system. The latter is comprised of minor and major calyces that coalesce into the renal pelvis. This distinction between the parenchyma and collecting system is important in renal injury grading (Table 2.1).
Table 2.1 AAST Renal injury classification, revised in 2018.
| Grade I | Contusion or nonexpanding subcapsular hematoma |
| Grade II | Nonexpanding perirenal hematoma |
| <1 cm cortical laceration without urinary extravasation | |
| Grade III | Cortical laceration >1 cm without urinary extravasation |
| Any injury in the presence of a kidney vascular injury or active bleeding contained within Gerota's fascia | |
| Grade IV | Laceration into collecting system |
| Segmental renal artery or vein injury | |
| Active bleeding beyond Gerota's fascia | |
|
Segmental or complete kidney infarction
|