Page 76 - JSOM Fall 2022

prompt broad spectrum antibiotics are the mainstays of ther­ decreased chest wall compliance and increased intrathoracic
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apy. If the patient remains hypotensive despite fluid resusci­ pressures, atelectasis, shortness of breath, and respiratory dis­
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tation, a vasopressor such as norepinephrine should be used to tress. In the setting of ACS, increased pressure on the inferior
maintain a mean arterial pressure of ≥65mmHg. 17,15,18 venous cava decreases cardiac preload and forward perfusion
to the kidneys. Additionally, direct pressure on the renal vas­
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Trauma culature causes further renal ischemia. 26
AKI in trauma patients has been shown to significantly in­
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crease mortality. Mechanisms increasing the risk of AKI When ACS is suspected, IAP can be measured by utilizing a Foley
include rhabdomyolysis from blast or crush injuries, hypovo­ catheter to obtain bladder pressures as a surrogate. Abdominal
lemia from acute blood loss causing acute tubular necrosis, hypertension is defined as an IAP of 12–20mmHg, compared
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abdominal compartment syndrome from aggressive fluid hy­ to a normal IAP of 0–5mmHg. Abdominal compartment syn­
dration or intrabdominal bleeding, and direct trauma to the drome results when the pressures exceed 20mmHg, and there
kidneys. One multicenter cohort study found prehospital is evidence of new organ dysfunction, to include AKI, altered
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variables affecting risk for developing AKI included minimum mental status, and respiratory distress. Surgical decompression
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mean arterial pressure (MAP), maximum heart rate, and trans­ is the gold standard treatment for ACS. However, several non­
fer to a secondary trauma center. Treatment is supportive surgical interventions can improve IAP and in turn renal perfu­
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and patients should have urine output monitored. To increase sion. These include gastric decompression with a gastric tube,
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the sensitivity of diagnosing renal injuries, contrast­enhanced removing restrictive dressings, adequate pain control, and re­
computed tomography of the abdomen and pelvis with de­ moving excess fluids via diuretics or paracentesis. 27
layed imaging is recommended to prevent missing late extrav­
asation of contrast seen with ureteral or renal pelvis injuries. 7 Intrinsic AKI
Intrinsic AKI is due to direct damage to the kidney parenchyma
Cardiorenal Syndrome and commonly due to nephrotoxic medications, acute tubular
Cardiorenal syndrome (CRS) is a form of AKI in which cardiac necrosis (ATN), or autoimmune disease. With ATN, ischemia
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dysfunction leads to secondary renal dysfunction (CRS type or direct damage to endothelial cells results in sloughing of the
1), or vice versa (CRS type 3), as this disease process is due to endothelial lining and subsequent obstruction of the renal tu­
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bidirectional interplay between the heart and kidneys. This bules. Increased hydrostatic pressure leads to leakage of filtrate
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is due to either decreased cardiac output or increased sodium into the bloodstream, causing reduced GFR. Classically, muddy
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retention resulting in venous congestion and decreased renal brown casts are seen on microscopy. Treatment of intrinsic
perfusion. In response to poor renal perfusion, the kidneys AKI is supportive care to include identification and cessation
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activate the RAAS and release antidiuretic hormone. The kid­ of nephrotoxic medications, fluid hydration, and management
neys also activate the sympathetic nervous system which causes of electrolytes. Additional etiologies of intrinsic AKI include
vasoconstriction, increased fluid retention, venous congestion, rhabdomyolysis, tumor lysis syndrome, glomerulonephritis,
and subsequent decreased cardiac output further exacerbating nephrotoxic medications, and drugs of abuse. Nephrotoxins
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poor renal perfusion pressure. Risk factors for cardiorenal and rhabdomyolysis are specifically highlighted below.
syndrome include a history of heart failure and chronic kid­
ney disease. In contrast to most prerenal AKI therapies, the Nephrotoxicity
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treatment for cardiorenal syndrome is not fluid resuscitation. In patients with suspected AKI, a thorough medication his­
It instead centers on optimizing cardiac function and decreas­ tory may reveal nephrotoxic medications. Patients should be
ing venous congestion through the use of diuretics. 23 advised to hold such medications unless the benefit outweighs
the risk. These decisions should be made in conjunction with
Hepatorenal Syndrome the prescribing physician.
Hepatorenal syndrome is similar to cardiorenal syndrome and
is caused by venous congestion leading to low renal perfusion • NSAIDs: Block prostaglandin production and cause affer­
pressures, subsequent neurohormonal dysfunction, and AKI. ent arteriolar vasoconstriction. 7
Unlike cardiorenal syndrome, however, the poor renal perfu­ • ACE inhibitors and ARBs: Inhibit angiotensin induced va­
sion is due to advanced liver disease causing worsening portal soconstriction leading to decreased glomerular filtration
hypertension and splanchnic vasodilation, leading to a low ef­ pressure and GFR. 7
fective circulating volume. Type I hepatorenal syndrome is the • Antibiotics (aminoglycosides, beta­lactams, fluoroquinolo­
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most severe form and is characterized by an acute rise in serum nes): Directly nephrotoxic.
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creatinine and a dramatic decrease in urine output. Treatment • Antivirals (acyclovir, valacyclovir): Direct damage caused by
is supportive and includes addressing triggers for acute on the precipitation of crystals and subsequent obstruction. 28
chronic liver disease, such as spontaneous bacterial peritonitis, • Drugs of abuse (cocaine, methamphetamine): Unknown
alcohol use, medication noncompliance, and hepatitis. 25 mechanism of toxicity but thought to cause direct nephrotox­
icity along with secondary insults such as rhabdomyolysis. 29
Abdominal Compartment Syndrome
Abdominal compartment syndrome (ACS) is defined as an in­ Rhabdomyolysis
traabdominal pressure (IAP) >20mmHg leading to decreased Rhabdomyolysis is an important cause of AKI that occurs when
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organ perfusion and end organ dysfunction. Risk factors for skeletal muscle breaks down and releases its cellular contents
ACS include aggressive fluid hydration, diminished abdomi­ into the serum. This can result in acute electrolyte derange­
nal compliance, increased intraluminal contents, increased ments, most notably, hyperkalemia, as well as release of myo­
abdominal cavity contents, such as hematoma or ascites, and globin and uric acid into the serum. Myoglobin is broken down
shock states leading to leaky capillaries and third spacing. into nephrotoxic byproducts which cause direct damage to
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The increased pressure in the abdomen can also result in the kidneys via intratubular cast formation and obstruction.
72 | JSOM Volume 22, Edition 3 / Fall 2022