Page 86 - JSOM Summer 2022

derangements, and if available, should be pursued. Renal pro- TABLE 4 Acute Kidney Injury Network (AKIN) Criteria
cessing of metabolic wastes depends on the proper function • Absolute increase in SCr ≥ 0.3mg/dL
of the glomerulus (the functional unit of the kidney). This • Increase in SCr ≥ 1.5 × above baseline
is best estimated by the glomerular filtration rate (GFR), a • UOP < 0.5mL/kg/h for > 6 hours
measurement not available with most point of care testing. SCr = serum creatinine, UOP = urine output.
However, serum creatinine (Cr) serves as an effective marker
of kidney function, helps estimate GFR and can establish a that significant gastrointestinal bleeding (from peptic ulcer
diagnosis of AKI, with assistance from blood urea nitrogen disease, cancer, or other causes) can increase BUN secondary
(BUN) levels. 68–70 A byproduct of natural muscle catabolism, to intestinal red blood cell digestion. 85,86 Additionally, other
creatinine is continuously produced and found in a normal less emergent causes of BUN elevation should be considered,
range of 0.6–1.2mg/dL. 68,71 The constant clearance of circu- including exogenous corticosteroid use (dexamethasone, pred-
latory wastes (with low and stable levels) signifies healthy re- nisone, methylprednisolone), general muscle catabolism (re-
nal function, while elevated levels establishing AKI. Military cent weight loss), and increased protein intake (namely from
literature varies on AKI incidence, with 13–34% of modern red meat). 84,85
battlefield casualties, but no significant trends for disease and
non-battle injury. 72–74 Additionally, rhabdomyolysis and crush A BUN/creatinine ratio less than 20:1 suggests intrinsic renal
injuries can cause significant AKI through traumatic cellular failure, which can result from a number of causes. 84,85 These
destruction. 72 include acute tubular necrosis from ischemic injury or toxins,
glomerulonephritis from infection complications (streptococ-
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Elevated creatinine levels indicate AKI with varying severity cal pharyngitis) or idiopathic complications. Ischemic injury
generally on a three-tier system alongside urine output (UOP) can result from decreased renal perfusion secondary to se-
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findings (Tables 2 and 3). While UOP levels are diagnostically vere hypovolemia, especially prominent in cases of traumatic
helpful, they are best used in cases of prolonged care and are hemorrhage. 72–74
difficult to quantify in the initial evaluation of the acutely pre-
senting patient. The use of creatinine as a surrogate marker for While there are numerous concerning causes for AKI described
GFR, and subsequent diagnosis of AKI, has been repeatedly above, in the absence of trauma immediate concerns for re-
trialed for diagnostic calculators, including the Acute Kidney mote medicine should focus on likely prerenal causes, primar-
Injury Network (AKIN) classification system for patients with- ily dehydration, and subsequent treatment with IV fluids. The
out prior kidney disease (Table 4). 75–77 As part of initial patient liberal use of IV crystalloids for resuscitation can significantly
evaluation, medics should be aware of nutritional supplements, improve subsequent laboratory findings and the overall clini-
as supplemental creatine is popular amongst military popula- cal picture, and may begin with clinical suspicion of diagnosis
tions and can result in artificially elevated serum levels. 78–81 or risk of AKI given non-hemorrhagic presentation (to include
initial treatment of crush injuries), but vigilance for compre-
TABLE 2 AKI Diagnostic Criteria hensive patient evaluation and continued monitoring is im-
Measurement Timeframe portant. Laboratory levels may temporarily improve after IV
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Increase SCr ≥ 0.3mg/dL Within 48 h fluids, but medics must continue to consider and evaluate for
Increase SCr ≥ 1.5 × baseline Known or presumed within 7 days other underlying causes with repeated laboratory checks every
of measurement 2–4 hours to evaluate for fluid responsiveness in addition to
UOP < 0.5mL/kg/h 6 continuous hours consultation depending on suspected mechanism.
SCr = serum creatinine, UOP = urine output.
Conclusion
TABLE 3 AKI Staging
Serum Creatinine With emergent evaluation in austere environments and the
Stage Multiplier from baseline Increase Urine Output possibility of protracted remote care in prolonged field care
1 1.5–1.9 × baseline ≥ 0.3mg/dL < 0.5mL/kg/h for scenarios, medics should be prepared to assess and treat com-
6–12 hours mon electrolyte derangements. The increasing availability of
2 2.0–2.9 × baseline n/a < 0.5mL/kg/h for point-of-care testing devices for electrolytes necessitates con-
> 12 hours current increased knowledge of these pathologies and initial
3 3.0 × baseline ≥ 4.0mg/dL < 0.3mL/kg/h for stabilization modalities.
≥ 24 hours
OR Conflicts of Interest
anuria ≥ 12 hours The authors have no conflicts of interest or relevant disclo-
sures to report.
During the course of initial evaluation, medics and telemedicine
consultants may find it helpful to utilize a BUN to creatinine Funding
ratio model, which helps discriminate prerenal causes, such as None.
dehydration, from those intrinsic to the kidney itself. 82,83 Urea
helps to regulate fluid and sodium levels in conjunction with Disclaimer
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the kidneys. Normal BUN levels range from 5–20mg/dL. A The views expressed herein are those of the authors and do
reduction in BUN excretion can stem from dehydration, in- not reflect the official policy or position of Madigan Army
creasing serum levels disproportionately above that of serum Medical Center, US Army Institute of Surgical Research, the
creatinine. 83,84 Therefore, an elevated BUN/creatinine ratio US Army Medical Department, the US Army Office of the Sur-
greater than 20:1 is suggestive of prerenal azotemia, generally geon General, the Department of the Army, or the Department
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secondary to dehydration. However, medics should be aware of Defense of the US Government.

84 | JSOM Volume 22, Edition 2 / Summer 2022