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Proceedings of the
57th Annual Convention of
the American Association of
Equine Practitioners
- AAEP November 18-22, 2011
San Antonio, Texas, USA
Next Meeting : Dec. 1-5, 2012 - Anaheim, CA, USA
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MEDICINE II
Review of Azotemia in Foals
Harold C. Schott II, DVM, PhD, Diplomate ACVIM
Author’s address: Department of Large Animal Clinical Sciences, College of Veterinary Medicine,
Michigan State University, East Lansing, MI 48824; e-mail: schott@cvm.msu.edu. © 2011 AAEP.
1.
Introduction
Azotemia in neonatal foals (ⱕ7 days of age) may be
an indicator of pre-renal failure, acute kidney injury
(AKI), obstructive disease, congenital renal disorders, or disruption of the collecting system leading to
uroperitoneum. Because clinical signs of renal failure may be similar to those with septicemia or asphyxia (weakness, recumbency, or poor nursing
vigor), performing a serum biochemical analysis in
compromised neonates is an essential part of the
minimum database to detect azotemia. Spurious
hypercreatininemia may also be a transient finding
in asphyxiated foals or foals delivered from mares
with placentitis.1 Neonates with spurious hypercreatininemia have normal serum electrolyte concentrations, supporting normal renal function, and
creatinine concentration, which may exceed 20 mg/
dL, typically drops by 50% or more over the first 1 to
2 days of life, as long as foals are well hydrated and
nursing well (Fig. 1). In older foals, azotemia and
renal failure are almost always a consequence of
another primary disease process, although limited
renal function with congenital anomalies may delay
onset of renal failure until foals are several years
old.
2.
Neonatal Renal Development and Physiology
Nephrogenesis, in terms of nephron numbers, is essentially complete at birth, and, as foals grow, the
kidneys increase in size through the first 1 to 2 years
of life. Foals are born with about 10 million glomeruli in each kidney, and these enlarge in size as the
kidneys grow.2 Of interest, low birth weight and
premature infants may be born with fewer
nephrons, and there is mounting evidence that this
reduced renal endowment may increase the risk of
developing hypertension and chronic kidney disease
(CKD) in later life.3
Normal term colts typically first urinate between
5 and 6 hours of age, whereas fillies initially urinate
later, at 10 to 11 hours of age.4 Initial urine may be
dilute or concentrated (specific gravity up to 1.040),
but hyposthenuria develops by 24 hours of age in all
foals that are nursing well. Urine pH is nearly
neutral, and significant proteinuria (2 to 3⫹ on reagent strips) is commonly observed from 24 to 48
hours of age in foals that received good passive
transfer of colostral antibodies.5 Serum urea nitrogen (BUN) and creatinine (Cr) concentrations are
variable during the initial 24 hours of life, with
values in the range of 15 to 30 mg/dL (⬃5–10
mmol/L) and 2 to 4 mg/dL (⬃175–350 ␮mol/L), respectively. BUN generally drops below the lower
limit of the adult reference range by 24 hours of age,
whereas Cr may not drop below 2 mg/dL until 48
hours of age. By 1 to 2 weeks of age, BUN is typically below 10 mg/dL (⬃3.5 mmol/L) and Cr may fall
below 1.0 mg/dL (⬃90 ␮mol/L). These low values
NOTES
328
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Renal tubular function remains essentially normal with pre-renal failure. Thus, serum electrolyte
concentrations are typically normal, and urine sodium concentration is ⬍20 mEq/L. Depending on
hydration status, urine specific gravity may be variable, but the classic finding that supports pre-renal
azotemia is a specific gravity ⱖ1.025 and a urine
osmolality (Uosm) exceeding 500 mOsm/kg.
serum creatinine (mg/dl)
25
20
a
15
a,b
10
4.
5
b,c
c
0
admission
day 2
day 3
day 4
Fig. 1. Decline in serum creatinine concentration in 28 equine
neonates that were admitted at 48 hours or less of age with a
serum concentration ⬎5 mg/dL attributed to spurious hypercreatininemia. Note the ⬎50% decline in serum creatinine concentration within the initial 24 hours of therapy (from admission to day
2).
can be attributed to the large volume of fluid intake
as milk (5-fold greater fluid intake as compared with
adult horses on a mL/kg basis) and associated diuresis that may persist for the first 3 to 4 months of life,
as long as foals continue nursing their dams.6
Renal function of neonatal foals, as assessed by
glomerular filtration rate (GFR), is similar to that of
adult horses.7,8 Further, the kidneys of foals are
capable of excreting a sodium load provided by fluid
administration,9 and fractional electrolyte clearance
values are similar to those of adult horses, supporting that renal tubular function in foals is similar to
that of adult horses.5
3.
Pre–Renal Failure
Renal hypoperfusion leading to pre-renal azotemia
is common in compromised neonates. Several compensatory mechanisms accompany decreased renal
perfusion to maintain renal blood flow and GFR over
a range of perfusion pressures (autoregulation).
These include a decrease in afferent arteriole tone
and intrarenal production of vasodilatory prostanoids (PGE2 and PGI2) to maintain blood flow, particularly in the medulla.10 Renal hypoperfusion
increases the risk of nonsteroidal anti-inflammatory
drugs (NSAID) associated AKI; for example, nearly
40% of premature infants that receive indomethacin
to speed closure of the ductus arteriosus develop
alterations in renal function.11 When the more selective COX-2 NSAIDs were initially introduced,
there was hope that they would be more sparing of
renal function than nonselective COX inhibitors.
However, it is now recognized that these newer
NSAIDs provide little benefit of limiting renal damage; thus, all NSAIDs should be used sparingly in
compromised foals.12
Intrinsic Renal Failure
Intrinsic renal disease and acute renal failure (ARF)
can develop as a consequence of hypoxic-ischemic
injury associated with birth asphyxia, septicemia,
or leptospirosis or treatment with nephrotoxic
medications (aminoglycoside antibiotics and
NSAIDs).11,13–17 It is often difficult to separate the
effects of these factors because many compromised
foals are routinely treated with nephrotoxic medications. Over the past decade, there has been a shift
away from routine use of penicillin and an aminoglycoside for broad-spectrum antimicrobial therapy
of neonatal foals (largely replaced by ceftiofur), and
this change has probably decreased the incidence of
aminoglycoside nephrotoxicity in foals. Further,
the shift away from multiple daily doses to oncedaily dosing regimens for aminoglycoside antibiotics
has been well documented to decrease the risk of
nephrotoxicity in infants.18 Unfortunately, during
the same time period there has been increased use of
oxytetracycline in foals with contracted tendons,
and tetracycline-associated ARF may go undetected
in compromised neonates unless a serum chemistry
profile is submitted as part of case management.
The incidence of ARF in foals in neonatal intensive
care units is not well documented, but human neonatal intensive care units have reported incidences
ranging from 6% to 24%, with cardiac surgery and
severe asphyxia being recognized risk factors. Of
interest, ARF was nonoliguric, oliguric, and anuric
in 60%, 25%, and 15% of patients, respectively.11
Consequently, adequate urine production cannot be
used to exclude AKI and ARF in compromised
equine neonates.
Although there are no specific values for BUN and
Cr that separate pre-renal failure from intrinsic renal failure, azotemia is generally greater with intrinsic renal failure. Further, there is not a sudden
transition from pre-renal failure to intrinsic renal
failure; rather, these are overlapping conditions.
To emphasize the point that some intrinsic renal
damage probably occurs with simple renal hypoperfusion, the term acute kidney injury, characterized
by a 50% increase in Cr, has been introduced to
describe early damage with intrinsic renal disease.19
This predominantly tubular damage may be characterized by proteinuria, microscopic hematuria, glucosuria, increased urine sodium and chloride
concentrations and excretion, increased urinary enzyme activities, and detection of novel biomarkers of
tubular epithelial damage in urine (kidney injury
molecule 1 and others). Examination of urine sedAAEP PROCEEDINGS Ⲑ Vol. 57 Ⲑ 2011
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MEDICINE II
iment may also reveal hyaline or granular casts.
These urinary changes can develop a few days before
onset of significant azotemia.
With both pre-renal and renal azotemia, acute
changes are better assessed by the comparatively
greater increase in Cr than BUN, due to the larger
size of Cr that slows its diffusion out of the extracellular fluid (ECF) space. Thus, following changes
in Cr over time is more reliable for assessment of
changes in renal function than is monitoring BUN.
However, it warrants emphasis that increases in Cr
are insensitive for detection early changes in renal
function (GFR must decrease by 75% or more before
azotemia develops). Further, an occasional foal
may have a more marked increase in BUN than Cr,
and, in such cases, upper intestinal ulceration with
blood loss into the intestine should be considered as
a potential cause for the increase in BUN. Next,
another simple question to ask is whether or not
acid-base status and serum electrolyte concentrations are normal. These parameters typically remain normal with pre-renal azotemia, whereas
alterations are common with intrinsic renal failure
(hyponatremia, hypochloremia, hyperkalemia, and
metabolic acidosis). A final hallmark of tubular
damage associated with AKI and intrinsic renal failure is loss of concentrating ability. Urine of affected foals is typically hyposthenuric (specific
gravity ⬍1.008 and Uosm ⬍300 mOsm/kg).
With AKI and intrinsic renal failure, it is important to determine whether or not affected neonates
are oliguric (urine output ⬍0.5–1 mL/kg/h) because
oliguric AKI carries a more guarded prognosis than
does nonoliguric AKI.11 However, most cases in
neonates are nonoliguric, and these may only be
detected by finding a progressive increase in Cr with
serial serum biochemical analyses. Fortunately,
neonatal kidneys are forgiving, and treatment can
sometimes be successful with anuria/oliguria lasting
up to 72 hours. Dialysis, either peritoneal or hemodialysis, is also feasible in foals as compared with
full-sized adult horses when anuria/oliguria persists.20,21 However, recent reports of peritoneal dialysis as a treatment for oliguric renal failure in
horses are not without controversy, as careful review of the reports reveals that urine output was not
well documented22 and that Cr had already begun to
decline before dialysis was initiated.21 The main
challenge of treating patients with anuric/oliguric
renal failure is not to control Cr; rather, it is to
maintain acid-base balance and serum electrolyte
concentrations within reasonable ranges while renal
tissue is repaired and urine production returns.
Of interest, recent evidence in management of ARF
in people provides further support for cautious IV
fluid support of compromised foals (so-called “running them dry”) because excessive fluid replacement
may increase intrarenal pressure and further compromise restoration of renal function.23
330
5.
Post-Renal Failure
Azotemia arising from disruption of the urinary
tract typically occurs in the face of nearly normal
kidney function, but failure to eliminate urine leads
to progressive abdominal distension and electrolyte
alterations. Hyponatremia, hypochloremia, and
hyperkalemia develop with “mixing” or “dialysis” of
the expanded peritoneal fluid compartment with the
remainder of the ECF compartment, including
plasma.24 Again, because Cr does not diffuse out of
the ECF compartment as rapidly as urea, finding a
peritoneal fluid Cr to serum Cr ratio ⬎2 is the clinicopathologic test of choice to confirm uroperitoneum. However, this test is being performed less
frequently than in the past because detection of a
large volume of hypoechic fluid within the abdomen
via transabdominal ultrasonography is essentially a
pathognomonic finding in foals with electrolyte alterations expected with uroabdomen.
The classic case of uroperitoneum occurs in 2- to
3-day-old colts that develop abdominal distension
consequent to a dorsal bladder wall tear sustained
as they pass through the pelvic canal with a full
bladder.24 However, silent uroabdomen can also
develop in compromised neonates in intensive care
units, especially when they are unable to stand and
void urine normally. Uroabdomen in these foals
may develop as a consequence of bladder distension
and leakage/rupture or can be due to a small leak in
association with sepsis of the urachus.25,26 Uroabdomen in these foals may not become a problem
until 4 to 7 days of age and is often first detected as
an increase in free abdominal fluid during routine
transabdominal ultrasonographic monitoring of sick
neonates to assess intestinal motility and bladder
size. At initial suspicion of uroabdomen, enough
time may not have elapsed for electrolyte alterations
to develop (or they may be attenuated by concurrent
IV fluid therapy), but uroperitoneum can be confirmed by comparing peritoneal fluid Cr to serum Cr.
Finally, another cause of “late onset” uroperitoneum
can be a ruptured ureter. Most ureteral leaks occur
near the kidney and may be associated with blunt
abdominal trauma during parturition or after
birth.27 The author has seen several cases of ureteral leakage in foals with multiple rib fractures,
supporting birth trauma and possible delivery with
the mare in a standing position as potential risk
factors. Urine initially accumulates more slowly in
the retroperitoneal space until it ruptures into the
peritoneal cavity. Further, with unilateral ureteral rupture, the bladder continues to fill from the
contralateral side and normal urination may still be
observed.
6.
Congenital Disorders
Anomalies of renal development reported in foals
include agenesis/aplasia, hypoplasia, dysplasia, and
polycystic kidney disease (PCKD).28 Although
present at birth, anomalies may not lead to azotemia
and renal failure until later in life, especially renal
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Fig. 2. Ultrasonographic appearance of a normal left kidney of an approximately 50 kg neonatal foal acquired transabdominally with
the probe placed on the left paralumbar fossa (left) or under the last few ribs and directed dorsomedially (right); length is ⬃10 cm and
renal parenchyma is hypoechoic when compared with the spleen; the renal medulla is also more hypoechoic than the cortex.
hypoplasia or PCKD. For example, the author diagnosed PCKD as the cause of CKD in a 19-year-old
Arabian mare. Anomalies of the collecting system
such as ureteral ectopia do not typically cause renal
failure and azotemia unless complicated by obstruction or ascending urinary tract infection. Megavesica, or a markedly enlarged bladder, has been
described in several foals in association with suspected urachal obstruction and can cause post-renal
failure and abdominal distension (due to the large
bladder) without actual disruption of the urinary
tract.29
7.
Evaluation and Management of Azotemia
When azotemia is detected in a neonatal foal, repeating the physical examination may detect subtle
findings that may not have been appreciated during
the initial exam. For example, mild edema or
“looseness” of the skin in the axillary and inguinal
regions may be appreciated with oliguria, and foals
with hyperkalemia may have fine muscle tremors
that may be easier to feel than to see. Evidence of
incontinence may support ectopic ureter, and moistness of the umbilicus may support localized sepsis
that may lead to subcutaneous urine accumulation
and/or uroperitoneum. In addition to physical examination and a clinicopathologic database, abdominal ultrasonography should be a standard part of
the work-up of neonatal foals. With regard to the
urinary system, the first question to answer is
whether or not the foal actually has two kidneys
that are of normal shape and size (about 5 ⫻ 10 cm
for a 50-kg foal, Fig. 2).30 Foals that have nursed
well or that have been started on IV fluid support
and are producing adequate urine often have mild
distension (to 1–1.5 cm) of the renal pelvis (Fig. 3),
but this should be a symmetrical finding in both
kidneys. Next, the bladder should be imaged to
determine whether it is small (supporting oliguria)
or possibly larger than normal (supporting intrauterine urachal obstruction or lack of detrusor tone).
If the bladder is larger than 10 cm in diameter and
urination is not observed within 30 to 60 minutes
after this finding, a catheter should be passed to
collect a urine sample and to empty the bladder.
Indwelling bladder catheters with closed collection
systems are being used more frequently in recumbent neonates and are certainly helpful in documenting rate of urine production. However, even
well-managed catheters are commonly colonized
with multidrug resistance bacterial spp.; thus,
short-term use (⬍3 days) is the goal and prophylactic antimicrobial treatment is warranted.
One of the hallmark treatments of azotemia is
supportive fluid therapy. However, the approach
should err on the side of caution. For example,
with pre-renal azotemia and spurious hypercreatininemia, fluid support can often be limited to enteral milk feeding or close observation to ensure
adequate nursing. With milk alone provided at
10% or more of body weight daily, foals will be receiving a fluid intake at a rate more than adequate
for maintaining hydration. Although adequate nutritional support with enteral milk feeding can be
accomplished in all neonates that tolerate milk feedings, it is important to remember that foals will
produce dilute urine (specific gravity ⱕ1.005) when
fed either 10% or 20% of body weight daily as milk.
However, they will produce a greater amount of
dilute urine when they are fed more. Thus, assessment of body weight gain daily is a superior method
of assessing adequacy of either nursing or enteral
feeding, as compared with only measuring urine
specific gravity. When enteral feeding is not tolerated well and/or when acid-base balance or serum
electrolyte concentrations are altered, judicious IV
fluid therapy support may also be required. A potassium-free IV fluid (0.9% saline solution) should
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Fig. 3. Ultrasonographic appearance of normal kidneys of equine neonates receiving IV fluids showing distension of the renal pelvis
to nearly 2 cm in diameter.
be used when significant hyperkalemia (⬎5.5
mEq/L) is present, whereas a polyionic replacement
fluid can be used when potassium concentration is
not elevated. The goal should be to limit fluid replacement to maintenance to 1.5 times maintenance
requirements (1.0 –1.5 mL/kg/h), and patients on IV
fluids should be monitored twice daily for development of edema and body weight change. Urine production can also be monitored with an indwelling
collection system, and central venous pressure
(CVP) can be monitored via the jugular venous catheter placed for fluid administration (as the catheter
end is often near or in the right atrium). Ideally,
CVP should be maintained below 10 cm H2O. Further, the enteral route, when it is working, can also
be used for administration of sodium chloride, sodium bicarbonate, potassium chloride, or potassium
bicarbonate. Once foals are tolerating enteral feeding well or are nursing adequately, they will have a
fluid intake that may be 3 to 5 times maintenance
requirements, and there is little benefit of additional
IV fluids. The resultant diuresis is generally adequate for resolution of azotemia, as long as damaged
renal tissue undergoes repair. Thus, IV fluid therapy does not need to be continued until azotemia has
fully resolved and can often be stopped once Cr
concentration has stabilized at values ⬍2.5 to 3
mg/dL (⬃250 ␮mol/L), although Cr concentration
should be measured again 1 to 2 days after discontinuing IV fluids to make sure that it is not increasing again. What is difficult (or impossible) to know
at the start of therapy is what the final Cr will be
after repair of damaged renal tissue. Many cases
will have Cr return to values within the reference
range within 5 to 10 days, whereas others will be
discharged with persistent elevations in Cr. In the
latter cases, Cr should be monitored at monthly
332
intervals and may still return to normal values over
1 to 3 months.
In foals with oliguric ARF, judicious fluid therapy
is even more critical to prevent volume overload.
Although efficacy remains unproven, furosemide
(1–3 mg/kg, q 2 hours, IV) may be used in an attempt
to increase urine flow rate. If no effect is observed,
mannitol (0.25–1.0 g/kg, IV) has also been used as
an osmotic diuretic but, again, supportive data are
lacking in foals, and this treatment has fallen out of
favor in human medicine. Similarly, use of a dopamine infusion in an attempt to increase renal blood
flow is no longer recommended in human medicine
because of the potential for development of arrhythmias and a lack of data substantiating improved
long-term outcome.31 Despite the lack of clinical
evidence for treatment of anuric or oliguric ARF,
continuous rate infusion of pressor agents, including
dopamine, norepinephrine, or dobutamine, may be
of benefit to foals with systemic hypotension, as part
of the overall neonatal supportive care although the
electrocardiogram (ECG) should be closely monitored during use of these drugs.32 Finally, peritoneal dialysis can be considered with refractory
oliguria and worsening azotemia. The goals of dialysis are to both correct electrolyte alterations and
acid-base status along with controlling azotemia,
but a more guarded prognosis should always be issued for owner consideration before this more invasive treatment is pursued.
Surgical correction of urinary tract disruption is
generally the treatment of choice for uroabdomen,
although small bladder rents may heal with placement of an indwelling bladder catheter alone.33
With uroabdomen, large volumes of urine in the
abdomen may compromise ventilation, and moderate to severe hyperkalemia (⬎6.5–7.0 mEq/L) may
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MEDICINE II
men is probably as important as fluid therapy in
overall management of hyperkalemia; thus, drainage should not be delayed while attempting to decrease serum potassium concentration. Once
affected neonates have been stabilized and serum
potassium concentration is ⬍5.5 mEq/L, surgical
correction of urinary tract disruption can usually be
safely pursued.
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Fig. 4. Drainage of uroabdomen in a foal, using a 16F trocar
chest tube.
cause life-threatening cardiac arrhythmias. Thus,
affected neonates must be stabilized before surgical
treatment is pursued. Drainage of accumulated
urine is indicated but can be challenging. The author prefers using a small trocar chest tube (16F),
placed abaxial to the linea alba (Fig. 4), over a teat
cannula or bitch catheter to allow more rapid removal of urine from the abdomen. Multiple holes
in the chest tube also make occlusion with omentum
or mesentery less of a problem.
Immediate treatment of hyperkalemia is directed
at membrane stabilization by administration of potassium-free IV fluids supplemented with calcium
and dextrose over 30 to 60 minutes (e.g., by addition
of 50 mL of a 23% calcium boroguconate solution and
200 mL of a 50% dextrose solution to 1 L of 0.9%
NaCl, after initially discarding 100 –200 mL of the
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the ECG may remain normal in some patients with
severe hyperkalemia.34 In foals with uroabdomen,
drainage of urine that has accumulated in the abdo-
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2011 Ⲑ Vol. 57 Ⲑ AAEP PROCEEDINGS
Proceedings of the AAEP Annual Convention, San Antonio, TX, USA - November 18 - 22, 2011