Acute renal failure (ARF)
Acute renal failure (ARF) is an acute
suppression of renal function. The insult causing ARF equally and abruptly
disrupts the function of all nephrons without time for compensatory
mechanisms which are involved in chronic renal failure to "kick in".
ARF is contrasted with
chronic renal failure (CRF) in which there is a gradual death of
nephrons with the remaining nephrons functioning in a normal or supra normal
capacity. ARF is potentially reversible whereas CRF is a progressive and
irreversible condition.
Most (~80 to 90%) of ARF patients are oliguric. Oliguria is defined as
urine production of less than 0.5 ml/lb/hr (1 ml/kg/hr). ARF patients which
are polyuric (increased urine output) have sustained a lesser degree of
renal injury compared to oliguric patients and therefore have a better
prognosis. The damaged nephrons of ARF patients have reduced ability to form
glomerular filtrate from blood, resulting in less filtration of urea
nitrogen, creatinine, phosphorus and potassium leading to an increase of
these substances in the blood.
It is important to differentiate ARF from
prerenal azotemia. Both prerenal azotemia and ARF can be caused by
hypovolemia and uncorrected prerenal azotemia can progress to ARF. The more
severe and sustained the hypovolemia, the greater the probability that ARF
will occur. The kidneys are able to "autoregulate" renal blood flow (RBF)
and GFR to keep these parameters normal when mean arterial blood pressure is
greater than 70 mm Hg. Mean blood pressures lower than 70 mm Hg are
associated with reduction in renal blood flow and GFR. The prognosis for
prerenal azotemia is good if the underlying disease causing prerenal
azotemia is reversible. The prognosis for ARF is usually poor.
Urine specific gravity (USG) and urine
sodium concentration are parameters which can be used to
differentiate prerenal azotemia from ARF. The USG is concentrated and
urine sodium is low in patients with prerenal azotemia. The USG is
isosthenuric (1.007 - 1.017) and urine sodium is high in patients with ARF.
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Possible causes of ARF include:
- ischemic injury
- toxic or chemical insults
- infection
- glomerular diseases
ARF is most often caused by chemical insults (drugs or toxins) or by
ischemic injury to the kidney.
Ischemic injury: The kidneys are very active organs. In order to function
properly, the cells in the kidneys must be supplied with large amounts of
oxygen and nutrients via the blood. If blood flow to the kidneys is
diminished by hypovolemia, the kidney cells are "deprived" of oxygen and
nutrients which results in cellular death. The death of epithelial cells
lining the renal tubules is called "acute tubular necrosis" (ATN). The
causes of hypovolemia include the same causes as those resulting in
prerenal azotemia but the insults are more profound and sustained to
result in ARF. An additional cause of reduced renal blood flow which will
result in ARF is thrombosis of the renal arteries. Renal artery thrombosis
may occur as part of a generalized hypercoagulable state (e.g.
disseminated intravascular coagulation).
Toxic Injury
The kidneys are highly susceptible to injury from drugs and toxins.
20-25% of cardiac output each minute reaches the kidneys delivering large
amounts of any drug in circulation to the kidneys. The glomerular blood
vessels have a large endothelial surface for contact with drugs and drugs
may be concentrated in tubular fluid by the normal reabsorption of water
from the tubules. The kidneys contain enzymes that metabolize drugs and drug
metabolites may be more toxic than parent compounds.
Chemical injury may occur as a consequence
of either endogenous or exogenous toxins. The mechanisms of chemical-induced
renal injury include direct toxicity, hypersensitivity reaction, immune
mediated damage, precipitation of drug causing obstruction, or renal artery
vasoconstriction with resultant renal ischemia.
Endogenous endotoxins include:
-
Hypercalcemia is an uncommon cause of acute renal failure.
Hypercalcemic patients often have polyuria, polydipsia and dilute urine
but infrequently develop irreversible renal failure.
- hemoglobin from hemolysis,
- myoglobin from rhabdomyolysis (muscle breakdown).
Normal kidneys can excrete hemoglobin and myoglobin without damage but in
the face of concurrent dehydration, nephrotoxicity and ARF may occur.
Pre-existing renal disease or dehydration may enhance the effects of
toxins. Renal lesions may be reversible in days to weeks or may be
irreversible.
Drugs which are renally excreted need to have the dose or dose interval
altered to prevent accumulation of toxic levels of the drug in patients with
renal disease.
Exogenous toxins
Many drugs and
chemicals have the potential to produce nephrotoxicity. Follows is a partial
list of possible nephrotoxins. An individual animal can have an
idiosyncratic reaction to any drug with a possible consequence of renal
injury.
Analgesics
- NSAIDs (acetaminophen, ibuprofen, etc.)
- selective cyclooxygenase (COX) inhibitors
Antibiotics
- aminoglycosides (gentamicin, paromomycin, etc.)
- cephalosporins
- nafcillin
- polymyxin B
- sulfonamides
- tetracyclines
Antifungal
Chemotherapeutic agents
- adriamycin (doxorubicin) in cats
- cisplatin in dogs
Heavy metals
- lead
- mercury
- arsenicals
- thallium
- turpentine
Plants & Foods
Misc.
- penicillamine (chelating agent/immune modulator)
- cyclosporin (immunosuppressive)
- radiographic contrast agents
- ethylene glycol
- Vitamin D toxicosis such as calcipotriol a synthetic analog of
calcitriol present in the topical psoriasis medication, Dovonex.
- pesticides, herbicides and solvents
Nonsteroidal anti-inflammatory drugs (NSAIDs) and selective
cyclooxygenase (COX) inhibitors commonly used for management of joint pain
and perioperative pain are potentially nephrotoxic. Vasodilatory renal
prostaglandin's counterbalance the vasoconstrictor effects of other
endogenous substances. The use of NSAIDs may precipitate ARF in predisposed
patients by depressing production of vasodilator prostaglandin's, leading to
reduced renal blood flow. Conditions in which renal function is dependent on
prostaglandin synthesis include congestive heart failure, liver failure with
ascites, volume/salt depletion, general anesthesia, diuretic use,
diabetes mellitus, and renal disease. Gastrointestinal toxicity is more
often observed in dogs receiving NSAIDs than is renal failure but dogs are
more susceptible to renal damage from NSAIDs and COX-2 inhibitors than are
people due to differences in anatomy and distribution of COX-2 in kidney
tissues. GI ulcers often precede development of ARF.
Although all NSAIDs are potentially toxic most toxicities involve
ibuprofen and occur due to ingestion of excessive amounts or occur in
animals with pre existent disease.
Aminoglycoside toxicity. Although increased awareness, monitoring of drug
levels and use of safer antibiotics have significantly reduced the
occurrence of aminoglycoside toxicity, several atypical cases have been
reported either from topical absorption of gentamicin from large soft tissue
wounds or systemic absorption of oral paromomycin which is used in treatment
of trichomoniasis or cryptosporidiosis in cats.
References:
Nephrotoxicosis associated with topical administration of gentamicin in
a cat.
Acute renal failure in four cats treated with paromomycin.
Infectious diseases that may lead to ARF include:
- Pyelonephritis
- Babesiosis
- Borreliosis
- Leptospirosis
Leptospirosis is an uncommon disease but
seems to be re emerging with new serovars. Infection with L pomona and L
bratislava are most likely to result in ARF. Untreated bacterial
pyelonephritis is more likely to compromise renal function over time
resulting in CRF but can cause an abrupt disruption of function (ARF).
Glomerulonephropathy, which is usually immune mediated, can cause ARF
but more often if glomerular disease results in azotemia, there is a gradual
loss of renal function (CRF) rather than an abrupt decline in function
(ARF).
All the etiologies of ARF are additive. For example, if a patient with
bacterial pyelonephritis is treated with a nephrotoxic antibiotic and also
becomes dehydrated, that patient is at greater risk for developing ARF than
if only one of these conditions were present. (infection =
pyelonephritis + chemical insult = nephrotoxic antibiotic + ischemia =
dehydration)
Very young and very old animals are at greater risk for development of
ARF; the young because the kidneys are immature and the old because
pre-existent renal disease is likely present.
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Pathophysiology
There is a large body of work which has been performed in an attempt to
elucidate the mechanisms responsible for the reduction of GFR and urine flow
in ARF patients. Four major mechanisms are believed to be involved in the
initiation and maintenance of reduced GFR and reduced urine output.
- reduced renal blood flow/renal artery vasoconstriction
- intratubular obstruction
- backleak
- decreased glomerular permeability
Renal artery vasoconstriction leads to a reduction of renal blood flow.
Vasoconstriction can be catecholamine induced, caused by alteration of renal
prostaglandin activity (reduced vasodilatory prostaglandins or increased
vasoconstrictor prostaglandins), or the renal arteries may be occluded by
thrombi.
Renal tubules can be obstructed from cell debris as tubular epithelial
cells die from what ever insult is responsible for causing ARF. Drugs such
as sulfonamides can precipitate in the lumen of the tubules causing
obstruction. In experimental models of ARF, tubular obstruction appears to
play a minor role in the genesis of ARF as the debris deposited in the
tubular lumen can be "flushed" from the tubule with low pressures. Therefore
tubular debris is probably a consequence of low fluid flow through the
tubule rather than a cause of it.
The backleak theory is described as reabsorption of filtrate into blood
after leakage through damaged tubular epithelium.
Decreased glomerular permeability caused by swelling of endothelial or
epithelial cells which comprise the glomerulus may impair formation of
glomerular filtrate.
All 4 of these mechanisms may contribute to the development of oliguria
and accumulation of wastes in ARF patients.
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Clinical course
The clinical course of ARF proceeds through a sequence of overlapping
phases:
- initiation phase
- oliguric phase
- polyuric phase
- phase of functional recovery
The initiation phase is defined as the time from renal insult to
recognition of decreased GFR, decreased urine output and increased BUN and
creatinine. This phase lasts 1-2 days. As an example, suppose a cat is under
anesthesia for an exploratory surgery and becomes hypotensive during the
procedure due to blood loss, the hypotensive effects of anesthesia and
inadequate fluid administration. If hypotension is severe and not corrected,
the kidneys are deprived of blood with resultant death of tubular epithelial
cells. The BUN will not increase immediately and unless urine volume is
being measured, it will not be immediately detected that urine production is
decreasing. Within 1 to 2 days it will become apparent that the cat is in
acute renal failure with decreased USG, reduced urine output and increased
BUN.
The oliguric phase which is also called the maintenance phase, is the
period of time during which oliguria persists. Some ARF patients are never
oliguric. Whether an ARF patient is oliguric or polyuric probably reflects
the severity of insult which caused the ARF. This has been demonstrated in
rodents with chemical or ischemic induced ARF. The more severe the insult,
the lower the urine output. As the majority (80 to 90%) of ARF dogs and cats
become oliguric, it indicates that the situations which cause ARF in these
species are severe and correlates with the poor prognosis for ARF patients.
In those patients which can repair the renal damage, the oliguric phase
lasts 1-2 weeks. Many animals die or are euthanized during the oliguric
phase because of the poor prognosis. The most life-threatening consequences
of the oliguric phase include hyperkalemia and overzealous fluid therapy
resulting in overhydration.
The polyuric phase = high output phase = diuretic phase is characterized
by a progressive increase in urine volume in patients which were initially
oliguric. The patients still have an increased BUN and creatinine and
isosthenuric USG. The polyuric phase may indicate the beginning of renal
repair and return of function or may be indicative of a less severe insult
to the kidneys. Glomerular filtrate is entering tubules that are not fully
functional and are acting as simple conduits for fluid without performing
any work on the fluid. There are several causes for polyuria in these
patients:
- impaired tubular sodium reabsorption causing loss of sodium in the
urine
- excretion of solutes retained in the oliguric phase (small molecules
like urea are osmotically active)
- impaired response of tubular cells to ADH (nephrogenic diabetes
insipidus)
- medullary washout of solute (It requires tubular work to maintain a
hypertonic gradient in the renal interstitium)
- iatrogenic over hydration during the oliguric phase
During the polyuric phase, renal loss of sodium and water can be
substantial. If the patient can not drink enough to keep up with the renal
loss of water, they will dehydrate resulting in a prerenal insult
superimposed upon the already existent renal disease. Fluid therapy must be
diligently managed to prevent dehydration. This phase lasts a few days to
several weeks or longer.
The phase of functional recovery has neither a clearly defined beginning
or end. In patients capable of repairing the renal injury, BUN, creatinine,
and urine volume gradually return to normal. Concentrating ability is the
slowest to return. Permanent defects in concentration, acidification, or
permanent decreases in GFR may persist.
Some ARF patients progress to CRF.
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Diagnosis
The patient history, physical examination and laboratory data may all
support a diagnosis of ARF.
The history may provide a clue as to the cause of ARF. For example the
animal may have had recent anesthesia/surgery causing hypotension, may have
been receiving a drug which has the possibility of being nephrotoxic or may
be a free-roaming animal which has the potential for exposure to toxins such
as antifreeze. Patients with chronic renal failure may have a history of
polyuria and polydipsia and may abruptly decompensate, presenting in a
crisis like an ARF patient. CRF patients can sustain acute insults (ARF
super imposed upon CRF).
Physical examination often reveals a depressed, hypotensive, hypovolemic
and sometimes hypothermic patient. Hypovolemia is due to fluid loss in
vomitus and diarrhea and lack of intake and in some patients, hypovolemia is
the cause of ARF.
Given the acute nature of their disease, the patient is often in good
body condition compared to the chronic renal failure patient which may be in
poor body condition.
Fever may be present if ARF is from an
infectious cause such as acute pyelonephritis or leptospirosis. Tachypnea
may be observed and is present to eliminate CO2 to compensate for metabolic
acidosis.
Bradycardia may exist due to hyperkalemia but hyperkalemic patients may
have a normal heart rate. As the patients are usually hypovolemic and the
cardiac response to hypovolemia is to increase the heart rate, the two
opposing influences on heart rate may result in a normal heart rate.
The kidneys may palpate normal to large. Enlarged kidneys may be painful
when palpated as pain receptors in the capsule of the kidney are stretched
as the kidney enlarges.
The most common change in mentation is depression but seizures may occur
in terminal uremia or due to toxins such as ethylene glycol.
Hematology
The CBC often discloses increased total protein and PCV due to
hemoconcentration, unless blood loss caused hypovolemia and subsequent renal
failure in which case total protein and PCV are decreased. Platelet number
is normal but function is abnormal (thrombocytopathia). Thrombocytopathia is
due to the retention of a waste product which makes the platelets less
aggregable (less sticky). WBC is either normal or shows a stress response.
Uremia interferes with the function of WBC which may predispose ARF patients
to infection.
Chemistry
Biochemical analysis will show increased BUN and creatinine.
Sodium may be increased, decreased, or
normal and depends upon the type of dehydration that is present and upon any
previous fluid therapy. Dehydration in the ARF patient is primarily due to
losses in vomiting and diarrhea and to lack of intake. Gastrointestinal
losses of fluid contain electrolytes in addition to water in proportions
comparable to blood resulting in
isotonic dehydration. Therefore the proportion of electrolytes to water
in the blood remains close to normal even though the actual amount of water
and electrolytes is decreased compared to health. Sodium will be increased
if the patient has greater than normal insensible losses (respiratory) as
insensible losses contain primarily water and little electrolyte.
 |
Elevated potassium (hyperkalemia)
is often associated with oliguria. There may be cardiac disturbances
when K > 6.0 mEq/L. Normal intracellular K is 160 mEq/L. The normal
ICF to ECF ratio for K is 40:1. When ECF K increases, this ratio is
reduced. This elevates the normal resting membrane potential (RMP)
to a less negative state, creating partial depolarization of
myocardial cells. The action potential produced is weaker and the
spread of depolarization across the myocardium is slowed. |
Inorganic phosphorus is increased. Calcium
is usually normal early in ARF but may decrease within several days of
onset. Calcium may deposit in damaged muscle with extensive rhabdomyolysis
(muscle breakdown) (example "heat stroke" or crush injury) causing a rapid
decline in serum calcium. This is followed by hypercalcemia during recovery
as the calcium is mobilized from muscle. Calcium may be decreased in
ethylene glycol poisoning due to the formation of calcium oxalate. Rapid
correction of acidosis results in a decrease in ionized calcium and may
precipitate hypocalcemic tetany. If
hypercalcemia exists, the patient should be evaluated for the source of
the increased calcium which could be the cause of ARF (primary or
pseudohyperparathyroidism).
 |
The urinalysis may show signs of tubular dysfunction which
include isosthenuric specific gravity (1.007-1.017), proteinuria,
glucosuria, increased urine sodium, or casts. Crystals may disclose
the cause of ARF (e.g., calcium oxalate crystals of antifreeze
poisoning). |
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Radiology can be used to determine kidney size if size cannot be
determined from palpation. Kidneys are normal to large in patients with ARF
as compared to small kidneys in CRF. Ultrasound can also be used to assess
renal size. Contrast studies of the kidneys
(IVP) should not be performed simply to determine renal size. The quality of
the contrast study is influenced by renal function as normal kidneys will
concentrate the injected dye which delineates their structure. Inability to
concentrate the dye results in a poor quality contrast study in patients
with renal disease. Additionally, the contrast agent can be nephrotoxic.
Renal biopsy is not necessary to make a diagnosis of
ARF but may yield prognostic information. The cause of ARF may be determined
from renal biopsy, for example oxalate crystals are observed in the biopsy
of patients with antifreeze poisoning. If a patient is not responding to
therapy after 7 to 10 days, a biopsy may give clues as to the potential for
reversibility based on the severity of renal damage and evidence for repair.
Renal biopsy can be performed "blindly", using ultrasound guidance, via a
laparotomy or via laparoscopy. Risks associated with biopsy include bleeding
as uremic patients have abnormal platelet function, and hypovolemia if the
animal is sedated or anesthetized for biopsy. The risks versus benefits of
biopsy must be weighed carefully.
A fine needle aspirate performed in an awake animal can sometimes yield
information such as the presence of oxalate crystals, without the need to
perform a biopsy.
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Conservative therapy of the ARF
patient: Depending upon the degree of renal damage, the kidneys may repair
themselves. The goal of treatment is to sustain life while the pathologic
process in the kidneys heals itself. Management of the ARF patient is
divided into 2 phases; immediate care when you first see the patient and
maintenance encompassing both the oliguric and polyuric phases. Immediate
care includes:
- identify if possible, and eliminate the inciting cause
- correct fluid deficits (dehydration) in an attempt to reestablish
adequate renal perfusion
| Mini quiz: |
A 25 kg dog is 10% dehydrated based on physical parameters. What
volume of fluid is required to rehydrate this patient? |
Initially
the patient must be rehydrated and the amount of urine produced evaluated in
response to fluid administration.
KEEP WRITTEN RECORDS OF ALL FLUID INPUT AND OUTPUT.
Isotonic saline or a
polyionic solution such as LRS should be used for rehydration and the fluid
deficit replaced over 2-6 hours at a rate of 10-20 ml/kg/hr or faster if the
animal is hypovolemic. Avoid K+ containing fluids (such as LRS) if urine
output is diminished, unknown or if K+ is increased.
A fluid pump is useful to deliver large volumes of fluid rapidly.
Failure to induce urine production of at least 1/2 ml/lb/hour (1
ml/kg/hr) indicates either that fluid replacement is inadequate or the
presence of intrinsic renal failure. The patient must be closely monitored
for signs of fluid overload.
Monitoring may include:
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Diuretics may be administered if after fluid
replacement urine production is inadequate. The value of diuretics in
intrinsic renal failure is questionable but as a single dose of a diuretic
carries minimal risk, diuretics are frequently tried in oliguric patients.
Diuretics which may be used include:
- furosemide (lasix)
- mannitol
- hypertonic dextrose
Dextrose and mannitol are osmotic diuretics, drawing water from cells
into extracellular spaces. Both can cause vascular overload if diuresis does
not occur. Do not administer osmotic diuretics if the patient already shows
signs of fluid overload. Do not repeat osmotic diuretics if diuresis fails
to occur. If diuresis occurs, mannitol can be repeated every 4-6 hours for
24 hours. If urine output increases in response to hypertonic dextrose, it
can be continued for 1-2 days. Divide the dextrose dose into several
portions and alternate with 2-3 cycles of 3-5% body weight LRS or normal
saline to maintain urine output. Furosemide (lasix) is the diuretic of
choice if the patient is already showing signs of fluid overload.
Dopamine causes selective renal arterial vasodilatation when administered
at 2-5 ug/kg/min. Dopamine has a duration of action of a few minutes so it
is delivered as a constant drip in 5% dextrose. Dopamine potentiates the
effects of furosemide. Dopamine should not be used in conjunction with
metoclopramide as their actions antagonize one another. It has recently been
demonstrated that cats do not have renal dopamine receptors.
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Hyperkalemia is
life threatening due to negative effects on myocardial cells. About 90% of
body potassium is located within cells. As cells die in response to normal
catabolic processes, intracellular potassium is released into extracellular
fluid. Uremia is a state of accelerated catabolism resulting in a greater
rate of cellular breakdown and release of intracellular potassium into
blood. With impaired renal function potassium cannot be excreted and serum
levels rise rapidly. The immediate management of hyperkalemia is based on
antagonizing its cardiotoxic effects or by driving potassium back into cells
in order to "buy" time until potassium elimination through urine or feces
can be increased.
There are 3 intravenous treatments which can have immediate impact on the
negative cardiac effects of potassium:
- sodium bicarbonate
- glucose (0.5 g/kg) with or without regular insulin
- calcium gluconate
Sodium bicarbonate combines with hydrogen ions in ECF. This creates a
gradient for additional hydrogen ions to move out of cells, into ECF. As
hydrogen ions move out of cells, potassium ions move into the cells.
 |
As glucose moves into cells under the influence of insulin,
potassium "tags" along into the cells. Glucose can be administered
without insulin, depending upon endogenous insulin release from the
pancreas or regular insulin can be administered with glucose.
Regular insulin (crystalline) is very soluble and readily available.
Do not administer insulin without administrating glucose or
hypoglycemia will result. |
 |
Calcium counteracts the effects of hyperkalemia on the cardiac
conduction system by re establishing the normal resting membrane
potential of -90 MV. Calcium should be administered slowly over
5-10 minutes with electrocardiographic monitoring as calcium itself
can be cardiotoxic. Calcium chloride can be used instead of calcium
gluconate but use ~1/10 the dose. |
All 3 treatments have rapid effect but are of short duration lasting
about 30-60 minutes. They can be repeated.
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Infections
are common complications of ARF. Infection aggravates the catabolic state of
the uremic patient resulting in a faster rate of protein breakdown and
generation of nitrogen containing wastes and potassium. Indwelling
intravenous and urinary catheters used in the management of ARF patients are
convenient avenues for infection. Strict attention to aseptic technique in
catheter placement and management is essential. The benefits of catheters
must be weighed against risks.
If an infection develops care must be taken in selecting antibiotics that
are not nephrotoxic. If an antibiotic is eliminated from the body by the
kidneys the dose may need to be altered to prevent accumulation of the
antibiotic. The package insert for the drug is a good source of information
regarding the need to alter the dose in patients with impaired renal
function.
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Once the immediately life threatening consequences of ARF are addressed,
it becomes a "waiting game" to maintain the animal until it can be
determined whether renal function can be re established.
Maintenance includes:
- maintaining normal hydration
- maintaining normal potassium concentration
- acid- base balance
- providing nutrition
- controlling vomiting and hemorrhagic gastritis
Maintaining normal hydration: During the oliguric phase of ARF one of the
most serious potential complications is iatrogenic fluid overload. After the
initial correction of dehydration, fluid therapy consists of replacing
ongoing losses including:
- insensible loss from skin and
respiratory tract (approximately 10-12 ml/lb/day (hypotonic))
- urinary loss (estimated or measured -
isotonic)
- losses from vomiting and diarrhea
(estimated or measured -
isotonic)
Careful records need to be kept of fluid
intake, administration and losses.
The patient should be monitored frequently for signs of overhydration or
dehydration by looking at:
- packed cell volume and total protein
- central venous pressure (CVP)
- blood pressure
- skin turgor
- body weight. An anorexic patient should lose 0.1 to 0.3 kg / 1000
calories required per day. Once this loss is considered any gain or loss
of 1 kg body weight should be regarded as an excess or deficit of 1
liter of fluid.
Daily fluid administration should be divided rather than all at once to
allow for easier correction of over or under assessment of fluid balance. As
the patient enters the polyuric phase of ARF, exogenous fluid administration
must be increased to prevent hypovolemia.
Sodium and potassium losses during the polyuric phase of ARF may be
substantial and must be replaced. If it is necessary to administer potassium
it should be done slowly, no faster than 0.5 mEq/kg/hr.
During the oliguric phase, hyperkalemia must be prevented. Sodium
polystyrene sulphonate (kayexylate) is an ion exchange resin which exchanges
sodium for potassium in the intestinal tract resulting in removal of
potassium from the body. The exchange resin is administered orally at 2 g/kg
in 3 divided doses. It can also be given as a high enema if the animal is
vomiting and cannot take oral medications. If the exchange resin is
unsuccessful in controlling hyperkalemia, dialysis is necessary.
Acid Base status: Most ARF patients are acidotic. Bicarbonate is
indicated to reestablish acid-base balance if blood pH < 7.2. The following
formula can be used to determine the amount of bicarbonate to administer.
Body weight (kg) x 0.3 x base deficit = bicarbonate dose in mEq
A similar formula using (0.6 x base
deficit) assumes that the bicarbonate will be immediately distributed
through
total body water which actually requires about 24 hours. Using a more
conservative estimate to calculate bicarbonate dose (0.3 x base deficit) is
often sufficient to improve the patient's acid base status to a point where
the body's own buffer systems will re establish a closer to normal, acid
-base status.
Example: (10 kg canine)
pH = 7.20
pO2 = 88 mmHg
pCO2 = 31 mmHg
HCO3 = 11 mEq/L
Base excess (deficit) = -15
10 kg x 0.3 x -15 = 45 mEq of bicarbonate
To be even more conservative, administer
1/2 the calculated dose immediately and the other 1/2 over 12- 24 hours. The
goal is to "add to" the body's own buffering systems, not to rapidly change
acid-base status. Rapid correction of acidosis can result in a
decrease in ionized calcium by increasing the amount of calcium bound to
proteins and may precipitate hypocalcemic tetany. Rapid correction of
acidosis can also cause neurologic dysfunction through the development of
paradoxical CSF acidosis.
If it is not possible to measure blood gas values, the degree of acidosis
can be estimated based on the degree of uremia:
| Uremic state |
Estimated base deficit |
| mild |
-5 |
| moderate |
-10 |
| severe |
-15 |
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Nutrition: To decrease the level of azotemia, the rate of protein
catabolism should be decreased. Glucose has a sparing effect on protein
catabolism in the fasting individual. If the patient can take food orally,
diets should be comprised of high caloric density fats, carbohydrates and
small amounts of high biologic value protein. The fluid content of the diet
needs to be considered when calculating fluid intake. Anorexia and vomiting
frequently preclude oral alimentation. Total parenteral nutrition (TPN)
solutions may be administered IV. TPN solutions contain an energy
source, usually 30-50% glucose, and protein hydrolysate to provide essential
amino acids. TPN solutions which contain hypertonic dextrose are irritating
and must be administered in a large vein such as the jugular vein. Also see
critical notes about PPN (partial parenteral nutrition).
Hemorrhagic gastritis
Gastrin levels in the blood are elevated in
ARF due to reduced clearance. Gastrin directly stimulates H2 receptors on
parietal cells or stimulates mast cells to release histamine which
stimulates parietal cell H2 receptors with the result being HCL liberation
by the parietal cell. Parietal cells also have acetylcholine receptors on
their surface. Increased gastric acidity plus abnormal platelet function
causes mucosal irritation and hemorrhage.
The administration of an H2 blocker (cimetidine
= tagamet, ranitidine = zantac, famotadine = pepsid) reduces the severity of
hemorrhagic gastritis in uremic patients.
Anti emetics may also be used to control vomiting including
metoclopramide, dolesatron, trimethobenzamide (Tigan), chlorpromazine or
ondansetron. The kidneys excrete metoclopramide and the dose should be
decreased 50% in patients with severe renal disease.
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Drug elimination:
The kidneys provide the
major route of elimination for many pharmacologic agents so avoid the use of
any unnecessary drugs. If drugs are used which are renally excreted,
after the initial loading dose is administered either the drug dose or dose
interval must be altered to prevent accumulation of the drug and subsequent
intoxication. The drug package insert is a good source of information
regarding the use of the drug in patients with impaired renal function.
Prognosis:
The prognosis for most
ARF patients is poor. These patients are usually very ill, unstable and
difficult to manage. ARF patients that are polyuric are much easier to
manage and therefore have a better prognosis than the oliguric patient. The
presence of oliguria indicates a more severe renal insult. If conservative
measures are not successful in the treatment of an ARF patient
dialysis should be considered.
Last Edited: Jul 26, 2007 1:51 PM
