Page 507 - ACCCN's Critical Care Nursing

484 P R I N C I P L E S A N D P R A C T I C E O F C R I T I C A L C A R E

short term (1–2 hours), nephrons remain structurally within the kidney, therefore reducing glomerular filtra-
normal and respond by limiting fluid lost by urine tion activity and affecting the reabsorption and diffusive
production while concentrating the excretion of waste process of the nephron. This reduction in blood flow is
products. The physiological process combines the neuro- exacerbated by degenerative vessel obstruction with ath-
endocrine control of the hypothalamus and the sympa- eromatous plaque, particularly pronounced in diabetic
thomimetic response, which then regulates both patients due to ineffective glucose metabolism. Diabetic
antidiuretic hormone secretion and the stimulation of patients are more likely to develop ARF associated with
the renin–angiotensin–aldosterone system (see Figure medical care in hospital from what may otherwise seem
18.4). This process is highly influenced by any preexisting to be a relatively trivial insult to the kidneys in a younger,
illness or concurrent factors such as diabetes and systemic healthy patient. The event may be enough to trigger ARF
infection. 12 in these patients, as they lack any degree of ‘renal reserve’
or tolerance to events such as low blood pressure or
INTRARENAL (INTRINSIC) CAUSES administration of nephrotoxic drugs normally filtered by
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Intrinsic damage to the nephron structure and function the kidneys.
can be due to infective or inflammatory illness, toxic
drugs, toxic wastes from systemic inflammation in sepsis, POSTRENAL CAUSES
vascular obstructive thrombus or emboli. In differentiat- Urinary tract obstruction is the primary postrenal cause
ing this type of ARF, a process of elimination has been of ARF, and is uncommon in the critical care setting as it
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suggested where failure of kidney function persists after is rarely associated with acute onset renal failure. Postre-
the restoration of adequate perfusion (blood flow), or nal obstruction is more common in the community and
where no loss of perfusion has occurred, and there is no is associated with urological disorders such as prostate
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obstruction to urine flow. Diagnosis is made by exclu- gland enlargement in males, urinary tract tumours and
sion of other causes. The common causes of this type of renal calculi formation impairing urine outflow. It is
ARF, glomerulonephritis, nephrotoxicity and chronic vas- essential that blockage of any urinary drainage device be
cular insufficiency, are discussed below. excluded in the critically ill patient when undertaking an
assessment of apparent oliguria.
Glomerulonephritis
This condition is caused by either an infective or a non- ACUTE TUBULAR NECROSIS AND
infective inflammatory process damaging the glomerular ACUTE KIDNEY INJURY
membrane or a systemic autoimmune illness attacking Intrinsic ARF (described above) is often associated with
the membrane. Either cause results in a loss of glomeru- typical microscopic changes on pathology examination
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lar membrane integrity, allowing larger blood compo- of kidney tissue. This pathology is termed acute tubular
nents such as plasma proteins and white blood cells to necrosis (ATN), and possibly explains how and why, in
cross the glomerular basement membrane. This causes a the acute setting, kidneys can fail abruptly to minimal to
loss of blood protein, tubular congestion and failure of no function (no urine output and therefore no waste
normal nephron activity. Resolution is based on treating clearance), and can then after a period of time, with arti-
the cause, such as an infection or autoimmune inflam- ficial support, recover to normal function in many
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matory illness. 16 patients. This is an interesting area for current research
into the mechanisms responsible for acute kidney failure
Nephrotoxicity that are yet to be fully understood.
Nephrotoxicity occurs as a result of damage to nephron Acute tubular necrosis describes damage to the tubular
cells from a wide range of agents, including many drugs portion of the nephron and may range from subtle meta-
used in critical care (e.g. antibiotics, anti-inflammatory bolic changes to total dissolution of cell structure, with
agents, cancer drugs, radio-opaque dyes). Toxic prod- tubular cells ‘defoliating’ or detaching from the tubule
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ucts of muscle breakdown in severe illness and trauma, basement membrane. Most ARF is multifactorial in
commonly called Rhabdomyolysis (see Chapter 23 for origin and may involve more than one causative mecha-
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trauma association), 4,13,18 blood product administration nism and is not always an ischaemic or necrotic event.
reactions and blood cell damage associated with major In critical illness, the most common combination causing
surgery are also causative agents. As these agents may ARF is the administration of nephrotoxic agents in
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often be given concurrently, a cumulative effect, along association with prolonged hypoperfusion or ischaemia
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with intermittent falls in renal perfusion, may result in (oxygen deprivation). This type of tubular necrosis can
the development of intrinsic ARF. be further mediated by infection, blood transfusion reac-
tions, drugs, ingested toxins and poisons, or be a compli-
Vascular Insufficiency cation of heart failure or major cardiovascular surgery.
One-third of patients who develop ARF in the ICU have The initial insult can also be compounded by metabolic
disturbances and subsequent systemic infection.
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chronic renal dysfunction. This chronic dysfunction
may be undiagnosed prior to the critical illness, and may ATN is the causative mechanism for up to 30% of acute
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be related to diabetes, the ageing process and/or long- kidney failure in the intensive care setting, with the
term hypertension. These factors create a reduction in precise causative illness not easily identifiable in critically
both large and microvasculature blood flow into and ill patients with multiple co-morbidities, for example