2. Must know Must do
• Must know
• Causes, types and management of ARF
• List of commonly used drugs, including
antibiotics and analgesics, known to cause
renal damage
• Principles of renal replacement therapy
3. Must do
• Clerk patients with chronic renal
disease/failure
• Follow patients being treated for ARF
• Become familiar with the biochemistry of
renal failure
4. Must do
• Become proficient in catheterizing male and
female patients
• Observe patients undergoing haemodialysis
and haemofiltration
• Observe cadaveric-donor and living-donor-
related renal transplantation
6. • Acute renal failure (ARF) is defined as the
rapid onset of renal impairment resulting in
the accumulation of nitrogenous waste
products, i.e. urea and creatinine, within the
body.
7. Causes of irreversibility
• 1-Pre-existing renal damage (acute-on-chronic
renal failure)
• 2-Irreversible damage
• 3-Delays in treatment
8. ATN/ ARF
• Acute tubular necrosis (ATN) is used to denote
ARF where there is intrinsic but reversible
damage to the kidney.
9. Sudden anuria or oliguria
• ARF commonly presents with sudden anuria
(no urine) or oliguria (< 400 mL/day).
10. Non-oliguric renal failure
• Non-oliguric renal failure may also occur and
is recognized by a persistently rising serum
creatinine level in the presence of normal
output of urine.
16. The causes of prerenal ARF
• Reduced cardiac output
• Acute myocardial infarction
• Cardiac arrest
• Cardiac failure
• Significant valvular disease
• Cardiac tamponade
• Depleted circulating volume
• Sepsis
• Haemorrhage
• Hypoalbuminaemia
• Depleted extracellular fluid volume
• Loss from gastrointestinal tract with diarrhoea, vomiting
• Loss from urinary tract due to excessive diuresis
• Loss from skin/body surface associated with sweating and
• Burns
• Vascular disease
• Renal artery thrombosis/embolism
17. Prerenal ARF
• Prerenal ARF can progress to ATN (intrinsic
ARF) if the underlying cause is not reversed
promptly, although instrinsic ARF may arise
directly from other causes
18. Postrenal failure
• Postrenal failure, which results from
obstruction to urinary flow, is categorized as
obstructive uropathy
• When the kidney is obstructed, glomerular
function does not cease completely because
the filtrate is reabsorbed by the renal
lymphatics and veins.
19. Postrenal failure
• Unrelieved, obstruction leads to ischaemic
renal damage mediated by vasoactive
hormones including renin, angiotensin,
endothelin, etc.
20. Postrenal failure
• Return to useful function depends on
duration/degree of obstruction and the
presence/absence of infection above the
obstruction.
21. Postrenal failure
• Following relief of obstruction, recovery of
tubular function lags behind restoration of
glomerular filtration rate (GFR), resulting in a
diuresis.
23. Inadequate/delayed treatment of
prerenal acute renal failure
• Most common cause in surgical practice:-
• 1-Ischaemia and toxin
• 2-Hypercalcaemia
• 3-Hepatorenal syndrome
31. ARF/ Shock/↓RBF
• ARF may occur as a consequence of shock.
• The reduction in circulating blood volume
produces a significant decrease in renal blood
flow, which may fall to one-third of its normal
level
32. ↓GFR
• The GFR is correspondingly reduced and the
patient becomes oliguric, producing only 400-
700 ml of urine per 24 h, or less than 20 mL/h.
• When oligaemic states cause a reduction in
renal blood flow, additional changes take
place.
33. ↓↓↓GFR
• There is a diversion of blood from the renal
cortex and this exacerbates the situation by
causing a further reduction in GFR
34. ↓RBF of Brief Duration
• If the impairment in renal blood flow is of
brief duration and blood volume is restored
rapidly, the condition can be reversed and
normal urine output resumed, although
sometimes there is a lapse of some hours
before this takes place
35. Prolonged ischaemic insult
• A more prolonged ischaemic insult causes
ATN, with oliguria persisting for 1 to 3 or 4
weeks, followed by a period of diuresis when
large volumes of dilute urine are passed each
day.
36. Profound Ischaemia
• More profound ischaemia gives rise to cortical
necrosis, an irreversible condition requiring
renal dialysis and eventually renal transplant
37. • Once ARF becomes established, serious water
and electrolyte disturbances occur
38. Oliguric Phase
• During the oliguric phase, water retention
with a relatively low Na+ may precipitate
cardiac failure, accompanied by pulmonary
and systemic oedema.
• The degree of dyspnoea may be sufficiently
severe to warrant ventilatory support.
39. Arrhythmias→ Cardiac arrest
• Inability to excrete K+ leads to dangerously
high plasma levels, which may give rise to
arrhythmias and, if uncontrolled, to cardiac
arrest.
40. Retention of H+ ions
• Retention of H+ ions precipitates metabolic
acidosis.
• At first, hyperventilation and respiratory
alkalosis compensate for this but these
mechanisms eventually fail and the pH of the
blood falls rapidly.
• This phase may be exacerbated by respiratory
failure and a developing lactic acidosis.
41. Retention of H+ ions
• Both the blood urea and serum creatinine
levels progressively increase and calcium
levels may fall.
48. Dyspnoea
• • Dyspnoea is a frequent problem and in
some patients respiratory failure may require
intermittent positive pressure ventilation
• The respiratory problems are due to fluid
retention, with fluid overload giving rise to
pulmonary as well as systemic oedema
• Metabolic acidosis and pulmonary infection
may contribute further to the respiratory
difficulties.
49. Hypertension
• • Hypertension may be a consequence of fluid
overload and retention of K+ may give rise to
arrhythmias.
50. Gastrointestinal symptoms
• Gastrointestinal symptoms range from
nausea and vomiting due to water intoxication
to hiccups and diarrhoea, which frequently
accompany uraemia.
• Stress ulceration and gastric erosions are
common with ARF following shock, and
gastrointestinal haemorrhage may be severe
51. Cerebral Edema
• • Cerebral oedema and toxic metabolites
cause :-
• Confusion
• Drowsiness
• Eventually coma
52. A progressive anaemia
• • A progressive anaemia may develop and
coagulation defects may occur.
• Disseminated intravascular coagulation is a
not uncommon development.
53. Generalized impairment of the
immune system
• Finally, there is a generalized impairment of
the immune system, increasing the risk of
serious infection, which is probably the
commonest cause of death in ARF.
• The indiscriminate use of antibiotics
exacerbates this risk by promoting the
development of resistant strains of pathogenic
bacteria.
57. Prevention
• Prevention ARF may be prevented by careful
attention to
• 1- Preoperative fluid balance
• 2- Proper monitoring of the patient
peroperatively
• 3- Avoidance of hypotension and sepsis.
58. Prevention
• Patients at risk of developing renal failure, e.g.
those with obstructive jaundice, should have
an intravenous infusion established the night
before surgery so that they are well hydrated.
59. Prevention
• Remember that patients are starved prior to
surgery and will not be allowed oral fluids for
about 12 h (but often longer) before surgery.
60. Prevention
• Patients undergoing major surgery should
have a urinary catheter for hourly
measurement of urine output during surgery
and in the postoperative period.
61. Prevention
• A central venous line and arterial line are
usually inserted by the anaesthetist for
haemodynamic monitoring
62. Drugs avoid renal failure
• Some drugs may help to avoid renal failure in
certain situations.
• Dopamine, which at low doses (< 5 ug/kg per
min) induces vasodilatation and increased renal
perfusion, is frequently given to at-risk patients in
an attempt to preserve renal function.
• Mannitol, an osmotic diuretic, may also protect
renal function in some patients, such as those
with obstructive jaundice or those at risk of
rhabdomyolysis (e.g. following arterial
embolectomy).
63. Patients receiving nephrotoxic drugs
• Patients receiving known nephrotoxic drugs
should have their renal function monitored
regularly.
64. Patients receiving nephrotoxic drugs
• In the case of aminoglycosides, plasma
concentrations should be measured 1 h after
intramuscular or intravenous administration
and just prior to the administration of the next
dose.
• This ensures that excessive and
subtherapeutic doses are avoided.
65. Patients receiving nephrotoxic drugs
• For gentamicin, the peak level should not
exceed 10 mg/L, while the trough level should
be less than 2 mg/L.
66. Conservative Treatment
• Identification and correction/removal of the
cause is essential and any sepsis treated with
a third-generation cephalosporin in the first
instance.
• In oliguric patients with adequate circulating
volume, intravenous diuretic is administered
and may promote a diuresis.
• Removal of obstruction is necessary in
obstructive anuria.
67. • Conservative management of intrinsic renal
failure is only possible when the patient's
condition is not so severe as to warrant
immediate renal replacement therapy (RRT).
68. Conservative management consists of:
• Restriction of fluid intake to cover daily estimated
losses (insensible perspiration and stools);
• Restriction of first-class protein to 30 g/day to
reduce nausea and anorexia;
• Restriction of potassium intake to 20 mmol/day
to minimize risk of hyperkalaemia
• Correction of biochemical abnormalities
• Maintenance of adequate nutrition, including
parenteral nutrition (if required)
69. Conservative management consists of:
• Hyperkalaemia is the most serious
biochemical abnormality since it can cause
cardiac arrhythmias and sudden death.
• Prompt detection and treatment are thus
essential
70. Treatment of hyperkalaemia
• Calcium gluconate or chloride of 10% 10-20
ml i.v.
• Dextrose 50% 50 ml of i.v. with 10 units of
soluble insulin
• Sodium bicarbonate of 1.4% 200-300 ml i.v.
• Calcium resonium 15 g three times daily orally
or by enema
• Dialysis
71. Treatment of hyperkalaemia
• 10-20 ml of 10% calcium gluconate or chloride
i.v.: has no effect on the serum potassium
concentration but stabilizes the myocardial
membrane
72. Treatment of hyperkalaemia
• 50 ml of 50% dextrose i.v. with 10 units of
soluble insulin:-
• drives potassium into the cells and should be
started directly after step 1
73. Treatment of hyperkalaemia
• 200-300 ml of 1.4% sodium bicarbonate i.v.:-
drives potassium into cells and helps to
correct the acidosis of acute renal failure.
• However, the fluid load necessary makes use
of this agent less desirable in hyperkalaemic
acute renal failure
74. Treatment of hyperkalaemia
• Calcium resonium 15 g three times daily orally
or by enema:-
• binds potassium in the gut and releases
calcium in exchange.
• Unlike the other actions listed this can control
the serum potassium for hours to days
75. Treatment of hyperkalaemia
• Dialysis: should be implemented if there is
severe hyperkalaemia and/or the patient
requires dialysis for other reasons, e.g. fluid
overload
77. RRT
• Abnormalities of potassium, calcium and
phosphate can be corrected by the various
forms of RRT using dialysate or replacement
solutions
78. The Indications For RRT
• • Uraemia (significant retention of
nitrogenous waste products with associated
clinical signs)
• • Metabolic acidosis
• • Hyperkalaemia
• • Significant fluid overload
79. Type of therapy
• Treatment for the majority of patients with
ARF requires adequate vascular access, most
commonly achieved using the internal jugular
vein with subclavian or femoral vein as lesser
alternatives
80. • The use of the subclavian route carries an
increased risk of pneumothorax and venous
stenosis.
• The femoral route is only suitable for short
periods because of the high infection rate.
81. • Temporary lines may have a single, double or
triple lumen.
• Double- and triplelumen lines are associated
with improved clearance of uraemic toxins,
and the triple-lumen line allows
administration of intravenous therapy without
interfering with RRT.
82. The choice is between the following
• Haemodialysis: efficient small-molecule and
volume removal.
• Haemofiltration: removes large molecules and
volume by convection.
• Haemodiafiltration: combination of
haemodialysis and haemofiltration
83. Haemofiltration
• Haemofiltration uses a highly permeable
synthetic membrane and negative pressure in
the dialysate compartment of the dialyser
without dialysate flowing such that up to 80 L
of fluid are removed from the patient in a 4-h
session.
84. Haemofiltration
• Solute removal is by 'convection', or passive
flow of solute with water.
• The desired proportion of the filtrate is
replaced by infusion usually from preprepared
sterile bags of replacement fluid.
85.
86. Haemofiltration
• Convection allows greater removal of solutes
in the 'middle molecular' range (110-500 Da)
but is less efficient at the smaller end of the
molecular spectrum, which contains most of
the lifethreatening compounds
87. Haemodialysis
• Haemodialysis is based on diffusion across a
semipermeable membrane porous to
molecules under 500 Da.
• It thus exhibits high efficiency with regard to
small molecule and volume removal and is
cost-effective but relies on well-trained
personnel
88.
89. Haemodiafiltration
• The combination of these two techniques is
called haemodiafiltration.
• With this modality, the benefits of diffusion
and convection are combined in a dialysis
circuit similar to that used for haemofiltration
but with dialysis fluid being pumped round
the dialysate circuit.
90. Venovenous haemofiltration
• Venovenous haemofiltration requires at least
a doublelumen venous line and relies on a
pumped system to create a gradient across
the filter and hence a fitrate from the patient.
91. Arteriovenous haemofiltration
• If the patient is normotensive, it is possible to
use an arterial and venous line to create the
pressure gradient across the filter line
(arteriovenous haemofiltration), thus
removing the need for a pump in the circuit.
92. • The choice between these types of support is
normally decided by the renal physician and
intensivist.
93. • All three modalities of RRT can be performed
on an intermittent or continuous basis.
95. Haemofiltration and
haemodiafiltration
• Patients with uncomplicated ARF whose
cardiovascular system is stable are usually
treated with intermittent techniques
• More unstable patients, in whom fluid
removal is more difficult, benefit from
continuous therapies.
96. Continuous Treatment
• Continuous treatment is especially useful for
patients with cerebral oedema or hypoxia.
Intermittent haemodialysis is the treatment of
choice when there is a need for rapid removal
of water-soluble substances such as
potassium, myoglobin and drugs.
99. Nutritional management
• All patients with dialysis-dependent ARF have
higher nutritional requirements than normal,
especially if the ARF arises as a complication
of other severe illness.
100. State of patients with ARF
• Relative insulin-resistant state
• Low triiodothyronine
• Decreased testosterone
• Increased energy expenditure above expected
resting levels.
101. • Hyperglycaemia (insulin resistance) is not
uncommon and glucose oxidation forms a
smaller component of total energy
consumption.
102. • Lipid and protein metabolism is also
disturbed, with increased plasma triglycerides
and increased protein catabolism.
103. • RRT adds a further strain.
• Whilst the glucose in haemofiltration fluids
provides a large number of calories, amino
acids are lost during RRT.
104. • The haemodynamic state of the patient may
restrict the ability to supply the patient's
nutritional requirements.
105. • Patients with ARF have the same daily
requirements as other acutely sick patients,
i.e. a caloric intake of 35 kcal/kg (147 kj/kg)
body weight and nitrogen 1.2 g/kg body
weight, with the ratio between glucose and
lipid in the non-protein part of the diet being
70/30.
107. Diuretic phase
• As ARF resolves there is often a diuretic phase.
• This occurs because although filtration is
restored, the concentrating ability of the
recovering tubules has not.
108. Diuretic phase
• During this phase there is a risk of
dehydration.
• The excessive fluid loss (as much as 20 L/day)
must be replaced intravenously until the
tubules are able to concentrate the urine.
• High urinary volumes such as these are
unlikely to persist for more than a few days.
•
109. Diuretic phase
• The diuretic phase of renal failure may last
several weeks to months but is usually shorter
if patients do not become anuric or severely
oliguric.
111. • The prognosis of ARF depends on the underlying aetiology.
• The overall mortality has not changed materially
• during the past three decades and averages 50%. However,
• the mortality rate associated with certain categories of
• ARF has improved, e.g. ARF associated with trauma and
• obstetric disorders. Comorbid disease influences the outcome:
• ARF in patients nursed in intensive care units has
• an overall mortality of 70%. For all patients if there is associated
• failure of one other system the overall patient survival
• is less than 30% and failure of two systems reduces
• survival further to less than 10%. Increasing age also
• impacts adversely on survival.
