Medical and Surgical Nursing Lecture

Support of Renal Function

Dr. Mary Grace Suplido, RN. MD DATE: 11/15/2022

 Acute Renal Failure of the original filtrate, allowing for a modest daily fluid
 A syndrome with numerous causes. intake of 1.5 L to achieve fluid balance.
 Causes: glomerulonephritis, prerenal azotaemia,
urinary tract obstruction and vasculitis.
 A rapid deterioration in renal function (hours to
days).  The ureters, bladder and urethra collect, drain and
 Easily detected by commonly measured markers of temporarily store the urine produced from each kidney.
kidney performance, including blood urea nitrogen,  The kidneys are located in the retroperitoneal space
serum creatinine, and a failed ability to adequately on the posterior wall of the abdominal cavity, encased
regulate electrolytes, sodium and water balance. in a protective combination of the ribs, muscle, fat,
 While generally reversible, it can be life-threatening tendon and the renal capsule.
in critically ill patients if acid-base balance,  Each adult kidney weighs approximately 140 g.
electrolyte levels (potassium) or fluid overloads are
not effectively diagnosed and managed.
 Occurs in 20–25% of intensive care patient
admissions, much higher than the broader hospital
rate of 5%.
 In critical care, it often forms part of the multiple
organ dysfunction syndrome, whose cause has
often been associated with sepsis, trauma,
pneumonia or cardiovascular dysfunctions.
 Acute Tubular Necrosis (ATN)
 Used to describe acutely deteriorating renal
function, reflecting pathological changes from
various renal insults of a nephrotoxic or ischemic
origin.  The glomeruli and nephrons lie in the cortical area of
 Serum Creatinine Level the kidney, while the collecting ducts gather together
 Preferred serum marker of renal function. into the renal pyramids, which lie in the medulla of the
 Exact level is considered excessive is disputed; kidney. The pyramids drain into the calyces of the
however, a doubling of the baseline serum kidney, which then drain into the renal pelvis where
creatinine or levels in excess of 200 μmol/L is urine is gathered to drain into the ureter.
commonly agreed on as being indicative of ARF.
 Urine Output Renal pyramids → calyces of the kidney → renal
 Also a key factor in determining the severity of pelvis → ureter
ARF.
 Oliguric Renal Failure is a urine output of less than  The major blood vessels of the kidney, the renal artery
0.5 mL/kg/h in adults and 1 mL/kg/h in infants, is and veins also enter the renal capsule through the
associated with poorer patient outcome than the pelvis of the kidney.
non-oliguric form.

a) Regulation and maintenance of fluid and electrolyte

balance.
b) Clearance of metabolic and other waste products.
c) An indirect role in the maintenance of blood pressure,
acid–base balance, and an endocrine function.

 Regulation and maintenance of the extracellular fluid

and electrolyte constituents is principally via the
process of filtration and reabsorption.
 The kidneys receive approximately 25% of the cardiac
output each minute and excrete approximately 180
L/day of glomerular filtrate. Fortunately, tubular
reabsorption accounts for approximately 178.5 L/day

1|A p r i l R o s e P a n e s B S N I V – A
 Medical and Surgical Nursing Lecture
Support of Renal Function
Dr. Mary Grace Suplido, RN. MD DATE: 11/15/2022
Three Stage Process of Urine Production (occurs in the
nephron):
1. Glomerular Filtration
2. Tubular Reabsorption
3. Tubular Secretion
 The glomerular filtration rate (GFR) is about 125
mL/min under normal conditions. Changes in the
diameter of the afferent and efferent arteriole help
regulate glomerular blood flow, but this is unable to
compensate for large variations of mean blood
pressure; hence, filtration rates may rise or fall
markedly over the course of a day.
 As the filtrate transgresses the glomerulus it is
collected into the Bowman’s capsule and delivered into
the proximal convoluted tubule, loop of Henle and then
the distal convoluted tubule, where a number of
processes result in the reabsorption of about 99% of
the glomerular filtrate.
Bowman’s Capsule → Loop of Henle → Distal
Convoluted Tubule → Collecting Tubule = Urine
 The remaining fluid within the tubule drains into the
collecting tubule to form urine. This fluid has
substantially different properties from the original
glomerular filtrate, as fluid and many electrolytes and
glucose are reabsorbed by the peritubular capillaries.
 Along with blood pressure, the sodium content of the
extracellular fluid is critical in maintaining fluid
balance, as it constitutes the major electrolyte and
osmotic agent of the glomerular filtrate.
 It is imperative that sodium intake and loss is equally
balanced, as excessive losses will result in associated
fluid loss and excessive intake will result in fluid
retention.
Excessive loss of sodium = Fluid loss
Excessive intake of sodium = Fluid retention
 If sodium balance is not maintained, other
compensations such as a rise in blood pressure may
result to restore fluid balance.
 As blood pressure rises, the excretion of sodium also
increases by way of the production of additional
glomerular filtrate.
↑ Blood Pressure = ↑ Excretion of Sodium
 Stimulation of the SNS by loss of blood volume occurs
by reflex via the low-pressure volume sensors in the
pulmonary and venous circulations.
 It widely innervates the kidney and is able to reduce
the filtration rate by constricting the afferent arteriole
of the glomerulus, thus inhibiting blood flow and
pressure necessary to create the glomerular filtration
rate.
 Increases the reabsorption of salt and water in the
tubule and stimulates the release of renin.
 It is excreted from the pituitary gland under regulation
of hypothalamic osmoreceptors (thirst center), and
reduces kidney diuresis (the excretion of water).
 By enhancing the kidney’s ability to concentrate urine,
it ensures that the excretory functions of waste
products and electrolytes continue while limiting fluid
loss.
 Essential to surviving limited periods of fluid
deprivation and fine-tuning the urine volume
production on a continuous basis.
RENIN
 The chemical trigger to initiate a cascade system that
results in two powerful hormones acting on the kidney
to significantly influence sodium and water excretion.
 Produced and released from the juxtaglomerular
apparatus, a collection of cells in the macula densa of
the distal tubule, and the adjacent afferent arteriole
next to the glomerulus, which monitors blood sodium
concentration.
 When released, it stimulates the activation of
angiotensin I from angiotensinogen. Under the
influence of coenzyme A, angiotensin I converts to
angiotensin II, a potent vasoconstrictor and stimulus
to reabsorb sodium and water. The vasoconstrictor
effect raises blood pressure and flow to the
glomerulus, inhibiting further renin release (negative
feedback mechanism) as perfusion pressure
normalizes. This allows the return of natriuresis
(sodium excretion) and diuresis.
2|A p r i l R o s e P a n e s B S N I V – A
 Medical and Surgical Nursing Lecture
Support of Renal Function
Dr. Mary Grace Suplido, RN. MD DATE: 11/15/2022
 This response is essential in assisting with retaining
fluid in the event of a falling blood pressure, or
boosting fluid excretion as blood pressure rises.
 It also responds effectively to a rise in sodium intake
by reducing angiotensin II formation and allowing a
larger natriuresis, resulting in maintenance of sodium
balance, a key to tissue fluid distribution and balance.
ALDOSTERONE
 It is a mineralocorticoid excreted from the adrenal
cortex in response to angiotensin II.
 It increases the reabsorption of sodium and hence
water, in the cortical collecting tubules and increases
the rate of potassium excretion. This has a dual effect
of regulating sodium balance and extracellular fluid
volume.
 As fluid volume accumulates, the rise in glomerular
filtration rate self-limits the volume effect by increasing
both diuresis and natriuresis.
 Hormone released from the atria of the heart in
response to atrial stretching during periods of
increased circulating fluid volume.
 Often described as having an antagonizing effect to
the RAAS (which acts primarily to preserve sodium
and water).
 These natriuretic, and hence diuretic, effects are mild
and self-limiting, and occur in response to mild rises in
GFR and reductions in sodium reabsorption. As blood
pressure falls, the drop in GFR compensates for the
effect of ANP, ensuring that excessive loss of sodium
and water does not occur.
 The kidney assists in the management of body pH by
regulation of the excretion of H+ and HCO3 − ions.
 During acidosis the kidney raises H+ secretion by
active transport to combine with ammonia (NH3 +) in
the renal tubule to form ammonium (NH4 +), which is
↑ H+ excretion = reabsorption of Na = ↑ HCO3-
unable to be reabsorbed. Coincidentally, raised H+
excretion increases the reabsorption of sodium, which
increases the alkalytic ion, bicarbonate (HCO3 −).
 During alkalosis the reabsorption of hydrogen ions is
increased. These changes in secretion of hydrogen ion
concentration in the renal filtrate alter the pH of the
urine down to a maximum level of 4. The buffering of
H+ with ammonia reduces the acidifying effect of the
hydrogen ions, particularly as some ammonium
combines with chloride to form ammonium chloride.
 Erythropoietin is important in stimulating the
generation of new red blood cells and is released from
the kidney in response to a sustained drop in arterial
blood oxygen levels.
 Calcitriol helps regulate the absorption of calcium from
the gut, which in turn promotes bone resorption of
calcium and the reabsorption of calcium in the kidney.
 The kidney also acts to convert vitamin D to its active
form, which is necessary for the maintenance of body
calcium levels.
 Pre-renal factors affecting blood supply to the kidneys,
such as: hypovolemia, cardiac failure or hypotension/
shock, can cause ARF.
 ↓ blood flow = ↓ glomerulofiltration occurs = urine
production diminishes and wastes accumulate. This
state can be reversed by restoration of blood volume
or blood pressure.
 In the short term (1–2 hours), nephrons remain
structurally normal and respond by limiting fluid lost by
urine production while concentrating the excretion of
waste products. The physiological process combines
the neuroendocrine control of the hypothalamus and
the sympathomimetic response, which then regulates
both ADH secretion and the stimulation of the RAAS.
 This process is highly influenced by any preexisting
illness or concurrent factors such as diabetes and
systemic infection.
INTRARENAL (INTRINSIC) CAUSES
Intrinsic damage to the nephron structure and function
can be due to infective or inflammatory illness, toxic
drugs, and toxic wastes from systemic inflammation in
sepsis, vascular obstructive thrombus or emboli.
Glomerulonephritis
 Causes: infective or a non-infective inflammatory
process damaging the glomerular membrane or a
systemic autoimmune illness attacking the membrane.
3|A p r i l R o s e P a n e s B S N I V – A
 Medical and Surgical Nursing Lecture

Support of Renal Function

Dr. Mary Grace Suplido, RN. MD DATE: 11/15/2022

 Either cause results in a loss of glomerular
membrane integrity, allowing larger blood
components such as plasma proteins and white
blood cells to cross the glomerular basement
membrane. This causes a loss of blood protein,
tubular congestion and failure of normal nephron
activity.
 Resolution is based on treating the cause, such as an
infection or autoimmune inflammatory illness.
Nephrotoxicity
 Result of damage to nephron cells from a wide range
of agents, including many drugs used in critical care
(e.g. antibiotics, anti-inflammatory agents, cancer
drugs, radio-opaque dyes).
 Toxic products of muscle breakdown in severe illness
and trauma, commonly called Rhabdomyolysis blood
product administration reactions and blood cell
damage associated with major surgery are also
causative agents.
 As these agents may often be given concurrently, a
cumulative effect, along with intermittent falls in renal
perfusion, may result in the development of intrinsic
ARF.
ACUTE TUBULAR NECROSIS (ATN) AND ACUTE
KIDNEY INJURY
 It is the damage to the tubular portion of the nephron.
 May range from subtle metabolic changes to total
dissolution of cell structure, with tubular cells
‘defoliating’ or detaching from the tubule basement
membrane.
 In critical illness, the most common combination
causing ARF is the administration of nephrotoxic
agents in association with prolonged hypoperfusion or
ischemia (oxygen deprivation).
 This type of tubular necrosis can be further
mediated by infection, blood transfusion reactions,
drugs, ingested toxins and poisons, or be a
complication of heart failure or major
cardiovascular surgery.
 It is the causative mechanism for up to 30% of acute
kidney failure in the intensive care setting, with the
precise causative illness not easily identifiable in
critically ill patients with multiple co-morbidities.

Vascular Insufficiency
 Prior to the critical illness, and may be related to
diabetes, the ageing process and/or long-term
hypertension.
 1/3 of patients who develop ARF in the ICU have
chronic renal dysfunction.
 May be undiagnosed.
 These factors create a reduction in both large and
microvasculature blood flow into and within the
kidney, therefore reducing glomerular filtration activity
and affecting the reabsorption and diffusive process of
the nephron. This reduction in blood flow is
exacerbated by degenerative vessel obstruction with
atheromatous plaque, particularly pronounced in
diabetic patients due to ineffective glucose
metabolism.  The clinical history is important in
differentiating preexisting renal disease and
cataloguing the numerous factors already discussed
 Urinary tract obstruction is the primary post-renal that can contribute to renal dysfunction.
cause of ARF, and is uncommon in the critical care  As the majority of renal failure patients in the ICU will
setting as it is rarely associated with acute onset renal succumb to the combination of pre-renal renal failure
failure. and ATN, the key assessments used in monitoring
 More common in the community and is associated with renal function are urine output, serum creatinine and
urological disorders such as prostate gland urea levels, combined with more general
enlargement in males, urinary tract tumors and renal hemodynamic measures including HR, CVP, BP,
calculi formation impairing urine outflow. PCWP.
 It is essential that blockage of any urinary drainage
device be excluded in the critically ill patient when
undertaking an assessment of apparent oliguria.  Where the management of ARF begins.
 It is based on the patient’s presenting signs
and symptoms linked to a patient history.

4|A p r i l R o s e P a n e s B S N I V – A
 Medical and Surgical Nursing Lecture

Support of Renal Function

Dr. Mary Grace Suplido, RN. MD DATE: 11/15/2022

 A long-term history of renal disease involving urinary
tract infections, diabetes, cardiac failure and
systemic inflammatory illnesses are all highly relevant.
 Immediate history of presentation to a
hospital involving surgery or any life-threatening
illness with associated shock is also highly relevant in
association with reduced urine output volumes over
time.
A useful classification system to grade loss of kidney
function, reflecting stages of injury to the kidney before
failure occurs.
o Ceasing or modifying the dose of any nephrotoxic.
o Drugs or agents and treating infection with alternative.
o Less toxic antibiotics.
Nutrition
 When ARF is persistent, providing nutritional support
is another important management strategy.
 An intake of 30–35 kcal/kg/day and a protein intake of
1–2 g/kg/day is essential due to the combined
increase in protein catabolism and caloric requirements
of associated critical illness.
RENAL REPLACEMENT THERAPY (RRT)
 If conservative measures fail, then the ongoing
management of the patient with ARF requires RRT.
 This enables control of blood biochemistry, prevents
toxin accumulation, and allows removal of fluids so
that adequate nutrition can be achieved.

Proposed Criteria for the Initiation of RRT in Adult

Critically Ill Patients
Oliguria Urine output <200mL/12h
Anuria/Extreme Oliguria Urine output <50mL/12h
Hyperkalemia K+ >6.5 mmol/L
Severe Acidemia pH <7.1
Azotemia Urea >30 mmol/L
Clinically significant Edema
organ (especially lungs)
Uraemic Encephalopathy
Uraemic Pericarditis
 In the critically ill patient, kidney function failure may Uraemic
be associated with an initial renal response to a fall Neuropathy/Myopathy
in perfusion associated with systemic shock. As the Severe Dysnatremia Na+ >160 or <115 mmol/L
majority of patients recover their renal function from Hyperthermia
ICU ARF, initial clinical management is aimed at Drug toxin with
reducing further renal damage. dialyzable toxin
 If kidney function becomes so compromised that blood
pH, fluid and electrolyte balance cannot be sustained, Renal Dialysis
then a replacement therapy will need to be  Human kidney function is able to be largely replaced
introduced. This is continued until kidney function is with a management program that includes an artificial
marked by the return of urine production or patients process of RRT that can sustain individuals for many
are moved to a more chronic form of replacement years in the community setting.
therapy, such as intermittent hemodialysis.  In critically ill patients with ARF, this program focuses
predominantly on RRT, rather than on the endocrine
REDUCING FURTHER INSULTS TO THE KIDNEYS functions of the kidney.
 After diagnosis, the next management principle is to
remove or modify any cause that may exacerbate the History
pathological process associated with ARF. Dialysis is a term describing RRT and refers to the
 Further interventions and investigations are performed purification of blood through a membrane by diffusion of
in relation to the findings from the history waste substances.
and presentation.
Historical Events in the Development of Dialysis
Time Period and Description
These may include:
Developer
o Further intravenous fluid resuscitation (despite an
1854: Thomas First used the term ‘dialysis’ to describe
oligo-anuric state) and restoration of blood pressure Graham, the transport of solutes through an ox
o Physical or diagnostic assessment for renal outflow. Scottish Chemist bladder, which drew attention to the
o Obstruction and alleviation if present.

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 Medical and Surgical Nursing Lecture

Support of Renal Function

Dr. Mary Grace Suplido, RN. MD DATE: 11/15/2022

concept of a membrane for solute removal  The drum with the blood-filled cellulose tubing wound
from fluid. around it was immersed in a bath of weak salt
1920s: George First human dialysis was carried out, solution, and as blood passed through, the
Haas, German performing six treatments on six patients.
rotating cellulose tubing allowed waste exchange to
Physician Has failed to make further progress with
occur by diffusion.
the treatment but is recognized as an
early pioneer of dialysis.
1920-30s Synthetic polymer chemistry allowed
development of cellulose acetate, a
membrane integral to the further
development of dialysis treatments.
1940s: Willem The discovery of heparin, an
Kolff, Dutch anticoagulant, enabled further
Physician development of dialysis during World
War II, the Kolff Rotating Drum Kidney.
1940-50s: Kolff Further modification of Kolff dialyser and
amd Allis- the development of improved machines.
Chalmers, USA
1950s: Fredrik Developed the parallel plate dialyser
Kiil, Norway made of a new cellulose, Cuprophane.
 This large extracorporeal blood volume became a
This required a pump to push the blood
through the membrane and return the
focus for further development of the therapy.
blood to the patient.  The goal was to develop a membrane for solute
1950-60s Dialysis began to be widely used to treat exchange with a greater surface area than the
kidney failure. cellulose membrane used by Kolff but needing
1960s: Richard The hollow-fibre membrane dialyser used less blood volume.
Steward and a membrane design of a cellulose acetate  This led to the development of the hollow-fiber
Dow Chemical, bundle, with 11,000 fibres providing a filter membrane structure in the 1960s, the same
USA surface area of 1m2.
design concept that is used today. Since then
1970s Use of first CAVH circuits for diuretic
significant developments have occurred, with new
resistant oedema by Kramer.
fibres using the polymer polysulfone or other artificial
1980s First continuous therapies using blood
pump and IV pumps to control fluids synthetic chemical structures that better imitate the
removal and substitution: Australia and nephron glomerulus and the ability to transfer wastes
New Zealand led the way. and plasma water for an effective ‘artificial kidney’.
1990s New purpose built machines used;  This combination of extracorporeal circuit (EC), blood
Gambro Prisma, Baxter BM 11+ 14 to pump and filter membrane (or artificial kidney or
provide pump controlled therapies with dialyser), and the associated nursing management is
integrated automated fluid balance using
now commonly known as hemodialysis.
scales to measure fluids. Cassette circuits,
 The major treatment components are essentially
automated priming: new membranes.
2000 Further purpose built machines using
the same as those first developed in the 1960s, with
direct measurement for waste and the key component being the device membrane.
substitution fluids via Hygiela-Kimal
machine. Introduction of high fluid Development of Renal Replacement Therapy in Critical
exchange rates for sepsis treatment. Care
Introduction of dialysis based machines in  Historically, ARF was treated in the ICU with the use
ICU for daily hybrid treatments: SLEDD of peritoneal dialysis (PD), which did not require
and SLEDDf.
specialist nurses or physicians.
2010 Multiple CRRT machines; more advanced
 This simple technique removes wastes by infusing
graphics interface and smart alarms.
Waste disposal systems. High flux, a dialysis fluid into the abdomen, allowing
porous membranes. diffusion and osmosis to occur between the
peritoneum and fluid before draining out again in
The Kolff Rotating Drum Kidney repeated cycles.
 One of the earliest attempts at RRT used  This was performed by the ICU nurse and
cellulose tubing rolled around a wooden skeleton built prescribed by ICU physicians, but was inadequate
as a large, drum-styled cage. in its clearance of waste and fluid volume, and was
 Cellulose acetate (material similar to ‘sticky tape’) associated with infection, limiting respiratory
tubing was strong, did not burst under pressure and function and exacerbated glucose intolerance.
could be sterilized.

6|A p r i l R o s e P a n e s B S N I V – A
 Medical and Surgical Nursing Lecture

Support of Renal Function

Dr. Mary Grace Suplido, RN. MD DATE: 11/15/2022

 In 1977, Peter Kramer, a German ICU physician,
frustrated with the limitations of PD and the delays in
gaining a dialysis nurse and machine to attend the ICU,
developed a new dialytic technique by inserting a
catheter into the femoral artery and allowing blood
to flow to a membrane and back to the femoral vein.
 As the blood passed through the membrane,
plasma water was filtered out.
 The technique was called continuous
arteriovenous haemofiltration (CAVH). It was later
renamed slow continuous ultrafiltration (SCUF),
as it enabled the removal of plasma water
in addition to dissolved wastes (convective
clearance of solutes) at a flow rate of 200–600
mL/h by passive drainage from the membrane as
blood flowed through it.
o Temporary catheters inserted via a skin puncture
into an artery (A) for drawing blood and a vein
(V) to return the blood (AV access).
o A surgical joining of an artery and vein (usually
in the forearm), making a large vessel that
is punctured with needles to both draw and
return the blood (AV fistula).
o A catheter with two lumens to draw and
return blood via a large central vein (veno-venous
access catheter).
Hemodialysis, hemofiltration and hemodiafiltration are
three common techniques used to achieve artificial
kidney support in ARF.

Refinement of Renal Replacement Therapy

 Continuous Veno-Venous Hemofiltration (CVVH)
 Use of roller blood pumps to generate pressure and
a reliable flow of blood.
 Eliminates the need for arterial puncture and
access.
 Introduced by two German groups.
 Reliably pumps blood at a constant rate and
achieve ultrafiltration volumes of 1000 mL/h.
 Able to remove large volumes of plasma water and,
if run continuously with similar amounts replaced
by a balanced plasma water substitute, an effective
clearance of wastes similar to a high-intensity
dialysis treatment could be achieved without
 The EC is a common factor in all these different circuit
cardiovascular instability.
designs.
 Continuous Veno-Venous Hemodiafiltration
 The difference between treatments is how the solutes
(CVVHDf)
(urea, creatinine and other waste products) and
 With further modifications to the circuit and filter
solvent (blood plasma water) are removed from the
set-up, a diffusive component was added to the
blood as it passes through the filter membrane
therapy by running a dialysate volume through the
(artificial kidney), and the intermittent versus
hemofilter, flowing between the membrane fibres
continuous prescription of the therapy.
and countercurrent to blood flow.
 This is determined by the way in which the dialysis
 To deliver continuous forms of veno-venous
fluids are mixed with or exposed to the blood, the rate
RRT required the introduction of blood pumps from
and direction of blood and fluid flows, and how fluid
modified dialysis machines into the ICU, and
loss or a negative fluid balance is achieved.
created a major education and training need for
 The three physical mechanisms of fluid and solute
critical care nursing
management are convection, diffusion, and
ultrafiltration.
Approaches to Renal Replacement Therapy
 Both IHD and CRRT require a machine to pump blood
and fluids; pressure and flow devices to monitor
• Process whereby dissolved solutes are removed with
treatment; a tubing and filter membrane set that
blood plasma water as it is filtered through the dialysis
together create an extracorporeal circuit (outside the
membrane.
body blood pathway); and a catheter connecting the
• Derived from the Latin convehere, meaning ‘to remove
patient’s circulation to the circuit.
or to carry along with’.
 This catheter enables blood to be drawn from
• This process is very similar to that occurring in the
and returned to the patient (known as ‘access’).
native kidney glomerulus, as plasma water is
 Access can be achieved by three different techniques:

7|A p r i l R o s e P a n e s B S N I V – A
 Medical and Surgical Nursing Lecture

Support of Renal Function

Dr. Mary Grace Suplido, RN. MD DATE: 11/15/2022

filtered across the nephron tubule via the Bowman’s

capsule.
• In RRT, the plasma water with the dissolved wastes
is discarded; the plasma water deficit is then
replaced with manufactured artificial plasma water in
equal or slightly lower amounts to achieve a desired
fluid balance. This blood washing (purification) process
is commonly known as hemofiltration. When applied
on a continuous basis in the ICU, hemofiltration
can adequately replace essential renal functions, and
is particularly effective in managing fluid balance.

 It is the physical movement of solutes across

a semipermeable membrane from an area of high
concentration to that of a relatively low concentration;
that is, solutes move across a concentration gradient.
 A higher concentration gradient results in a greater
rate of diffusive clearance.
 As blood passes through the dialysis membrane,
dialysate fluid, reflecting normal blood chemistry, is
exposed to the blood on the opposing side of the
membrane fiber. Diffusive clearance is continuous as
solute exchange occurs by diffusion with the dialysate
fluid and the blood continually moving in and out of
the membrane. As ‘dirty’ or waste-laden blood enters
the membrane and ‘clean’, fresh dialysate is in
continuous supply, this process performs an effective
waste-removal process. The two mediums are usually
established in countercurrent or opposing flow to each
other, making diffusion another process, mimicking the
normal nephron function of the kidneys.
 The technique of solute removal using diffusion alone
is termed dialysis; when used with blood, the process
is termed hemodialysis (HD). When applied on
an intermittent basis, as is normal for
patients receiving RRT for chronic renal failure, it
is called intermittent hemodialysis.
 Process that allows plasma water to leave the blood,
achieving body fluid or water loss.
 Dialysis nurses measure a fluid loss by weighing
the patient before and after a treatment.
 Primarily used to achieve fluid balance, an
important function of the kidneys.
 The only difference between this process and
the convective clearance of solutes is that this fluid is
not replaced, and it is therefore not considered
an adequate solute management method.
 Cannot be undertaken in large amounts without fluid
replacement, as it would cause hypovolemia. It
is therefore implemented during a dialysis period by
removing small amounts each hour (e.g. 250 mL/h for
4 hours) of the intermittent treatment cycle.

8|A p r i l R o s e P a n e s B S N I V – A
 Medical and Surgical Nursing Lecture

Support of Renal Function

Dr. Mary Grace Suplido, RN. MD DATE: 11/15/2022

term arteriovenous (AV) is used.

Blood Pump
 In veno-venous modes, a pump component is
MAJOR CIRCUIT COMPONENTS FOR CRRT
essential as part of the patient’s blood volume flows
Membranes
externally to the body via the EC.
 The filter or hemofilter (blood filter) is the
 Blood flow is maintained by a ‘roller pump’, that
primary functional component of the RRT system.
propels the blood along the tubing in a peristaltic
 Responsible for separating plasma water from
fashion (milking along by compression of the tubing),
the blood and/or allowing the exchange of solutes
compressing the blood-filled tubing but having no
across the membrane by diffusion.
contact with the blood itself. This roller rotates at a
rate providing a flow of fresh unfiltered blood to the
hemofilter, enabling it to clear metabolic waste
products.

Vascular Access
 Blood is most commonly accessed from the
venous circulation of the critical care patient via a
catheter placed in a central vein (e.g. femoral). Venous Return Line Bubble Trap Chamber
 Blood is both withdrawn from the vein and returned to  Purpose: to prevent any gas bubbles in the EC from
the same vein – that is, venovenous (VV) access by entering the patient’s circulation by allowing them to
means of a double (dual)-lumen catheter. rise to the top of a small, vertically positioned collection
 When the same procedure is carried out by reservoir.
accessing the blood from the patient’s systemic
circulation via an artery and returning it to a vein, the

9|A p r i l R o s e P a n e s B S N I V – A
 Medical and Surgical Nursing Lecture

Support of Renal Function

Dr. Mary Grace Suplido, RN. MD DATE: 11/15/2022

Not useful when liver

failure present, citrate
is converted to
bicarbonate by the
liver providing the
necessary buffer for
RRT. Acidosis may
occur in liver failure.
No anti- No side effects, May encounter very
clotting agent no exacerbation short circuit life that
(with saline of unstable consumes remaining
flushes) hematological hematological
status, liver components, risk of
failure. fad overload if saline
flushes not part of
fluid balance.

Anticoagulation No evidence saline

 There are several different drugs utilized to prevent flushes have any
blood clotting in the EC; heparin, prostacyclin and benefit.
sodium citrate have been used separately or in various
combinations. Fluids and Fluid Balance
 A key component of any CRRT is the administration of
Commonly Used Anti-clotting Agents for CRRT a replacement solution for the fluid removed during
Drug Benefits Precautions hemofiltration.
Heparin Inexpensive, Sensitivity reactions,
wide experience heparin-induced Typical Replacement/Dialysate Fluid Constituents for CRRT.
easily reversed, thrombocytopenia, to Component Bicarbonate-based Lactate-based
easily be effective means Solution (mmol/L) Solution (mmol/L)
monitored, short Increased risk of
Buffer 25.00 45.00
half-life bleeding systemically
Potassium 0.00 1.00
Low- Moderately Difficult to monitor,
Sodium 140.00 140.00
molecular- inexpensive not easily reversed,
Glucose 0.00 10.00
weight increasing longer half-life,
Calcium 1.63 1.63
heparin experience less dosing varies
Magnesium 0.75 0.75
(LMWH) likely to result in between types of
sensitivity LMWH. Chloride 100.75 100.75
reactions.
Prostacyclin Very short- Expensive, no
acting, has a measure of
physiological effectiveness, narrow
role in inhibiting dose range with
platelet activity, associated
does not hypotension,
exacerbate individual patients
other drug sensitive to Comparisons of CRRT and IHD
reactions. hemodynamic effects, Factors CRRT IHD
unstable in solution. Blood pressure Less Instability Removal of large
Citrate-based Limit anticlotting Substantial metabolic stability because of lower volumes of fluid in
solutions effect to EC- effect if not blood and a short time frame,
‘Regional adequately managed dialysate flow causing
anticoagulation,’ serum ionised rates and the hypotension and
results suggest calcium must be continuous nature blood pressure
very effective in monitored closely of the treatment instability during
prolonging requires additions to with slower fluid treatment.
circuit life. extracorporeal circuit removal rate.
to administer and Waste clearance Control of urea Removal of large
reverse and use of and creatinine volumes of fluid in
specialised (key wastes) a short time frame,
replacement/dialysate achieved slowly causing
solutions. and steadily, hypotension and

10 | A p r i l R o s e P a n e s B S N I V – A
 Medical and Surgical Nursing Lecture

Support of Renal Function

Dr. Mary Grace Suplido, RN. MD DATE: 11/15/2022

critical in blood pressure 4. Fluids/electrolyte 3. Treatment orders

managing patients instability during incorrect. cross-checked
with intracranial treatment. with settings.
pathologies. 4. Double-check
Nutritional Larger volumes of Continuous fluids used, e.g.,
support nutritional fluid feeding difficult any additives
can be because of fluid required.
administered with volume
concurrent requirement and Recommendation:
clearance of accumulation patient in bed,
products of while off supine position and
protein digestion treatment. MAP>70, stable.
and fluid load. Connection to 1. Access catheter 1. Prep access
Electrolyte, acid- Ability to adjust Potential acute the system obstruction/failur connections with
base and body dose of treatment changes in pH and Initiation e. antiseptic and
water and replacement during treatment, of therapy. 2. Hypotension test flush return
homeostasis of electrolytes, add and (venous) lumen
acid-base balance electrolyte and aspirate
and body water accumulation outflow (arterial)
balance to meet while off lumen.
patient needs as treatment. 2. Connect both
necessary. circuit lines to
Neurotrauma and Fare much better Fluid shirts can access catheter
surgery patients when managed by aggravate cerebral administering
CART without oedema and be priming volume
acute changes in life-threatening, to patient.
solute levels such IHD a) Increase
as urea and contraindicated vasoactive
sodium. for patients with drugs first to
raised ICP. maintain
Sepsis or severe Blood-borne Diffusive and MAP.
infections mediators in intermittent b) Start blood
sepsis and process in HD not pump slowly
Inflammatory as effective at with small
illness cytokines) removing the increases
better removed by mediators of until blood
the convective Inflammation due fills all of the
process in CRRT to molecular size. circuit.
(WH).
Recommendation:
use two nurses for
connection routine.
Start fluid
replacement and
removal only after
Key nursing management themes found in the literature blood circuit is full
useful for application of CRRT are: education and training; and at prescribed
methods for fluids management and fluid balance; speed.
anticoagulation approaches; and machines used. In-use 1. Low pressure 1. Maintain access
troubleshootin arterial alarm. catheter
g and 2. High pressure alignment,
Troubleshooting Guide
maintenance, venous alarm preventing kinks.
Nursing Area Potential Problem Key Nursing
particularly 3. High TMP alarm. 2. Do not place
Interventions
fluid balance. 4. Air detected extra
Required
alarm connections or
Patient and 1. Machine alarms 1. Machine test
5. Hypothermia taps between
machine/syste and technical and/or checklist
6. Fluid balance access catheter
m preparation failure on starting completed.
errors and circuit lines.
before use. treatment 2. Double-check all
7. Electrolyte 3. Blood pump
2. Air entrainment. line connections
imbalance speed>150
3. Fluid setting around circuit.
mL/min.
errors.
4. Ensure venous
chamber filled

11 | A p r i l R o s e P a n e s B S N I V – A
 Medical and Surgical Nursing Lecture

Support of Renal Function

Dr. Mary Grace Suplido, RN. MD DATE: 11/15/2022

well above air Recommendation: if

sensor, bubbles frequent failure,
removed. always check for
5. Heater set to blood flow
37°C. obstruction before
6. Use fluids chart more
or similar to anticoagulation, e.g.
account for all request change or
fluids used replacement access
including catheter if
anticoagulant. obstructed.
7. Potassium Access care 1. Access 1. Ensure catheter
additive to CRRT and dressings dislodgement. sutured in place
fluid is often 2. Access catheter and well secured
required after infection. with dressing.
24-48 hours of 3. Access catheter 2. Use asepsis
treatment some obstruction. when flushing or
patients are connecting to
hypokalemic access catheter,
despite acute monitor site for
renal failure. infection.
3. Use heparin to
Recommendation: fill catheter
assess and reset deadspace when
fluid balance not in use for>-4
settings hourly, hours.
particularly in
unstable patients Recommendation:
and for use flexible dressing
inexperienced staff. with application to
Monitoring 1. Premature 1. Check and both sides along
and clotting in circuit monitor effect of catheter allowing
adjustment to and filter. anticoagulant movement away
anticoagulatio therapy after from skin surface,
n. first 6 hours and preventing
then daily. obstruction during
a) Maintain patient care
adequate positioning.
dose to Vital sign 1. Arrhythmias, 1. Monitor vital
therapeutic monitoring hypotension, signs hourly,
range. fever. consider any link
b) Use between
predilution changes and use
fluid of RRT; e.g. low
administratio CVP and
n. inadvertent fluid
c) Use blood loss occurring
flow greater
than 150 Recommendation:
mL/min. CVP readings
d) Use large- should be performed
bore access 2-4-hourly during
catheter and CRRT; CVP can be
take care not used as a target for
to obstruct daily fluid loss
catheter. prescription
e) Keep blood Assessment 1. Filter clotting 1. If
pump of filter abruptly with transmembrane
operating function and inability to return pressure (IMP) or
minimize patency circuit blood to prefilter pressure
stops >30 the patient. (P-IN)>250
sec. 2. Inadequate mmHg consider
solute removal. electively

12 | A p r i l R o s e P a n e s B S N I V – A
 Medical and Surgical Nursing Lecture

Support of Renal Function

Dr. Mary Grace Suplido, RN. MD DATE: 11/15/2022

returning blood should not be used

by saline infusion for other
into circuit and purposes/infusions
ceasing when RRT is not
treatment. connected.
a) Observe for Temporary 1. Maintenance of 1. Flush out any
venous disconnection circuit before excess blood
chamber dot for reconnection. residue in circuit,
development. procedures. 2. Infection. keep blood
If excessive 3. Inadvertent fluid pump
and venous administration. operational with
pressure saline in circuit.
>200 mmHg 2. Circuits in use
consider for>24 hours
electively before
returning disconnection or
blood by not restarted
saline after 6 hours
infusion into following
circuit and temporary
ceasing disconnection,
treatment. consider
2. Assess patients’ discarding.
urea and 3. After restarting
creatinine circuit, increase
measures; they fluid loss to
should be remove fluid
reducing or used to re-
stable. establish RRT.

Recommendation: Recommendation:
blood flow into add heparin 5000 IU
venous chamber to circuit when
should be visible, le temporarily
not full to identity disconnected, but
clot, reduce level of flush this out with
blood to detect clot 200-300 ml saline
and or perform a before reconnection;
small saline flush (- always use additive
100 ml) into circuit label for this
to check for clot procedure.
formation.
Cessation of 1. Blockage and/or 1. Use
treatment and clotting in access concentrated
disconnection catheter. heparin to fill
from the 2. Inadvertent deadspace of
extracorporeal blood loss. catheter when
circuit. 3. Infectious risk. not in use >4
hours. Use 1000
IU/mL and follow
manufacturer's
specifications for
volume required.
2. Always cease a
circuit before it
dots, return
patient blood.
3. Use asepsis for
disconnection
procedure.

Recommendation:
access catheter

13 | A p r i l R o s e P a n e s B S N I V – A
 Medical and Surgical Nursing Lecture
Multiple Organ Dysfunction Syndrome (MODS)
Dr. Mary Grace Suplido, RN. MD DATE: 11/15/2022
 The term was established by an expert consensus
conference in 1992 to describe a continuum of
physiologic derangements and subsequent dynamic
alterations in organ function that may occur during a
critical illness.
 Associated with widespread endothelial and
parenchymal cell injury because of hypoxic hypoxia,
direct cytotoxicity, apoptosis, immunosuppression and
coagulopathy.
 Cellular damage in various organs in patients who
develop MODS begins with the onset of local injury
that is then compounded by activation of the innate
immune system. This includes a combination of
pattern recognition, receptor activation and release of
mediators at the microcellular level, leading to
episodes of hypotension or hypoxemia and secondary
infections.
 Typically occurs because of unchecked systemic
inflammation as seen in the systemic inflammatory
response syndrome (SIRS) or sepsis.
1. Increasing volume requirements and mild respiratory
alkalosis, accompanied by oliguria, hyperglycemia and
increased insulin requirements
2. Tachypnea, hypocapnia and hypoxemia, with
moderate liver dysfunction and possible
haematological abnormalities
3. Developing shock with azotemia, acid–base
disturbances and significant coagulation
abnormalities.
4. Vasopressor dependence with oliguria or anuria,
ischemic colitis and lactic acidosis.
 MODS is a state characterized by aberrant cellular
responses involving multiple organ systems and
sequential processes. The pathogenesis of MODS is
complex, simultaneously involving every cell type,
neuro-hormonal axis, and organ system.
 In brief, hypoxic hypoxia results from altered
metabolic regulation of tissue oxygen delivery which
contributes to further organ dysfunction.
 Microcirculatory injury as a result of lytic enzymes, and
vasoactive substances (nitric oxide, endothelial growth
factor), is compounded by the inability of erythrocytes
to navigate the septic microcirculation.
Altered metabolic regulation of tissue O2 delivery →
hypoxic hypoxia = further organ dysfunction
 Mitochondrial electron transport is affected by
endotoxins in sepsis, nitric oxide, and TNF-alpha,
leading to disordered energy metabolism. This causes
cytopathic or histotoxic anoxia (the inability to use
oxygen, even when available).
 This context of impaired oxygen utilization rather
than delivery results from diminished mitochondrial
production of cellular energy (ATP), despite normal or
even supranormal intracellular PO2 levels. Cytopathic
hypoxia appears resistant to resuscitation measures,
and this may ultimately worsen already-existing organ
dysfunction. During sepsis or ischemia mitochondria
respond by facilitating cell death rather than the
restoration of homeostasis.
 Apoptosis is normal physiological programmed cell
death and is the main mechanism to eliminate
dysfunctional cells. It involves chromatin condensation,
membrane blebbing, cell shrinkage and subsequent
breakdown of cellular components into apoptic bodies.
 This normally orderly process is deranged in critical
illness, leading to tissue or organ bed injury and
MODS. Pro-inflammatory cytokines released in sepsis
may delay apoptosis in activated macrophages and
neutrophils, but in other tissues, such as gut
endothelium, accelerated apoptosis occurs.
 Necrosis is a form of cell death characterized by
cellular swelling and loss of membrane integrity as a
result of hypoxia or trauma. It has been termed ‘cellular
energy crisis’, and is unregulated resulting in loss of
membrane sodium/potassium/ATP-ase pumps.
 This loss leads to cell swelling, rupture and spillage of
intracellular contents into surrounding regions
creating collateral damage. Therefore, it can involve
significant amounts of tissue and organ bed damage.
 Apoptosis differs from necrosis in that it does not
seem to involve the recruitment of inflammatory cells
or mediators to complete its task. Activation of an
enzyme cascade systematically cleaves proteins,
including the cell’s nuclear DNA, with the end-result
being death of the cell. This requires energy from
mitochondria and if not available necrosis of the cell
occurs.
 In ischemia/reperfusion, endoplasmic reticulum loses
its ability to process proteins which induces the
expression of heat shock proteins, affecting
transcription of proteins necessary for organ specific
functions. For example, liver cell metabolism, renal cell
function or cardiac cell contractility may be affected.
 Cellular communication is also altered in MODS. Cells
normally communicate through highly interactive
bidirectional networks. The endothelium acts as a
communication interface between cells, organs and
systems and is involved in orchestration of systemic
responses, including hemodynamic regulation,
inflammation and coagulation; oxygen and nutrient
delivery; oxidative stress and sensing of psychological
stress and neuroendocrine alterations.
14 | A p r i l R o s e P a n e s B S N I V – A
 Medical and Surgical Nursing Lecture
Multiple Organ Dysfunction Syndrome (MODS)
Dr. Mary Grace Suplido, RN. MD DATE: 11/15/2022
 In critical illness, endothelia release molecules that
trigger the immune and neuroendocrine systems to
produce a generalized inflammatory response. The
combination of the pathophysiological processes
involved with the development of MODS,
compensatory mechanisms and the effect on target
organs and systems is now discussed.
 The complex host-response generated involves the
inflammatory immune systems, hormonal activation
and metabolic derangements, resulting in multiple
organ system involvement. These are initially adaptive
to maintain nutrient perfusion to the tissues, however
eventually organ systems become dysfunctional and
fail, and the body is no longer able to maintain
homeostasis.
 Initially, pro-inflammatory mediators are released
locally to fight foreign antigens and promote wound
healing. Anti-inflammatory mediators are also
released to down regulate the initial response to the
insult. If the local defense system is overwhelmed,
inflammatory mediators appear in the systemic
circulation and recruit additional leucocytes to the area
of damage. A whole-body stress response ensues,
further compounding the situation.
 If pro-inflammatory mediators and anti-inflammatory
response is imbalanced, the patient may develop
systemic inflammatory response syndrome (SIRS) and
subsequent immunological dissonance of organ
dysfunction.
 Regardless of the trigger event, lymphocytes (T cells,
B cells, natural killer cells) and macrophages are
activated by cytokines (cellular signalling agents) to
commence the inflammatory or anti-inflammatory
response. A number of Interleukins (IL) have been
identified as key cytokines in pro-inflammatory (e.g. IL-
1, IL-6; and similar to tumour necrosis factor alpha
[TNFα] actions) or anti-inflammatory (e.g. IL-10, IL-6,
IL-4) responses. The inflammatory response results in
clinical signs of hypoperfusion, culminating in shock
 Intracellular transcription factors, in particular nuclear
factor kappa B (NFκB), are important in innate and
adaptive immunity, as they regulate the transcription
of genes involved in the inflammatory and acute stress
response, leading to the expression of TNFα,
interleukins, and tissue factor. NFκB, therefore, plays
an important role in response pathways in critical
states including hypoxia, ischemia, hemorrhage,
sepsis, shock, and MODS.
 The inflammatory cascade activates a number of
prostaglandins and leucotrienes that also have pro-
and anti-inflammatory effects. Thromboxane A2 plays
a role in the acute phase, in part due to stimulation of
platelet aggregation, leading to microvascular
thrombosis and tissue injury; it may also play a role in
pulmonary bronchoconstriction and myocardial
depression.
Trigger event → pro-inflammatory and anti-inflammatory
mediators are released → cytokines trigger lymphocytes
(T cells, B cells, and natural killer cells) and macrophages
→ pro-inflammatory and anti-inflammatory response =
hypoperfusion → shock
 A part of innate immunity, a generic response to injury,
and is normally an excellent mechanism to localize
injury and promote
 Neutrophils, macrophages, natural killer cells,
dendrites, coagulat,ion and complement are the
principal active components of the innate host
response.
CLASSIC SIGNS OF INFLAMMATION:
 Pain
 Edema
 Erythema and heat (from vasodilation)
 Leucocyte accumulation and capillary leak
 Occurs as a consequence of alterations to tissue
endothelium, with increased microvascular
permeability (‘capillary leak’).
 Infection exists when there is one of the following:
positive culture, serology, presence of
polymorphonuclear leucocytes in a normally sterile
body fluid except blood, and clinical focus of infection
such as perforated viscus or pneumonia.
 In sepsis, the most common sites of infection are the
lungs (34–54%), intra-abdominal organs (15–28%)
and urinary tract (5–10%). The incidence of
15 | A p r i l R o s e P a n e s B S N I V – A
 Medical and Surgical Nursing Lecture

Multiple Organ Dysfunction Syndrome (MODS)

Dr. Mary Grace Suplido, RN. MD DATE: 11/15/2022

bloodstream infections is 30–40%, although one-third

of cases with septic shock have negative blood
cultures; one reason suggested for this is antibiotic
administration prior to sample collection.
 The type of infecting organism has also changed over
time, with Gram-positive bacteria predominant,
accounting for at least one-third of pathogens in septic
shock; Gram-negative, fungal, viruses and parasitic
organisms are also involved.
 The increasing incidence of resistant organisms
partially as a result of the indiscriminate use of
antibiotics, is an ongoing concern.
 Tissue injury and the production of inflammatory
mediators lead to:
o coagulation via the expression of tissue factor and
factor VIIa complex (tissue factor pathway; the
primary cascade for initiation of coagulation;
previously termed the ‘extrinsic’ pathway)
o Coagulation amplification via factors Xa and Va,
leading to massive thrombin formation and fibrin
clots (common coagulation pathway).

16 | A p r i l R o s e P a n e s B S N I V – A