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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3080_Библиотеки_им_академика_М_И_Перельмана
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The Patient with a Raised Temperature
89
What are the indications for RRT in critical care?
Metabolic acidosis (pH <7.1).
Hyperkalaemia refractory to medical management (K
+
>6.5 mmol/L).
Uraemic complications (e.g. encephalopathy, pericarditis, myopathy or
bleeding).
Removal of dialysable toxins (e.g. salicylate, methanol, ethylene
glycol, lithium).
Pulmonary oedema unresponsive to diuretics.
Hyperthermia (temperature >40 °C).
Anuria or oliguria.
Management of uid overload.
Has optimal timing been established for when CRRT
should be initiated in the critical care patient?
There is still no consensus on the optimal timing of when to start CRRT acutely
in these patients. Several trials have attempted to review this but there has been
inconsistency regarding methodology and even denitions of what constitutes
‘early’ and ‘late’ initiation of therapy (notable trials include AKIKI, ELAIN
and IDEAL- ICU). To date, no signicant mortality benet has been found in
association with the timing of CRRT.
Where creatinine and urea were historically used in studies as substitutes
for the severity of AKI, they do not necessarily determine outcome for patients
requiring CRRT. Mortality associated with AKI requiring CRRT in the critically ill
is usually associated with volume overload, hyperkalaemia and severe metabolic
acidosis. Thus, current practice continues to include early commencement of
RRT in the setting of oliguria, established volume overload, metabolic acidosis or
electrolyte derangements (local guidelines should also be followed). The rapidity
of initiation of RRT within an intensive care unit can depend a great deal upon
Describe the characteristics that form the basis of RRT
Mode of delivery–RRT is either continuous or intermittent. Continuous
treatments result in a slow and steady clearance of solutes and permit
lower average serum urea levels compared to intermittent techniques.
Continuous methods also avoid the hazardous peaks of solute clearance
After 12 hours of supportive management, Jane's creatinine has risen to
600
μmol/L, her potassium has increased to 6.5 mmol/L and her urine
output has decreased signicantly. You decide to initiate continuous renal
replacement therapy (CRRT).
You successfully insert a VasCath™ into the right internal jugular vein to
enable commencement of CRRT.
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Clinical Cases in Critical Care
90
that can occur when using intermittent RRT. Compared to intermit-
tent therapies, continuous forms of RRT (e.g. CVVH) result in a greater
average mass clearance of urea (Figure6.1) and better acid–base control.
Method of removing solutes–using diusion, convection or a combination
of both methods.
Access–this is usually via either large veins (venovenous) or arteriove-
nous stulae.
Briey describe the different methods for delivering RRT
Haemofiltration (e.g. continuous venovenous haemofiltration) –this
method uses a hydrostatic pressure gradient to move large volumes
of plasma water and solutes across a semipermeable membrane by
convection. This describes mass transfer due to the bulk motion of a
uid (e.g. the ow of plasma water transports the molecules and ions
that are located within this physiological compartment). An extracor-
poreal pump is used to power the movement of venous blood through a
hollow-
bre cartridge. Certain solutes and plasma water pass through
the semipermeable membrane, forming an ultraltrate. This ultraltrate
is then removed and replaced with a physiological crystalloid solution
that can be infused either prelter or postlter. Prelter replacement
dilutes the blood entering the lter and acts to reduce the incidence of
clots forming within the haemolter. However, it also dilutes the solute
content of the blood and reduces the eective solute clearance. Postlter
replacement has no eect on clot formation or solute clearance. This
is the least ecient method of RRT and is conducted continuously for
24 hours per day. However, it is ecient at removing large molecules
(<60 kDa) and water (Figure6.2a).
Haemodialysis (e.g. intermittent haemodialysis)–in this method, the sol-
utes are removed by utilising a concentration gradient. It relies on the
process of diusion, a term that describes (a) the random movement
40
30
20
10
0
Urea (mmol/L)
Hours
12 24 36 48
Figure 6.1: RRT patterns of urea removal using continuous (green line) versus
intermittent techniques (orange line). Note the potentially hazardous peaks associated
with intermittent techniques.
Source: Theophilus Samuels.
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The Patient with a Raised Temperature
91
of particles and (b) movement of particles from regions of high
concentration to low concentration. Blood and dialysate run counter-
current to one another, also separated by a semipermeable membrane.
Solutes that have high concentrations in the plasma will preferentially
move down their concentration gradients into the dialysate (e.g. urea,
creatinine). This is an intermittent procedure and is typically performed
for 3–4 hours per day, 3–4 times a week. This method is avoided in criti-
cally ill patients as it causes hypotension. It is very ecient at removing
small molecules, less than 20 kDa (e.g. ammonium, potassium, creat-
inine), but not at removing larger molecules and water (Figure6.2b).
Haemodialtration (e.g. continuous venovenous haemodialtration)–this
method combines both diffusion and convection to remove fluid
and solute.
Peritoneal dialysis (PD)–this method typically makes use of an intra-
peritoneal catheter. This permits a glucose- rich (hypertonic) solution
to be inserted into the peritoneal cavity, which then acts as a dialysate.
Following a specied period, this solution is removed and discarded. It
contains the extra uid and toxins that have crossed into this dialysate
from the peritoneal blood vessels. PD is rarely used for the treatment of
AKI in developed countries and is more suitable for chronic dialysis.
Slow low- eciency dialysis (SLED)–this method is performed by using
dialysis machines that can deliver a slow dialysate ow for periods ranging
from 8 to 12 hours per day. This technique has an excellent solute removal
capability, is well tolerated haemodynamically, and does not require any
additional equipment to perform if access to haemodialysis machines is
readily available. SLED has similar uraemic clearance and haemodynamic
stability to CVVH or CVVHD and can be used without anticoagulation.
This potentially makes it less labour intensive compared to CVVH.
(a) (b)
Figure 6.2: (a) In CVVH, blood (red arrows) is pumped through the circuit, creating
a hydrostatic pressure gradient (yellow arrows) that moves large volumes of water
and solutes across a semipermeable membrane (blue dashed line). This creates an
ultraltrate (blue arrow) that is removed and then discarded. Replacement uid can
be infused prelter (dark grey arrow) or postlter (light grey arrow). It is an ecient
method for removing larger molecules (green dots) and water (blue dots). (b) In IHD,
blood (red arrows) and dialysate (blue arrows) move countercurrent to one another
separated by a semipermeable membrane (blue dashed line). It is an ecient method
for removing smaller molecules (orange dots).
Source: Theophilus Samuels.
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Clinical Cases in Critical Care
92
What dose (mL/kg/h) would you prescribe for Jane?
Evidence from two large clinical trials, the VA/NIH Acute Renal Failure
Trial Network (ATN) study and Randomized Evaluation of Normal versus
Augmented Level of RRT (RENAL) study, demonstrated no benet in high
doses of CRRT (e.g. >35 mL/kg/min) for critical care patients with AKI. This
data suggested that the minimal dose of 20–25
mL/kg/h would be satisfactory
in most cases. However, in clinical practice, higher doses can often be employed
in patients with sepsis and liver failure.
Why are continuous therapies preferred over
intermittent therapy in critical care?
Reduce risk of hypotension or cerebral oedema–changes in plasma osmo-
lality occur at a lower rate. This makes it the mode of choice in patients
with haemodynamic instability.
Increase systemic vascular resistance (SVR) –the continuous nature
of ltration tends to lower body temperature despite the presence of
a warming element in the system. This unintended consequence can
lead to an increase in systemic vascular resistance, making it less hae-
modynamically unstable.
Safety prole–this therapy can be safely conducted by critical care nurses.
What are the disadvantages of continuous RRT
therapies in critical care?
Anticoagulation–in almost all patients, the circuit needs to be anticoagu-
lated, particularly if low ow rates are used. Heparin is most commonly
used, but its anticoagulant eect may become systemic. Alternatively,
citrate can be used–this possesses the best regional eect, but calcium
and pH must be carefully monitored and corrected.
Labour intensive–CRRT can be used safely in critical care, but it requires
a one- to- one nurse- to- patient ratio as each day a large volume of euent
must be discarded and replaced with an appropriate electrolyte solution.
Cost–the volume of replacement electrolyte solution required for a
single patient during the length of stay can be very high.
Limited patient mobility–as the therapies are continuous, patients can
be literally conned to bed, especially in the presence of venous access
that is ‘position dependent’. As such, mental well- being should be con-
sidered in awake patients with single organ dysfunction and the use of
lter- free periods is encouraged if appropriate (e.g. in between changing
expired circuits), allowing the patient to mobilise if able.
Your unit uses CVVH.
Since Jane has no immediate family that can be contacted, and she has had
to be intubated and ventilated without discussion or consent, one of your
team suggests that deprivation of liberty has taken place.
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The Patient with a Raised Temperature
93
What is a Deprivation of Liberty Safeguards
(DoLS) order?
A DoLS is designed to protect vulnerable people in a hospital or care home
(or even their own home) where they are deprived of their ‘freedom’ (i.e. the
freedom to do the things they want to do and live where they want to live)
and who lack the capacity to consent to the care or treatment needed. In legal
terms, a person is deprived of their liberty if they are both ‘under continuous
supervision and control and not free to leave’.
How does DoLS apply in intensive care?
In 2017, the Court of Appeal passed judgement in R(Ferreira) v HM Senior Cor-
oner for Inner South London & Ors and stated that in general, when life-
saving
medical treatment is required then there shall be no deprivation of liberty. The
court armed that the test for deprivation of liberty as dened above requires
that the patient themselves wants to leave but is being prevented by the hospital
or care institution they are being held in. Therefore, when their underlying
medical condition prevents them from ‘leaving’ then this test is not met.
Should Jane be referred for DoLS?
No. Given that her medical condition deteriorated to the point where she
required intubation and mechanical ventilation to treat her persistent and
life-
threatening hyperpyrexia, she has not been deprived of her liberties and
therefore does not require a DoLS referral.
Further reading
Toxbase. www.toxbase.org (accessed 1 February 2022). Denitive online reference
for clinical toxicology for UK medical professionals.
Tandukar, S. and Palevsky, P. (2019). Continuous renal replacement therapy. Chest
155: 626–638. Excellent review on who, when, why and how to use CRRT.
KDIGO AKI Work Group (2012). KDIGO clinical practice guideline for acute kidney
injury. Kidney Int. Suppl. 2: 1–138. Seminal work on the various aspects of AKI by
world leading experts.
Jane spends 48 hours on your intensive care unit and is successfully extu-
bated on day 2, having required only 12
hours of RRT. She makes a full
recovery and is discharged within 1week of admission.
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Clinical Cases in Critical Care, First Edition. Alice Myers and Theophilus Samuels.
© 2023 John Wiley & Sons Ltd. Published 2023 by John Wiley & Sons Ltd.
7
Y
ou are called urgently to your HDU to review John, a 46- year- old man who
was admitted from the ward with hepatic encephalopathy. Around 4
hours
into his admission, he suddenly had a single episode of haematemesis. Vital
signs are HR 100
bpm, BP110/60 mmHg and RR 20 breaths per minute. His
oxygen saturations are 96% on room air despite him refusing supplementary
oxygen. He is confused and agitated.
The Patient
with Haematemesis
How would you initially assess John?
Airway–John is confused but able to maintain his airway at present.
However, his neurological status could quickly deteriorate which could
necessitate emergency intubation. Haematemesis could make this a
dicult airway due to potential blood in the oropharynx altering the
view at laryngoscopy. Endotracheal intubation is usually required in
cases of signicant haematemesis where the airway is compromised or
when urgent endoscopy is required.
Breathing–ideally, John should receive high- ow oxygen therapy, but
due to his agitation and confusion this is not possible.
Circulation–ensure that two large- bore intravenous cannulae are in
situ. Care needs to be taken, as attempting to site a cannula in agitated
and combative patients increases the risk of a needlestick injury. Given
that John is tachycardic, commence resuscitative uids. He should have
a blood group and save sample sent and ask the lab to cross-
match
at least four units of packed red cells (or according to your local unit
policies).
Disability/exposure–easily correctable factors, such as hypoglycaemia,
should be identied and corrected, as well as appropriately exposing the
patient to assess for other sources of bleeding (e.g. PR bleeding).
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The Patient with Haematemesis
95
How might you assess bleeding severity at
the bedside?
Assessment of haemodynamics and vital signs allows broad categorisation (as
per ATLS
®
).
Mild bleeding–when the approximate blood loss is between 15% and
30%, this usually produces few physiological changes. Vital signs (e.g.
pulse rate, respiratory rate, blood pressure, mental status, urine output)
remain relatively unchanged.
Moderate bleeding–when the approximate blood loss is between 31%
and 40%, this usually results in detectable changes in postural blood
pressure, tachycardia, tachypnoea and oliguria. Metabolic acidaemia
may be present, with attempted compensatory increases in minute ven-
tilation (e.g. respiratory rate and tidal volumes). However, it should be
noted that aspiration of blood and/or agitation and anxiety may also
contribute to the increase in respiratory rate.
Severe bleeding–when the degree of lost blood exceeds approximately
40%, a shocked state will most likely develop. This results in profound
hypotension, marked tachycardia and tachypnoea, greatly diminished
urine output and mental status, and requires a massive transfusion.
What primary prophylaxis is available for preventing
upper gastrointestinal bleeding (UGIB) in acutely
unwell critical care patients?
The National Institute for Health and Care Excellence (NICE) UK guidance
(CG141) recommends offering these patients acid suppression therapy
(H
2
- receptor antagonists or proton pump inhibitors) for the prevention of
UGIB, and where possible to use the oral form of the drug.
How useful is the haematocrit at this initial stage?
In the acute setting, it is important to understand that the patient is losing
whole blood. Therefore, the loss of both plasma and red blood cells (RBCs)
will result in the percentage of RBCs (the haematocrit) remaining at a similar
level as before the acute bleeding occurred. As uid from the extravascular
space moves into the intravascular compartment between 24 and 72 hours
after the bleeding event, and along with resuscitation using crystalloid solu-
tions, the haematocrit will begin to decrease. Therefore, in the acute stages the
haematocrit can remain nearly normal despite massive losses until resuscitative
uids are administered.
Following insertion of your second large- bore cannula, you withdraw
blood samples and send them to the laboratory for urgent full blood count,
cross- matching and coagulation studies. You are informed that John’s
haematocrit is 45%.
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Clinical Cases in Critical Care
96
How can you differentiate clinically between
an upper and lower gastrointestinal bleed?
An upper GIB may present with:
haematemesis or coee grounds vomiting (indicating recent but not
active UGIB)
melaena (black, tarry stools), which indicates that the blood has been
present within the GI tract for at least 14
hours. However, brisk upper
GI bleeding may result in rapid GI transit and present with fresh rather
than transformed blood
hyperactive bowel sounds
raised serum urea, due to blood proteins absorbed in the small intestine.
A lower GIB typically presents with fresh blood per anus (haematochezia).
Discuss the potential sources of non- variceal upper
gastrointestinal bleeding
Peptic ulcers –these are the most common causes of UGIB, with an
approximate incidence between 30% and 50%. Prognostic information can
be obtained at endoscopy by examining these lesions. Approximately 20%
of these patients will demonstrate ndings of active bleeding, adherent
clot or a non-
bleeding viable vessel. Around one- third of this cohort will
experience further bleeding and therefore benet from endoscopic therapy
with bipolar electrocoagulation, heater probe, injection therapy (e.g. abso-
lute alcohol, 1:10000 adrenaline) and/or clips. Clean- based ulcers seen at
endoscopy have nearly zero risk of rebleeding. If no measures are taken in
this cohort to prevent rebleeding, then approximately 10–50% will suer
another episode. Prevention is focused on three main strategies:
Helicobacter pylori eradication decreases rebleeding rates to
less than 5%.
Stopping non- steroidal anti- inflammatory drugs (NSAIDs) if
being taken.
Indefinite proton pump inhibitor (PPI) therapy (42% incidence of
rebleeding at 7 years if not adhered to).
Erosive gastritis, oesophagitis or duodenitis –these occur in approximately
10–15% of cases and are conned to the mucosa. As there are no arteries or
veins within the mucosa, these ‘breaks’ do not cause major bleeding. The
most important precipitating factor for these erosions is the use of NSAIDs.
It is estimated that 50% of patients taking long- term NSAIDs may have
gastric erosions. Other causes include stress, alcohol consumption and H.
pylori infection. Critically ill patients are most prone to stress-
related gastric
mucosal injury where reduced splanchnic blood ow disrupts the integrity
of the mucosa. Severe bleeding should not occur unless ulceration develops.
Due to their critical illness, the mortality rate is very high in these patients.
Mallory–Weiss tear –accounts for approximately 2–10% of UGIB hospi-
talisations. The patient will usually give the classic history of vomiting,
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The Patient with Haematemesis
97
retching or coughing followed by haematemesis. In 80–90% of patients,
bleeding from these tears will stop spontaneously. They are usually found
on the gastric side of the gastro-
oesophageal junction. Recurrence rates
are low, with estimates being up to 10%. Actively bleeding tears should
be managed endoscopically.
Other causes –malignancies, oesophagitis, angiodysplasia or vascular
malformations (e.g. Osler–Weber–Rendu syndrome, Dieulafoy lesion),
and aortoenteric stulae are other less common causes of UGIB.
What are the options for patients who need to
continue NSAIDs after they present with bleeding
peptic ulcers?
Cyclo- oxygenase- 2 selective NSAID with PPI therapy.
If taking low- dose aspirin for secondary prevention of established
cardiovascular disease, then this should be restarted as soon as possible
(between 1 and 7 days) after the bleeding event.
For primary prevention of cardiovascular disease, aspirin should be
discontinued in most patients who develop an UGIB.
How could cirrhosis contribute to the development
of varices in John?
The hepatic venous pressure gradient (HVPG) is the dierence between the portal
vein pressure and free hepatic vein pressure. Portal hypertension occurs when this
pressure is greater than 5
mmHg and is most associated with cirrhosis. Interest-
ingly, if the HVPG remains less than 12
mmHg, varices do not develop and there
is therefore very little risk of bleeding. When the HVPG exceeds 12 mmHg, there
is little correlation between the risk of bleeding and the pressure gradient. In
response to portal hypertension, portosystemic collateral venous drainage results
in variceal formation, most commonly in the distal oesophagus and stomach. Var-
ices can also occur within the small and/or large bowel and in the anorectal area.
Non- cirrhotic causes of portal hypertension include Budd–Chiari syndrome,
portal vein thrombosis and constrictive pericarditis.
Describe the Child–Pugh classication of cirrhosis
This score is used to predict survival in many liver diseases and for cirrhosis
can predict the likelihood of major complications, such as variceal bleeding and
spontaneous bacterial peritonitis. The classication scores the patient between
5 and 15 on bilirubin, INR, albumin, ascites and encephalopathy:
Score 5–6: class A (‘compensated cirrhosis’).
Score 7–9: class B.
Score 10–15: class C.
You determine from John's clinical history that he has been recently
diagnosed with cirrhosis of the liver due to alcohol.
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Clinical Cases in Critical Care
98
A score of 7indicates decompensated cirrhosis. The Child–Pugh score
was used to assess a candidate for liver transplantation and prognosticate in
cirrhotic patients. However, for listing patients for transplantation, it has been
superseded (see Case 19).
What do you think is the source of John’s bleeding?
The most likely source of bleeding in this case is ruptured oesophageal varices.
This remains the most common site of portal hypertensive bleeding in these
patients. In all patients with cirrhosis, approximately 50% will have oesophageal
varices. However, varices will develop in most cirrhotic patients eventually.
What is the recommended haemoglobin level
for transfusion in variceal bleeding?
Currently, transfusion is recommended when the haemoglobin level falls below
70 g/L. Evidence suggests that adhering to this threshold when compared to a
threshold of 90 g/L decreases rebleeding, multiorgan failure and death. In addition,
transfusing a patient to a haemoglobin level above 100 g/L should be avoided.
However, you should consider other factors that might require
transfusing at
a higher threshold, such as underlying cardiac disease (e.g. peripheral vascular
surgery, heart failure or ischaemic heart disease), the presence of tissue hypox-
aemia (suggested by rising lactate levels) and haemodynamic status.
In rapid exsanguination, it may not be possible to use laboratory haemoglo-
bin level as a guide to transfusion. In these circumstances, repeated clinical
assessment of haemodynamics, regular estimation of overt blood loss and pos-
sibly the use of real- time thromboelastography are used to guide transfusion.
What is the role of tranexamic acid in acute UGIB?
The HALT- IT study investigated the eects of a high- dose 24- hour infusion
of tranexamic acid on death and thromboembolic events in patients with
acute gastrointestinal bleeding. The trial suggested that the use of tranexamic
acid does not reduce death and should not be incorporated into management
strategies to treat GI bleeding.
Describe the treatment options available
for variceal bleeding
Non- endoscopic
Pharmacotherapy – this aims to reduce intrahepatic resistance or
decrease portal blood ow. Several agents can or have been used.
Terlipressin –a synthetic analogue of vasopressin, this has a longer
duration of action and safer profile. It is the only agent that has been
Despite the ongoing administration of IV fluid boluses, John remains
tachycardic (now 120 bpm) and his BP is lower than before (95/60 mmHg).
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