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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 Haematemesis
99
shown to reduce mortality when compared to placebo. In the UK, it
is licensed for bleeding from oesophageal varices.
Somatostatin –this naturally occurring peptide causes splanchnic
vasoconstriction without affecting systemic vasculature. It reduces
portal pressure and has fewer side-
effects when compared to
vasopressin.
Octreotide – a somatostatin analogue, it is best used in conjunction
with endoscopic therapy and is used in the United States due to the
unavailability of somatostatin.
Balloon tamponade –generally used in cases of exsanguinating variceal
haemorrhage, this can be used to control active variceal bleeding when
other forms of therapy fail or are not immediately available or while
awaiting endoscopy. It is best seen as a temporising measure until den-
itive treatment can be given. However, as endoscopic techniques have
improved, experience in the use of balloon tamponade has dramatically
fallen. Nevertheless, control of bleeding can be achieved in most patients,
but the risk of rebleeding is high after balloon deation. The most com-
monly used balloon device is the Sengstaken–Blakemore tube, which has
three ports: one for oesophageal balloon ination, one for gastric balloon
ination and one for gastric aspiration. The tube is passed to the 50
cm
mark and the gastric balloon is inated to its full recommended volume
of air, around 400–500
mL. Once correct placement is conrmed using a
chest radiograph, the tube can be pulled back gently until resistance is
felt (due to the diaphragm). Ination time should be limited due to the
risk of perforation, which is highest when the oesophageal balloon is
also needed for haemorrhage control. Duration and timing of removal
should be co- ordinated closely with the endoscopic team. In current
practice, the oesophageal balloon is rarely inated.
Transjugular intrahepatic portosystemic shunt (TIPS) –using a percuta-
neous approach, this technique creates a portosystemic shunt. An expand-
able metal stent is advanced under angiographic guidance and creates a
direct portocaval shunt between the portal and hepatic vein, bypassing
the liver parenchyma and signicantly decreasing portal pressure. When
acute variceal bleeding fails to respond to endoscopic and pharmacolog-
ical therapies, this procedure should be considered. In more than 90% of
patients, this technique can control active bleeding, with less than 20%
experiencing a rebleeding episode. Performing a TIPS procedure within
24–48 hours in a patient with an HVPG >20 mmHg or with Child–Pugh
class C disease has been shown to reduce mortality. Encephalopathy
develops in up to 20% of patients undergoing this procedure and stenosis/
complete occlusion of the shunt occurs in 5–15% of cases.
Endoscopic
Band ligation –this technique is the preferred choice for controlling
active oesophageal variceal bleeding and for subsequent eradication of
oesophageal varices. Ligation involves suctioning a varix into a cap tted
on the end of the endoscope, which is then ligated by a rubber band that
is released from the cap. Band ligation will control acute bleeding in up
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Clinical Cases in Critical Care
100
to 90% of patients. Oesophageal stenosis and postligation ulcer bleeding
are uncommon complications following band ligation. In addition, this
technique is less successful when oesophageal varices extend into the
proximal stomach.
Sclerotherapy –this involves injecting a sclerosing, thrombogenic solu-
tion into or next to the varices. This technique is generally used to con-
trol bleeding when band ligation fails but it is associated with a higher
incidence of complications.
Stenting –this has been demonstrated to increase 15- day survival without
serious complications or further bleeding when compared to balloon
tamponade. It is also associated with less need for transfusion and has
a greater success at controlling bleeding
What is the role of prophylactic antibiotics
in patients with variceal bleeding?
Evidence from randomised controlled trials and a meta- analysis suggests that
prophylactic antibiotics in patients with variceal bleeding decreases overall
mortality, death from bacterial infection, rebleeding and length of hospital
stay. As bacterial infection can be present in up to 20% of these cases and up
to 50% will develop a hospital- acquired infection, the use of prophylactic anti-
biotics appears self- fullling. In addition, variceal bleeding is more likely to
occur in cirrhotic patients who are infected. Quinolones and cephalosporins
have been used with good success, but antibiotic resistance can dramatically
lower their eectiveness and local guidelines should be followed.
How would you proceed?
This is a life- threatening situation.
Emergency intubation and ventilation –the decrease in conscious level
puts John at very high risk of aspiration due to the potential loss of
protective airway reexes and a stomach full of blood. Therefore, secure
a denitive airway and intubate his trachea (see Introduction Section 2).
Care should be taken as massive haematemesis may obscure the airway,
so eective suction and experienced airway support are essential. In
addition, ensure that appropriate personal protective equipment is avail-
able and used (e.g. faceshield, aprons, gloves).
Declare a major haemorrhage –as part of the ongoing uid resuscitation,
John will need blood products. It should be clear that he is undergoing a mas-
sive haemorrhage and so alerting your transfusion service to this emergency
will ensure that blood products are made available as rapidly as possible.
Consult your local hospital policies for the major haemorrhage protocol.
About 1 hour after you began reviewing John, he has another larger episode
of haematemesis. He is much quieter and only responds to pain. His oxygen
saturations are now 85% on high-
flow oxygen and his blood pressure is
70/50
mmHg.
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The Patient with Haematemesis
101
Consider balloon tamponade – as described previously, balloon
tamponade can be considered as a bridging measure to definitive
endoscopic treatment.
Get expert help –alert the on- call endoscopy team to facilitate emergency
endoscopy.
How can massive transfusion (MT) be dened?
The most common denitions of MT are as follows:
Transfusion of 10 units within 24 hours.
Transfusion of >4 red blood cell units in 1 hour with the anticipation of
a continued need for blood product support.
Replacement of >50% of the total blood volume by blood products
within 3 hours.
However, these definitions do not direct attention to the coagulopa-
thy that also exists in these patients and fuels the process underlying the
haemorrhage.
What are the complications associated with a
massive transfusion?
There are multiple ways to categorise the complications, e.g. immediate, early
and delayed or immune versus non- immune. Here we divide the complications
into six categories:
1.
Coagulation abnormalities
Dilutional abnormality due to use of crystalloids or massive
transfusion.
Dilutional thrombocytopenia.
2. Related to blood storage
Increased inammatory response.
Immunosuppression.
Blood cell haemolysis.
Metabolic acidosis.
Hyperkalaemic cardiac arrest.
Hypocalcaemia.
Hypomagnesaemia.
3. Immunosuppression and infection
Infection (bacterial, viral, etc.).
Increased length of stay.
Increased mortality.
With trained airway assistants, you successfully intubate John. You begin
transfusing him according to your local major haemorrhage protocol (e.g. 1:1
RBC/FFP transfusion). As the on-
call consultant for emergency endoscopy
is mobilising their team, you are informed that the international normalised
ratio (INR) is 2.3.
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Clinical Cases in Critical Care
102
4. Lung- associated injury
Transfusion- related acute lung injury (TRALI).
Acute respiratory distress syndrome (ARDS).
5.
Metabolic
Anaerobic metabolism.
Lactate production.
Hypothermia.
6.
Fluid overload.
In general, non-
massive transfusion can also be associated with the
complications of pain, fever and anaphylaxis.
In the UK, serious adverse reactions associated with blood transfusion
should be reported to SHOT (Serious Hazards Of Transfusion), the UK
haemovigilance scheme.
How does this INR result affect the ability to
perform endoscopy?
Endoscopy should not be delayed while treatment is ongoing to normalise the
INR. It is useful to seek expert haematological advice regarding these coagula-
tion abnormalities. Usually, coagulation defects due to liver disease or warfarin
therapy can be treated using fresh frozen plasma (FFP). In patients with cir-
rhosis, the INR only reects changes in procoagulant factors. However, there
is often a balanced coagulopathy present with altered levels of anticoagulant
factors (e.g. protein C, protein S) in addition. In this context, thromboelas-
tography may help guide blood product administration. If patients are tak-
ing antiplatelet therapy (e.g. clopidogrel or aspirin) then platelet transfusion
may be warranted. If taking warfarin, the INR may be corrected with FFP
or administration of prothrombin complex concentrate (e.g. Beriplex
®
). In
addition, platelet transfusion is also indicated when platelet levels fall below
50
× 10
9
/L in patients with acute GIB.
Describe factors that increase the risk of death after
hospital admission for acute UGIB
The mortality rate for patients presenting with UGIB ranges between
3% and 14%. The following risk factors are associated with an increased
risk of death:
Presenting in a shocked state (e.g. systolic BP <100 mmHg).
Advanced age.
Presence of advanced upper gastrointestinal malignancy.
Co- morbidities such as renal or hepatic failure or disseminated cancer.
Certain endoscopic ndings such as active, spurting haemorrhage from
a peptic ulcer, non- bleeding visible blood vessel.
Rebleeding, which increases mortality 10- fold.
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The Patient with Haematemesis
103
Further reading
Jameson, J., Fauci, A., Kasper, D. etal. (2018). Harrison’s Principles of Internal Med-
icine. NewYork: McGraw- Hill Education. Chapter44. Authoritative information
on gastrointestinal bleeding.
Kamboj, A., Hoverston, P., and Leggett, C. (2019). Upper gastrointestinal bleeding:
etiologies and management. Mayo. Clin. Proc. 94 (4): 697–703. Succinct review on
the aetiologies and management of UGIB.
García- Pagán, J., Caca, K., Bureau, C. etal. (2010). Early use of TIPS in patients
with cirrhosis and variceal bleeding. N. Engl. J. Med. 362: 2370–2379. Formative
RCT showing that early use of TIPS resulted in signicant reductions in treatment
failure and mortality.
The endoscopy team arrive and perform emergency endoscopy. They nd
bleeding oesophageal varices and perform variceal band ligation successfully.
With the ongoing resuscitative measures you and your team have employed,
John begins to show signs of stabilising.
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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.
8
A
t the start of your night shift, you are asked to review 45- year- old Susan.
She was admitted earlier in the day with sepsis secondary to a lower
respiratory tract infection. She was agitated and severely hypoxic on arrival in
ED so was intubated and brought to ICU. Throughout the day, she has been
becoming increasingly dicult to ventilate. The nursing sta say that her blood
gases have deteriorated, and she is now ‘ghting the ventilator’.
The Patient Who Is
Dicult to Ventilate
What may be causing lack of synchrony with the
ventilator?
Ventilator dyssynchrony due to inappropriate settings or mode of
ventilation –Susan probably received neuromuscular blockade at the
time of intubation. Initially, the ventilator would need to have been set
to deliver mandatory breaths. The paralysing agent is likely to have been
metabolised by now, allowing Susan to initiate her own breaths.
Modes of ventilation can be divided into spontaneous, mandatory
or a combination. There are multiple parameters which can be
programmed inappropriately, e.g. inspiratory:expiratory ratio,
respiratory rate,
inspiratory ramp time, etc. In a spontaneous or
combination mode, the ventilator can be set to detect and augment
breaths initiated by the patient. Support is usually delivered as a target
pressure or volume and the success of these breaths will depend
upon the patient’s respiratory mechanics, clinical condition and
flow dynamics within the system. If augmentation is inadequate, the
patient may increase their work of breathing to try and compensate.
If mandatory breaths are delivered out of sync with the patient’s own
breathing, a situation may develop where the patient wants to inspire
when the ventilator is programmed for expiration, or vice versa. This
results in a pattern of respiration which looks uncomfortable and is often
accompanied by erratic tidal volumes and high peak pressures. Work of
breathing may be increased, there is a risk of alveolar damage from shear
forces within the lungs, and there may be a worsening of gas exchange.
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The Patient Who Is Dicult to Ventilate
105
Pain, distress, or inadequate sedation –many patients nd the presence
of an endotracheal tube painful and distressing and therefore sedation
is often needed for tube tolerance. There are many potential sources of
distress for Susan; for example, she may have delirium and be experi-
encing hallucinations. She could have pleuritic pain from her infection
or pain from vascular access devices, etc. Other sources of pain in critical
care include chest drains, surgical wounds or pre-
existing chronic and
atypical pain syndromes. While Susan requires ventilatory support, she
will need to be appropriately sedated, usually aiming for a RASS of 0 to
−2 (see Case 11). Commonly, this is achieved using a combination of an
opioid with a hypnotic agent (e.g. remifentanil and propofol).
Equipment problem or misplaced ETT –search for an equipment problem
systematically by assessing every element of the circuit from patient to
ventilator, including all gas pipes and ow sensors. Perhaps the ETT has
migrated, leading to endobronchial intubation and ventilation of one lung
only. Alternatively, especially if high PEEP is being used, the cu may have
herniated above the vocal cords, causing a leak and reduction in the positive
pressure generated by the ventilator. If ow-
triggering is being used, a gas
leak or impaired ow through ventilator tubing could mean Susan needs to
work harder to compensate for the leak to trigger support from the ventilator.
Increased resistance in the system – a water- logged HMEF (heat mois-
ture exchange lter) or kinked tubing massively increases resistance to
ow. Since resistance to ow is equal to the change in pressure divided
by the ow rate
R
P
Q
(R = resistance to ow, P = pressure dierence, Q = ow).
By combining this relationship with the Hagen–Poiseuille Law below
Pr
l
4
8
(Q= ow, P = pressure dierence, r = radius, η = viscosity, π = pi, and
l = length), we see that the following inverse relationship is apparent
R
r
1
4
assuming the viscosity of the gas and length of the breathing circuit
remain constant. Hence, any small reduction in radius can lead to an
increase in the work of breathing (use of accessory muscles, tachypnoea,
tachycardia, etc.) as the patient struggles to overcome this increased resis-
tance and decreased gas ow.
Worsening chest sepsis –it is possible that Susan’s apparent discomfort
could be due to deterioration in her clinical condition. She was admitted
recently, and the trajectory of her illness is not yet clear. Her chest sepsis
may be getting worse and her initial ventilatory support might now be
inadequate. Antimicrobial agents are unlikely to have made a positive
impact yet. Ensure a full septic screen has been sent (including blood
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Clinical Cases in Critical Care
106
cultures, a urinary antigen screen for pneumococcus and Legionella,
nasopharyngeal aspirates, and u swabs) and review her current anti-
microbials with a microbiologist.
New pathology –Susan could have developed a new problem in addition
to her chest sepsis. This could be related to her lung pathology, inter-
ventions the critical care team have instigated, or something else coinci-
dental. Keep an open mind when reviewing Susan, looking for evidence
of pneumothorax, pleural eusions, lung collapse or sputum plugging.
Ensure a complete assessment is performed to rule out problems with
other organ systems which may have been missed by focusing on the
acute problems. Don’t forget to examine the skin for rashes (e.g. menin-
gococcal septicaemia, measles etc.) and the abdomen for peritonitis, and
ensure all invasive cannulae are clean and appropriately sited.
What is the likely cause of Susan’s chest sepsis?
Chest sepsis can result from community- or hospital- acquired pneumonia.
Susan’s case is one of community-
acquired pneumonia (CAP) and is probably
bacterial or viral.
Bacterial causes in previously well adults include the following:
Typical
Streptococcus pneumoniae (approximately 50% of cases).
Haemophilus influenzae.
Moraxella catarrhalis.
Atypical
Mycoplasma pneumoniae.
Legionella pneumophila is a possibility, particularly if there has been
exposure to stagnant water.
Chlamydia spp.
Staphylococcus aureus and gram- negative pathogens should also be con-
sidered given the severity of Susan’s condition. Secondary bacterial infec-
tion can complicate recovery from viral infection.
Viral causes include the following:
Inuenza virus–‘seasonal u’ due to inuenza A or B. After S. pneu-
moniae, inuenza A is the most common cause of CAP. Surface proteins
(haemagglutinin and neuraminidase) are used in classication. Empirical
treatment may be started (e.g. oseltamivir) if unable to rule this out imme-
diately. Inuenza C causes only mild infection and D mainly aects cattle.
Coronavirus –consider the need to isolate the patient and wear an
FFP3mask if there is any chance of contagion, e.g. SARS- CoV (see Case 24).
Other causes include the following:
It would be wise to explore causes of immune suppression (e.g. HIV,
use of immunosuppressants) underlying lung disease (e.g. brotic or
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The Patient Who Is Dicult to Ventilate
107
obstructive processes), and exposure to unusual pathogens (e.g. recent
foreign travel, exposure to moulds). If none of these are present, the
cause is less likely to be fungal, though this should be reviewed as a
possibility if Susan fails to respond to treatment.
20
16
12
8
4
0
Flow (L/min)Pressure (cm H
2
O)
60
40
20
0
–20
–40
–60
Figure 8.1: Pressure and ow curves for the patient.
Source: Theophilus Samuels.
You review Susan and nd the following on examination. Weight 82 kg, height
165
cm, BMI 30.1. The ventilator is in synchronised intermittent mandatory
ventilation (SIMV) mode: FiO
2
0.85, PEEP12 cmH
2
O, set RR 14 per minute
(actual RR 35–40 per minute), V
T
120–700 mL (ideal body weight [IBW] 57 kg).
From the end of the bed, you can see that her HR is 125–130
bpm (sinus
rhythm), BP95/50
mmHg giving a MAP65 mmHg on noradrenaline
0.45
mcg/kg/min. Her chest is moving asynchronously with the ventilator
(Figure8.1), and she is using accessory muscles of respiration. You can hear
the peak pressure alarm intermittently.
Her temperature is 38.4 °C. She is prescribed co- amoxiclav and clarithro-
mycin. She is sedated with propofol 150
mg/h and fentanyl 100 mcg/h with
a RASS -
2.
You also note that her urine output has dropped to 0–10
mL/h for the
last 6 hours.
The remainder of the examination is unremarkable.
Initial blood results–Hb 104
g/L, WBC 14.2 × 10
9
/L, CRP256, platelets
92
× 10
9
/L, urea 9 mmol/L, creatinine 157 μmol/L.
ABG– pH
7.10, PaO
2
7.2 kPa, PaCO
2
9.3 kPa, base excess −6.4 mmol/L.
Lactate is now 3.6
mmol/L (3.1 mmol/L on admission).
Plain chest radiograph shows widespread pulmonary inltrates.
What is your assessment of the clinical situation?
From examination and review of the flow and pressure curves, Susan is
dyssynchronous with the ventilator, leaving her at risk of barotrauma and
atelectrauma. She appears to be deteriorating with increasing vasopressor
requirements and poor urine output. She has reduced oxygen delivery and
increased oxygen requirements with increased work of breathing and pyrexia.
Intervention is required at this point to prevent further deterioration.
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Clinical Cases in Critical Care
108
What is synchronised intermittent mandatory
ventilation?
Synchronised intermittent mandatory ventilation is a volume control mode where
the ventilator is set to deliver mandatory breaths at a programmed respiratory
rate while also allowing spontaneous breathing. For example, a set respiratory
rate of 14 breaths per minute means the ventilator would deliver 14 breaths
spread evenly throughout the 60-
second time period (time- cycled). All 14 breaths
would be mandatory in the way they are delivered (i.e. cycling from inspiration
to expiration). The ventilator will attempt to synchronise the mandatory breaths
with the patient’s own breathing up to the maximum set rate. If the patient takes
a breath during that time-
window, the ventilator will synchronise that breath
with the patient. If they do not, then a preprogrammed mandatory breath will
be delivered. The patient can breathe additionally, but unless pressure support is
set for those breaths (i.e. pressure- SIMV [P- SIMV]), they will be unaugmented.
Categorise the available modes of mechanical
ventilation
There are several ways to categorise modes of ventilation. With huge numbers
of ventilator manufacturers creating increasing numbers of new modes, many
modern modes may cross several categories and nomenclature is variable.
This is one approach to answering the question:
Conventional modes
Pressure–pressure assist control, pressure SIMV, pressure support.
Volume–volume assist control, volume SIMV.
Adaptive modes
Simple –adaptive assist control, adaptive SIMV, adaptive
volume support.
Advanced–adaptive support ventilation.
Biphasic modes
BIPAP (biphasic positive airway pressure).
APRV (airway pressure release ventilation).
Other ways to approach categorisation could include:
Mandatory versus spontaneous
Control (ventilator triggered) versus support (patient triggered)
Triggering modes–time, pressure, volume, ow, shape- signal, neural
assist (NAVA)
Cycling modes–time, volume, ow.
What types of ventilator asynchrony do you know?
Trigger asynchronies
Delayed triggering–there is a delay between the patient’s effort and
delivery of supported breath.
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