Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / @xirurgi_2025 / @xirurgi_2025 - 1159 - файл.pdf
Chapter 8: Capillary leak and fluid resuscitation 85
Increased
IAP
Mesenteric Vein
Compression
CAUSE
Visceral
Swelling
Oliguria
Venous
Hypertension
Effect
Intestinal
Oedema
Fluid
Resuscitation
Figure 8.4
This has direct consequences on fluid management in the
critically ill patient with IAH. Patients at risk of GIPS require
restrictive fluid strategies and fluid removal guided by extended
haemodynamic monitoring, including EVLW
measurements. Restrictive fluid management may require a
greater use of vasopressor therapy, resuscitation with
hyperoncotic solutions (e.g. albumin 20%) and early initiation
of diuretics and renal replacement therapy.
Figure 8.5 illustrates the GIPS and its relation to the three
hits theory.
Table 8.3 lists the consequences of fluid overload.
Table 8.4 lists the risk factors for the development of IAH
and ACS in the context of capillary leaks.
When it starts to get better (day 3)
The dual response to acute inflammatory insult is characterized
by a turning point on day 3. Homeostasis of cytokines allows
86 Section 2: Underlying predisposing conditions: when to worry?
Trauma, infection, burns,
sepsis, bleeding
First HIT
Neutrophil Activation & Cytokine Release
Shock & Ischamia
Dilutional coagulopathy,
clot disruption, decreased
blood viscosity, interstitial
oedema
Second HIT
Resuscitation & Reperfusion
Third HIT
Global
Peripheral Oedema Cerebral Oedema
Lung Oedema
Increased
Permeability
Syndrome
Gut Oedema
Kidney Oedema
Figure 8.5
initiation of correction of the microcirculatory disruptions
and ‘closure’ of the capillary leaks. Microcirculatory blood
flow seems to normalize on day 3 in patients with abdominal
sepsis.
Key points
Capillary leak is a result of the inflammatory response and
its diverse triggers, including ischaemia–reperfusion.
Plasma volume expansion to correct hypoperfusion
predictably results in extravascular movement of water,
electrolytes and proteins.
Chapter 8: Capillary leak and fluid resuscitation 87
Table 8.3 Consequences of capillary leaks and fluid
overload
System Effect
Central nervous system Cerebral oedema increases
Impaired cognition
Delirium
Intracranial pressure increases
Cerebral perfusion pressure decreases
Intraocular pressure increases
Intracranial hypertension
Respiratory system Pulmonary oedema
Impaired gas exchange
Hypercarbia
and PaO2/FiO2decrease
PaO
2
Extravascular lung water increases
Prolonged ventilation
Difficult weaning
Increased work of breathing
Renal system Renal interstitial oedema
Renal venous pressure increases
Renal blood flow decreases
Interstitial pressure increases
Glomerular filtration rate decreases
Uraemia
Renal vascular resistance increases
Salt retention increases
Water retention increases
Renal compartment syndrome
Abdominal wall Tissue oedema increases
Lymphatic drainage decreases
Microcirculation decreases
88 Section 2: Underlying predisposing conditions: when to worry?
Table 8.3 (cont.)
System Effect
Poor wound healing
Wound infection increases
Pressure ulcers
Endocrine system Release of cytokines
Gastrointestinal system Gut oedema increases
Malabsorption
Ileus
Abdominal perfusion pressure decreases
Bowel contractility decreases
IAP increases and incidence of IAH and ACS increase
Successful enteral feeding decreases
Intestinal permeability increases
Bacterial translocation increases
Hepatic system Hepatic congestion
Impaired synthetic function
Cholestasis
Impaired cytochrome P450 activty
Hepatic compartment syndrome
Cardiovascular system Myocardial oedema
Conduction disturbances
Impaired contractility
Diastolic dysfunction
Plasma volume expansion in the context of GIPS can lead
to IAH, and sometimes ACS.
A variety of strategies are available to the clinician to
reduce the volume of fluids used during resuscitation and this
may affect the occurrence of IAH.
Chapter 8: Capillary leak and fluid resuscitation 89
Table 8.4 Risk factors for the development of IAH and ACS
In the context of capillary leak and fluid resuscitation
Acidosis (pH below 7.2)
Hypothermia (core temperature below 33°C)
Coagulopathy [platelet count below 50 000/mm
thromboplastin time (APTT) greater than twice normal or a prothrombin time
(PTT) below 50% or an international standardized ratio (INR) greater than 1.5]
Polytransfusion/trauma (>10 units of packed red cells/24 hours)
Sepsis
Severe sepsis or bacteraemia
Septic shock
Massive fluid resuscitation (3–5 L of colloid or >10 L of crystalloid/24 hours with
capillary leak and positive fl uid balance)
Major burns
FURTHER READING
Cordemans C, De laet I, Van Regenmortel N et al. Fluid
management in critically ill patients: The role of
extravascular lung water, abdominal hypertension, capillary
leak and fluid balance. Annals of Intensive Care 2012; 2
(Suppl. 1): S1.
Cuthbertson DP. Post-shock metabolic response. Lancet
1942; 239: 433–7.
Fishel RS, Chandrakanth A, Barbul B. Vessel injury and
capillary leak. Critical Care Medicine 2003; 31(8): S502–11.
Matsuda N, Hattori Y. Vascular biology in sepsis:
pathophysiological and therapeutic significance of vascular
dysfunction. Journal of Smooth Muscle Research 2007; 43
(4): 117–37.
3
or an activated partial
90 Section 2: Underlying predisposing conditions: when to worry?
Maxwell RA, Fabian TC, Croce MA, Davis KA.
Secondary abdominal compartment syndrome: an
underappreciated manifestation of severe hemorrhagic
shock. Journal of Trauma 1999; 47(6):
995–9.
Section 3
Specific conditions: when to worry more?
Chapter 9
Pancreatitis
Introduction
IAH is an important contributor to early organ dysfunction in
severe acute pancreatitis, and is associated with pancreatic
necrosis. Up to 80% of patients with severe acute pancreatitis
will develop IAH. ACS is observed in 30% of these patients.
Prompt recognition, prevention of IAH and treatment of the
ACS are essential to avoid irreversible deterioration.
Why and when do patients with severe acute pancreatitis develop IAH and ACS?
IAH can be present at admission or occur shortly thereafter,
with ACS developing mostly within the first few days. IAH is
caused by the inflammatory process causing retroperitoneal
oedema, fluid retention, ascites, ileus and decreasing
abdominal wall compliance. Aggressive fluid resuscitation will
contribute to IAH. Figure 9.1 shows an abdominal CT scan
obtained early after admission of a patient with pancreatitis.
Retroperitoneal inflammation and fluid collections are present.
IAH and ACS can appear later, 1 or more weeks after initial
presentation. This late appearance is often associated with local
94 Section 3: Specific conditions: when to worry more?
Figure 9.1
pancreatic complications such as bleeding or infected
peripancreatic necrosis.
Consequences of IAH and ACS in the patient with severe acute pancreatitis
IAH and ACS are associated with impaired organ dysfunction,
especially of the cardiovascular, respiratory and renal systems.
It can be difficult to differentiate between the systemic
inflammatory response syndrome (SIRS) of the pancreatitis
process itself and the effects of ACS. Respiratory insufficiency in
the non-ventilated patient or increased ventilatory issues in
ventilated patients should raise the possibility of IAH or ACS.
Elevated hemidiaphragms and bilateral pleural effusions may
be observed. Oliguria is a common feature and additional fluid
loading will further exacerbate IAH or ACS.