Page 590 - ACCCN's Critical Care Nursing

Multiple Organ Dysfunction Syndrome 567

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The alarm reaction (flight-or-fight response) is initiated
when stress is detected, increasing the amount of glucose TABLE 21.2 Acute organ dysfunction 46,98
and oxygen available to the brain, skeletal muscle and
heart. Two-thirds of total blood volume is also redistrib- Organ system Clinical parameters
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uted to support central circulation. A rise in glucose
production and the breakdown of glycogen in skeletal Cardiovascular Patient requires vasopressor support (systolic
BP <90 mmHg) or MAP <70 mmHg for 1
muscle increases circulating glucose levels, providing an hour despite fluid bolus
immediate energy source. The long-lasting second stage
is a resistance reaction, involving hypothalamic, pituitary Respiratory Patient requires mechanical ventilation: P/F
ratio <250, PEEP >7.5 cmH 2 O
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and adrenal hormone release. Response exhaustion
occurs when these physiological changes can no longer Renal Low urine output <0.5 mL/kg/h; raised
maintain homeostasis. creatinine >50% from baseline or requiring
acute dialysis
3
Haematological Low platelet count (<1 000 000/mm ) or APTT/
COMPENSATORY MECHANISMS PTT > upper limit of normal
Internal equilibrium (homeostasis) is maintained by the Metabolic Low pH with increased lactate (pH <7.3 and
nervous and endocrine systems, and these work symbio- plasma lactate > upper limit of normal)
tically with other compensatory mechanisms, such as Hepatic Liver enzymes >2 × upper limit of normal
endothelial cells, to maintain cellular perfusion. The
nervous system responds rapidly to maintain homeosta- CNS Altered level of consciousness/reduced
Glasgow Coma Scale score
sis by sending impulses to organs to activate neurohor-
monal responses (see Chapters 16 and 20). Endothelins Gastrointestinal Translocation of bacteria, possible elevated
(ET-1, ET-2, ET-3) are potent vasoconstrictors produced pancreatic enzymes and cholecystitis
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by endothelial cells that regulate arterial pressure. The
endocrine system works in a slow and sustained manner
by secreting hormones, which travel via the blood to ORGAN DYSFUNCTION
end-organs.
Organ dysfunction is a common clinical presentation in
An initial acute-adaptive response is activated when an ICU. Patients with dysfunction in the respiratory, cardio-
insult or stress occurs. For example, the body senses a vascular, hepatic or metabolic systems were 50% more
disruption of blood flow through baroreceptor and che- likely to require ICU treatment and had a higher mortal-
moreceptor reflex actions: baroreceptors located in the ity than patients not requiring intensive care. Timely
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carotid sinus detect changes in arterial pressure; chemo- identification of organ dysfunction is therefore critical, as
receptors co-located with the baroreceptors detect O 2 , early intervention reduces damage and improves recovery
+
CO 2 and H concentration. When alterations are sensed, in organ systems. As each organ fails, the average risk of
the cardiovascular centre in the brain adjusts autonomic death rises by 11–23%, with up to 75% of patients in
outflow accordingly. In a patient with decreased tissue sepsis clinical trials having at least two failing organs.
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perfusion, there is increased peripheral vasoconstriction, The organ system that most commonly fails is the pul-
contractility and heart rate. Blood flow is shunted to the monary system, followed by the cardiovascular, renal and
vital organs (brain, heart, lungs), and away from less vital haematological systems. Organ and systems dysfunc-
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areas (e.g. gastrointestinal and reproductive organs). tion are a result of hypoperfusion, inflammation, cellular
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Important hormonal regulators of blood flow are also dysfunction and oedema. Dysfunction of the cardiovas-
activated from decreased blood flow to the kidneys, cular (Chapters 10 and 12), respiratory (Chapters 14 and
including adrenocorticotrophic hormone (ACTH), and 15), renal (Chapter 18), and hepatic and gastrointestinal
the renin–angiotensin–aldosterone system (see Chapter systems (Chapter 19) have been previously addressed.
18). Adrenal medullary hormones, adrenaline and nor- This next section addresses the haematological, endo-
adrenaline, vasopressin (antidiuretic hormone) and atrial crine and metabolic systems. Neurological dysfunction is
natriuretic peptide also regulate blood flow to maintain also common in the patient with MODS and comple-
adequate circulation and tissue oxygenation. 13,38,39 ments previous discussions in Chapter 17.
Arterial pressure is a major determinant of tissue perfu-
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sion as it forces blood through the regional vasculature. HAEMATOLOGICAL DYSFUNCTION
Hypotension (systolic blood pressure <90 mmHg or Systemic inflammatory response syndrome (SIRS) and
mean arterial pressure [MAP] <70 mmHg) results from disseminated intravascular coagulation (DIC) have
either low systemic vascular resistance or a low cardiac pivotal and synergistic roles in the development of
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output. Glomerular filtration falls, leading to reduced MODS. The coagulopathy present in MODS results
urine output; low cerebral blood flow results in an altered from deficiencies of coagulation system proteins (e.g.
8
level of consciousness; and other manifestations reflect protein C, antithrombin 3 and tissue factor inhibitors).
low-flow states in other organ systems. To maintain Inflammatory mediators initiate direct injury to the vas-
oxygen supply, respirations and heart rate increase to cular endothelium, releasing tissue factor, triggering the
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meet organ oxygenation demands. Organ dysfunction extrinsic coagulation cascade and accelerating thrombin
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ensues if balance is not sufficiently restabilised production. Coagulation factors are activated as a result
(see Table 21.2). of endothelial damage with binding of factor XII to the