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2 Endocrine Aspects of Acute and Prolonged Critical Illness 23
Mitochondrial dysfunction is correlated with disease severity, particularly with
long-term adverse clinical outcomes such as prolonged mechanical ventilation and
extended stays in the intensive care unit (ICU) and hospital. In this stage of
mitochondrial metabolic-bioenergetic downregulation, an excessive supply of metabolic substrates may exacerbate cellular damage, as mitochondria are incapable of
utilizing substrates for energy purposes.
Several factors, including excess inflammatory mediators, altered thyroid hormone function, and reduced mitochondrial protein production, may contribute to the
diminished mitochondrial capacity for oxygen utilization and oxidative phosphorylation. This mitochondrial downregulation should be considered when providing
energy substrates through artificial nutrition in the various metabolic phases of
critical illness [33–35].
Metabolic Aspects of Stress Response
The changes in metabolism associated with acute illness are proportional to the
severity of the illness and also involve changes in body temperature and heart rate
[36]. Essentially, there is a reduct ion in energy metabolism in the hyperacute phase
of the injury (“ebb” phase), while the subsequent phase (“flow” phase) is characterized by a catabolic response with high consumption of glycogen, fat, and muscle
proteins. The final resumption of prote in synthesis and lean mass reconstitution
occurs only in the anabolic phase once the critical illness is under control [
In the hyperacute phase of critical or posttraumatic illness, the purpose of the
neuroendocrine response is to maintain homeostasis to ensure the survival of the
organism. From a metabolic standpoint, this response is characterized by reduced
oxygen consumption, decreased body temperature, and increased urinary excretion
of nitrogen [37, 38].
An imp
directly proportional to the severity of the initial injury in terms of the magnitude
of trauma and tissue damage. Early in the ebb phase, hepatic glycogen stores are
rapidly utilized for a period of about 12–24 h. Thereafter, glucose synthesis is
ensured by amino acids, lactates, pyruvate, and glycerol, all used for hepatic and
renal gluconeogenesis. At this stage, gluconeogenesis may produce about 360 g of
endogenous glucose, equivalent to about 1300 kcal. Such production cannot be
inhibited by exogenous administration of substrates or insulin [
gluconeogenesis delivers glucose to noninsulin-dependent cells such as neurons,
erythrocytes, and inflammatory cells. Quantitatively, in this phase, lactates are the
most important substrates used for gluconeogenesis, while in the later catabolic
phase, amino acids derived from muscle proteins are primarily used. Lactates are
derived from anaerobic glucose metabolism in peripheral tissues and in the liver
through the Cori cycle [40,
ortant metabolic feature of this phase is the hyperglycemic response,
39, 40].
41].
36].
Hepatic
24 M. G. Annetta
Time
STRESS
Seconds
Minutes
Sympathetic nervous system
Hours
Days
Weeks
Fig. 2.2 Neuroendocrine response to critical illness and trends in plasma concentrations of the
most important pituitary and peripheral hormones during critical illness
Hypothalamic –Pituitary axis
and Peripheral Hormones
Immune System
(Cytokines, Chemokines,
Heat shock proteins)
Behavioural
Hypersecretion of certain hormones (glucagon, catecholamines, cortisol, and GH)
and inflammatory react ion generated by cytokines also result in peripheral insulin
resistance, and this worsens hyperglycemia and inhibits anabolism (Fig. 2.2).
Conclusion
In conclusion, exploring the endocrine aspects of both acute and prolonged critical
illness reveals a complex interplay of physiological responses. The initial stress
response, marked by autonomic, endocrine, and immune system modifications, is
geared towards maintaining homeostasis and ensuring survival during the acute
phase. With advancements in intensive care treatments, the landscape of critical
illness has evolved, leading to a prolonged or “chronic” phase characterized by
distinct neuroendocrine alterations. The transition from the acute to the chronic
phase, though not precisely defined, is estimated to occur around 10 days of illness.
This extended phase unveils mitochondrial dysfunction, particularly associated with
hypoxia and hypoperfusion, prompting a metabolic and bioenergetic hibernation of
cells. This adaptive mechanism appears to have a protective purpose, preventing
cellular deterioration and death during the acute phase of critical illness. Notably, the
challenge lies in navigating the delicate balance of inte rvention, especially
concerning nutritional strategies. Aggressive nutrition in the early hyperacute
phase may prove detrimental, exacerbating oxidative stress and adversely impacting
clinical outcomes. Understanding these intricate endocrine dynamics is crucial for
refining therapeutic approaches in the care of critically ill patients. In this chapter, we
have aimed to provide an overview of the current understanding of the endocrine
2 Endocrine Aspects of Acute and Prolonged Critical Illness 25
aspects of acute and prolonged critical illness, acknowledging the nuanced and
evolving nature of this multifaceted medical condition. Continued research in this
field is essential for unraveling further complexities and refining therapeutic strategies to enhance patient outcomes in the face of critical illness.
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Chapter 3
Disorders of Fluid, Electrolytes, and Acid
Base Balance
Zaccaria Ricci, Luigi Diaferia, Giulio Iacopetti, and Filippo Pelagatti
Introduction
Disorders of fluid balance and electrolytes pose significant challenges in the management of critically ill patients. The intricate interplay between fluid administration,
electrolyte disturbances, and acid-base imbalances underscores the complexity of
maintaining homeostasis in the human body. Fluid balance, a cornerstone of physiological stability, is intricately linked to cardiovascular dynamics and tissue perfusion. Meanwhile, electrolyte imbalances such as dysnatremias and dyskaliemias can
lead to profound clinical manifestations, exacerbating patient morbidity and mortality. Moreover, disruptions in acid-base equilibrium further complicate patient care,
necessitating prompt evaluation and intervention to mitigate adverse outcomes. In
this chapter, we explore the multifaceted landscape of disorders of fluid balance,
electrolytes, and acid-base balance encountered in critically ill pati ents. We delve
Supplementary Information The online version contains supplementary material available at
https://doi.org/10.1007/978-3-031-66541-7_3.
Z. Ricci (
Pediatric Intensive Care Unit, Department of Anesthesia and Critical Care, Meyer Children’s
Hospital, IRCCS, Florence, Italy
Department of Health Sciences, Section of Anesthesiology and Intensive Care, University of
Florence, Florence, Italy
L. Diaferia
Department of Health Sciences, Section of Anesthesiology and Intensive Care, University of
Florence, Florence, Italy
Department of Interdisciplinary Medicine – ICU Section, University of Bari, Bari, Italy
G. Iacopetti · F. Pelagatti
Department of Health Sciences, Section of Anesthesiology and Intensive Care, University of
Florence, Florence, Italy
e-mail: giulio.iacopetti@unifi.it; filippo.pelagatti@unifi.it
© The
A. Cotoia et al. (eds.), Nutrition, Metabolism and Kidney Support,
https://doi.org/10.1007/978-3-031-66541-7_3
✉)
Author(s), under exclusive license to Springer Nature Switzerland AG 2024
27
28 Z. Ricci et al.
into the pathophysiology, clinical manifestations, diagnostic approaches, and therapeutic interventions aimed at restoring equilibrium and optimizing patient outcomes.
Through an in-depth examination of these interconnected phenomena, we endeavor
to provide clinicians with a comprehensi ve understanding of the complexities
inherent in managing these conditions, thereb y facilitating informed decisionmaking and enhancing patient care.
Disorders of Fluid Balance
Sixty percent of adult human body is composed by water. The continuous balance
between fluids that are given to the body and those that are expelled from it is a
fundamental aspect of human physiology and it is at the base of homeostasis. Fluid
balance is significantly associated with fluids running in the bloodstream even if
volemia and fluid homeostasis should not be considered synonyms. In fact, even if
impaired oxygen delivery due to hypovolemia and congestion secondary to
hypervolemia have been long recognized as major determinants of organ dysfunction, recently the literature has focused on the use of fluids in terms of quantity
(volume/time) and quality (type of fluids administered), emphasizing the undesired
effects that may result from their “inappropriate” administration, regardless of blood
circulation and volemia [
of the alveolar–arterial membrane and on the distance from capillaries to tissues.
Fluid excess stagnating in the interstitial space compromises oxygen diffusion and is
one of the components of multiple organ dysfunction in critically ill patients [2].
Many s
tudies a
outcomes. Two approaches to the administration of intravenous fluids in surgical and
critically ill patients have been classically compared: “liberal” and “restrictive.” In
the liberal approach, the use of fluids is more permissive, and traditionally generous
amounts of fluids are administered perioperatively to correct and sometimes to overcorrect the preoperative fasting (whose relevance is significantly reduced), other
fluid deficits (such as the use of intestinal preparations), the so-called insensible
losses (related to perspiration through the skin and peritoneum), and diuresis. In the
restrictive approach, on the other hand, a lower amount of fluid administration is
envisaged, supported by the results of numerous trials showing a lower incidence of
postoperative complications as well as a reduction in length of stay in patients who
tend to receive less “corrective” fluids. Similar approaches have been described in
septic critically ill patients [3, 4]
Overall, no definitive conclusion can be derived by initial prospective studies
[
5]. The restrictive approach is one of the cornerstones of the Enhanced Recovery
After Surgery (ERAS) pathway, which promotes a reduction in preoperative fasting
and rapid reintroduction of oral diet among the strategies to promote rapid recovery
after surgery [4]. However, an overly restrictive approach can also lead to some
complications such as hypotension, reduced perfusion of vital organs, and delayed
1]. Clearly, oxygen diffusion is dependent on the thickness
ttempted to verify the effects of fluids and fluid balance in patients’
.
3 Disorders of Fluid, Electrolytes, and Acid Base Balance 29
b
a
c
Fig. 3.1 There is a spectrum of fluid balance for the critically ill patients, that is a U-shaped curve.
(A) This spectrum can swing between positive fluid balance (+FB) and negative fluid balance (-FB)
with varying levels of clinical impact depending on the severity of the abnormal fluid balance.
(B) Depending on the case-mix and/or resources available, the U-shaped curve may have more or
less tolerance for a positive or negative fluid balance. (C) For any given sick patient, there are
several factors (i.e., host factors, interventions, adverse outcomes) that may push them towards a
greater +FB or -FB or pull them back towards a state of neutral fluid balance at the center. These
may vary over the course of the hospitalization and can be constantly changing [Acute Disease
Quality Initiative 26, www.ADQI.org][13]
wound healing. On the other side, fluid overload has been repeatedly identified as an
independent predictor of worse outcomes in retrospective studies [6], but its impact
in randomized
trials does not seem to be confirmed. It is important to consider that
positive fluid balance is often strongly influenced by patients’ disease status. The
maintenance of a septic-inflammatory state with vasodilation and capillary leak
(or capillary spillover) implies hypovolemic hypotension and imposes, in a certain
way, aggressive fluid resuscitation. In these patients the balance between tissue
rdia
edema due to fluid resuscitation and low ca
ventr
icular
ad must be carefully considered. This concept is well expressed
prelo
graphically by the Bellamy U-curve (Fig.
c output determined by insufficient
3.1a).
The risk of mortality related to fluid overl oad in critically ill patients can be
mitigated by the application of restrictive strategies, aggressive and timely use of
decongestive drugs (loop diuretics) and renal replacement therapy, today routinely
applied in the intensive care unit [7]. In the 2022 CLASSIC Clinical Trial, for
example, it has been shown that in adult critically ill patients with septic shock,
90-day mortality was almost the same whether they were treated with a standard or
restrictive fluid strategy. There was no difference between the two groups in the total
number of days of respiratory support [
In the same line, the RADAR2 and
8].
30 Z. Ricci et al.
REVERSE-AKI trials showed that pharmacologic strategies for decongestion can be
feasibly applied and may imply better renal outcomes [9, 10].
We can therefore say that
tailored to their clinical needs (Fig.
each patient should receive individualized fluid therapy
3.1b, c): the volume to be administered oscillates
like a “pendulum” on the patient’s susceptibility and metabolic demands. Such
amount has to avoid the risk of hypoperfusion, but it must prevent organ edema.
Precisely for this reason, in recent years new evidence has emerged showing that
fluid therapy based on objectively measurable fluid responsiveness parameters
would be able to improve outcomes, both in critically ill patients and those undergoing major surgery [
5]. The latest approach, called Hemodynamic Goal Directed
Therapy (GDT), is based on objectively measurable fluid responsiveness parameters
that include hemodynamic response to fluid challenge, dynamic tests such as pulse
pressure variation, stroke volume variation, leg raising test, echocardiography with
analysis of cardiac chambers and inferior vena cava, monitoring of hemoglobin
concentration in non-bleeding patients, heart rate, and urinary output. Hemodynamic
GDT is encouraged in the resuscitation phase, but that should be followed by a phase
of volume optimization and stabilization [11]. Furthermore, in hemodynamically
unstable patients, vasopressor and/or inotropic agents should be initiated simultaneously with fluid administration. Once hemodynamic stabilization is achieved, in
the evacuation phase, the volume overload gained in the previous phases must be
timely removed. If spontaneous diuresis is insufficient, excess fluid must be removed
with the use of diuretics or, in case of diuretic resistance, of renal replacement
therapy. Interestingly, the same GDT approach of resuscitation can be applied in
the decongestive phase, in order to verify patients’ tolerance to fluid removal [12].
Dysionemias
Electrolyte disturbances are frequently encountered among critically ill patients and
are typically associated with increased morbidity and mortality in the intensive
care unit (ICU). Therefore, prompt evaluation, diagnosis, and therapy are essential
[14–16].
Dysnatremias
Dysnatremias ([Na+ ]
relative imbalance between the total amount of sodium and the total water content.
Many cases of dysnatremia are acquired after a patient is admitted to the ICU.
Careful monitoring of plasma and urinary sodium, judicious use of hypertonic and
hypotonic saline solutions, and removal of non-osmotic stimuli for vasopressin
secretion (nausea, pain, hypovolemia) are essential components in the prevention
of iatrogenic dysnatremia. The severity of symptoms correlates with the severity and
< 135 mEq/L or > 145 mEq/L) are essentially due to a
PL
3 Disorders of Fluid, Electrolytes, and Acid Base Balance 31
rate of development of dysnatremia. Clinical manifestations are nonspecific and may
be related to changes in serum osmolality, implying neurologic symptoms (lethargy,
irritability, restlessness, convulsions, coma), and death in the most severe alterations.
There may be signs of hypovolemia or hypervolemia. It is important to consider that
the neurol ogical manifestations and their course are not clinically evident in sedated
and ventilated patients (Table
). Most cases of hyponatremia in patients with
3.1
neurologic or neurosurgical diseases are caused by two mechanisms: the syndrome
of inappropriate secretion of antidiuretic hormone (SIADH) and the cerebral salt
wasting syndrome (CSWS). It can be difficult to distinguish between these two
syndromes and volume status must be accurately assessed; in fact, SIADH is treated
with fluid restriction, while CSWS requi res fluid and sodium replacement due to
hypovolemia.
The speed of correction
of dysnatremia is of fundamental importance to avoid
repercussions at the level of the central nervous system (cerebral edema, herniation,
pontine myelinosis). Correction speeds higher than 0.5 mEq/L/h are to be reserved
for symptomatic or acute hypo-hypernatremia (occurring within hours) without ever
exceeding plasma sodium variations of 10–12 mEq/L/die.
Dyskalemias
Dyskalemia ([K+ ]
< 3,5 mEq/L or > 5 meq/L) can develop due to cellular shifts of
Pl
potassium, increased-decreased potassium ingestion, or impaired potassium elimination. In the context of the critically ill patient, these mechanisms are often present
due to the patient’s underlying conditions (diabetic ketoacidosis, insulin resistance,
rhabdomyolysis, blood transfusions, burns, trauma, kidney dysfunction, adrenal
insufficiency, hypomagnesemia) and pharmacological therapies (Table
3.2). Evalu-
ation of urinary potassium may help in the differential diagnosis. The symptoms of
hypokalemia include neuromuscular (paralysis, weakness, nausea, vomiting, constipation, respiratory muscle weakness) and cardiological (electrocardiographic
changes and arrhythmias) manifestations. Intravenous potassium supplementation
is reserved for the treatment of severe (<2.5 mEq/l) and/or symptomatic hypokalemia or when the gastrointestinal tract cannot be utilized, with oral adminis tration
preferred when possible. Rapid potassium infusion (i.e., > 10–20 mEq/h) requires a
central venous catheter to avoid phlebitis and venous damage. Correction of underlying hypomagnesemia and hypocalcemia makes it easier to correct potassium
values. Total daily potassium supplementation should not exceed 240–400 mEq/day.
The clin
ical manifestations of hyperkalemia, often absent for [K
+
]
Pl
< 6–6.5-
mEq/L, include neuromuscular symptoms (muscle contractions, cramps, weakness,
ascending paralysis) and cardiological symptoms (electrocardiographic changes,
bradyarrhythmias, ventricular fibrillation, asystole). The goals of the hyperkalemia
therapy are to antagonize the cardiac effects of potassium, reverse symptoms
(if present), and return serum potassium to normal while avoiding overcorrection.
32 Z. Ricci et al.
Table 3.1 Pathophysiology and main causes of dysnatremias. (Modified from [17])
Hyponatremia Hypernatremia
Increased free-water intake Decreased effective
Polydipsia Malnutrition No access to water Medications
Hypotonic fluids NPO Hypertonic fluids
Surgical irrigation Loss of thirst
Decreased free-water
output
SIADH Renal losses Renal losses Rarely a cause of
Physiologically appropri-
ate increase in AVP (states
of decreased effective
intravascular volume, e.g.,
HF, CLD, sepsis,
hypothyroidism)
HF heart failure, CLD chronic liver disease, AVP arginine
SIADH syndrome of
drome, GIT gastrointestinal
TIN tubulointerstitial nephritis
osmole intake
Increased effective
osmole output
Diuretics (primarily
thiazides)
CSWS Osmotic diuresis
Hypocortisolemia Reduced renal
Hypoaldosteronemia Non-renal losses
Hypothyroidism Sweating
Salt losing
nephropathy
Non-renal losses Respiratory
Bleeding
GIT losses with high
effective osmolarity
secretory
(e.g.,
diarrhea)
Burns
inappropriate antidiuretic
tract, NPO nil per Os, DI diabetes insipidus, ATN acute tubular necrosis,
Decreased freewater intake
drive (e.g., hypothalamic lesions)
Increased freewater output
DI (central and
nephrogenic)
(e.g., hyperglycemia, mannitol,
urea)
concentrating
capacity (e.g.,
myeloma, ATN,
TIN)
Osmotic diarrhoea
(e.g., high flow
oxygen without
humidifier)
vasopressin (antidiuretic hormone),
hormone, CSWS cerebral-renal salt wasting syn-
Increased effective
osmole intake
Salt poisoning
Decreased effective
osmole output
clinically important
hypernatremia
Hyperaldersteronemia
Hypercortisolemia
Glucocorticoids
losses