Jozef Firment1*, Peter Firment2, Vladimír Hudák1 and Janka Vašková3
1Department of Anaesthesiology and Intensive Medicine, Pavol Jozef Šafárik University in Košice, Slovak Republic
2Department of Anaesthesiology and Intensive Medicine, JA Reiman University Hospital, Slovak Republic
3Department of Medical and Clinical Biochemistry, Pavol Jozef Šafárik University in Košice, Slovak Republic
Submission: May 01, 2017; Published: October 27, 2017
*Corresponding author: Jozef Firment, 1st Clinic of Anaesthesiology and Intensive Medicine, Louis Pasteur University Hospital, Faculty of Medicine, Pavol Jozef Šafárik University in Košice, Trieda SNP 1040 66 Košice, Slovak Republic, Email: email@example.com
How to cite this article: Firment J, Firment P, Hudák V, Vašková J. Sepsis and Volume Resuscitation. J Anest & Inten Care Med. 2017; 4(1) : 555630.
New definitions of sepsis have been published in 2016 to facilitate and refine the identification and early treatment of septic patients. One of the first steps after identifying a septic patient is to supplement circulating blood volume, monitor blood flow, and, if necessary, indicate the necessity of vasopressor support of blood circulation.
The first comprehensive definitions of sepsis were published in 1992 , and subsequently reformed in 2001 . Under their influence, recommendations for the diagnosis and treatment of sepsis were issued in 2004, 2008 and 2012 [3-5]. The most recent recommendations were revised during 2016 and published in early 2017 . It is currently recommended to follow the Third Consensus Definition of Sepsis and Septic Shock, valid since 2016 (Sepsis-3) . The shortcomings of the previous definitions were evident in the excessive emphasis on inflammation and the disproportionate sensitivity and specificity of the SIRS criteria. The definition’s indication that sepsis develops through severe sepsis into septic shock has, in practice, created unclear situations in which cases potentially treated as ambulant are instead treated as severe sepsis in the Intensive Care Unit. Also, ambiguous definitions and terminology for sepsis, septic shock and organ dysfunction have led to different incidence and mortality outcomes for these nosological units. For these reasons, a group of experts agreed that the term severe sepsis is superfluous and should not be used .
Sepsis is now defined as life-threatening organ failure caused
by the inadequate response of the host to infection. The previous
concept of sepsis, presenting SIRS due to infection, is unified with
the original content of heavy sepsis, which was characterized by
the failure of at least one organ system, to the wider concept of
sepsis. Therefore, a patient suffering from sepsis is that with
an infection present and a SOFA score elevated by at least two
points. Septic shock is a subset of sepsis (meaning that sepsis
criteria are met) and, in addition, there is a circulatory disorder
(which can be easily identified by the need to maintain mean
arterial pressure above 65mmHg using noradrenaline) and the
additional presence of cell-metabolic changes (the simplest
method of identification is the increase in lactate). The most
important aspect of these circumstances is the increase in the
risk of death. The abbreviated term qSOFA (quick SOFA) has
been introduced into identification, and expresses simplified
criteria selected from SOFA, aiming to simplify the identification
of a patient whose worsening clinical condition can be caused by
sepsis (Table 1 & 2).
Sepsis and septic shock are urgent developments in the health
state, so it is recommended to start treatment and resuscitation
immediately. Resuscitation with sepsis-induced hypoperfusion
should be given with at least 30ml/kg crystalloidsintravenous
for the first 3 hours. This recommendation is considered strong,
but is supported by the low quality of the evaluated studies.
After initial resuscitation with crystalloids, the subsequent
administration of the solutions should be reassessed by frequent
assessment of the haemodynamic status. If clinical examination
does not lead to a clear diagnosis, further reassessment of
haemodynamics, including cardiac function, is recommended to determine the type of shock. If possible, to reassess the
response to fluid delivery, it is recommended to favour dynamic
variables over static ones. For patients with septic shock
requiring vasopressors, it is recommended to achieve an initial
mean arterial pressure (MAP) of 65mmHg. If there are elevated
levels of blood lactate in the patient, which are considered to be
markers of hypoperfusion of the tissues, it is recommended to
normalise them during resuscitation.
Repeated re-evaluation of blood circulation response to
administered solutions should include clinical examination and
evaluation of static physiological variables (heart rate, blood
pressure, arterial pO2, breathing, temperature, diuresis) as well
as other available dynamic non-invasive or invasive methods.
In practice, passive leg raising (PLR) is often used to evaluate
changes in blood pressure, which can also be performed in
spontaneously breathing patients. The blood that moves into the
heart from the lower limbs is able to increase the preload of the
left heart. The advantage of the method is also the possibility to
reverse its effects by returning the patient to the semirecumbent
position (Figure 1). Therefore, PLR is also referred to as
“reversible autotransfusion” . It should be noted, however, that
the test is only orientational. It is therefore necessary to measure
real-time changes in CO (echo, analysis, and curve, oesophageal
doppler) for more accurate interpretation during the PLR test,
and not only to provide invasive or non-invasive blood pressure
measurements. CO must be measured continuously in real time
during the test, as the effect may disappear within 1 minute .
Another dynamic way to evaluate hypovolaemia is to observe the
fluctuations of invasively-measured arterial systolic pressure
under the influence of positive pressure ventilation. The maximal
increase in systolic pressure occurs at the end of inspiration and
the maximum drop in systolic pressure during exspiration .
In the initial steps of treating septic shock, it is necessary
to emphasize the so-called parallax MAP 65mmHg. The rise in
MAP from 65mmHg to 85mmHg after administration of NA does
not significantly affect O2 metabolism, skin microcirculation,
diuresis or splanchnic perfusion. The rise to 85mmHg from
65mmHg may not yet be a significant indicator of improvement.
It is a picture of the macrocirculatory state (under the influence
of NA): microcirculation can be closed and the shock can persist!
However, if the patient worsens in the sense of decreasing MAP
to 65mmHg, it must be evaluated as a significant indicator of
deterioration  (Figure 2).
It is still necessary to highlight the importance of lactate
in the initial resuscitation of septic shock. Lactate levels serve
as a more objective indicator of tissue perfusion than clinical
examination or diuresis. In the resuscitation of septic shock by
lactate, there is a significant decrease in mortality comparing
resuscitation with and without its monitoring.
While it is important to add that tissue perfusion disturbances
in sepsis are proven (direct microcirculation in the sublingual
and intestinal tract), direct evidence that hyperlactataemia is the
direct consequence of hypoperfusion of tissues is lacking and,
on the contrary, the evidence does not confirm it. These studies
showed a much higher level of lactate in muscle tissue compared
to plasma levels in patients with hyperdynamic sepsis, despite
the higher partial pressure of oxygen observed in muscle tissue
by direct tissue oximetry. Could there not be a higher production
of lactate for purposeful sepsis than as a consequence of
hypoperfusion? Does the elevated lactate level not have any
important metabolic, protective or backup functions in the stress
response of the organism? A lower lactate level at the onset of
the disease will result in lower insulin intensity, and early lactate
reduction during treatment of sepsis will be a consequence of
overall treatment and elimination of the source, or other insult
(right antibiotic, early drainage of the identified abscess) [11,12].