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 / Библиотека им академика М.И. Перельмана / Книга_1520_Библиотеки_им_академика_М_И_Перельмана
.pdf
491
34 Intensive Care: The Basics
Case Scenario 1
A 56-year-old lady is on the surgical HDU 72 h after having had an Ivor-Lewis
esophagectomy. She is becoming increasingly tachycardiac and tachypneic.
CXR and blood gas results are as follows:
Date 18/3
Time 19:30
FiO
2
0.6
pH 7.31
pCO
2
4.71
pO
2
16.4
BE −4.5
Assessing Oxygenation
Although the PaO
2
is 16.4, the patient is breathing 60% oxygen. This is evi-
dence of signifi cant compromise of oxygenation and is a cause for concern.
Assessing Acid–Base Status
1. What is the pH?
2. What is the PaCO
2
?
3. What is z the base defi cit?
4. Is there evidence of compensation?
492
J.R. Goodall
34.4.1 Assessing Oxygenation
The oxygenation status can be determined from the PaO
2
, which refl ects the partial
pressure of oxygen in the arterial blood sample, along with the SaO
2
, which describes
how much of the hemoglobin present in the sample is saturated with oxygen. Both
of these results can only be interpreted when the inspired oxygen concentration is
known: although a PaO
2
of 11.7 kPa when the patient is breathing room air is nor-
mal, if the patient is breathing supplementary oxygen via a face mask with reservoir
bag, it most certainly is not!
34.4.2 Assessing Acid–Base Status
The assessment of acid–base status is easier if the following steps are followed:
1 . What is the pH ?
A pH of <7.35 means that the patient has an acidemia.
A pH of <7.45 means that the patient has an alkalemia.
2 . What is the PaCO
2
?
This will determine if there is a respiratory component to the acid–base
disturbance.
(a) If the pH indicates that the patient is acidotic and the PaCO
2
is high, there is
a respiratory component to the acidosis.
(b) If the pH shows that the patient has an alkalemia and the PaCO
2
is low, there
is a respiratory component to the alkalemia.
3 . What is the base excess ( BE )?
This will determine if there is a metabolic component to the acid–base
disturbance.
(a) If the pH <7.35 and the BE <−2, there is a metabolic component to the
acidemia.
(b) Likewise, if the patient is alkalemic (pH >7.45) and the BE >+2, there is a
metabolic component to the alkalemia.
Remember, in certain circumstances, there may be both respiratory and meta-
bolic components to an acidemia or alkalemia. Using the system order above will
help identify such mixed causes of acid–base disturbance.
4 . Is there evidence of compensation ?
It must be remembered that compensatory homeostatic mechanisms will try to
correct any acid–base disturbance when possible. A patient with a metabolic
acidemia will increase respiration and minute volume in an attempt to “blow off”
CO
2
and bring the pH back to normal. Similarly, a patient with respiratory failure
will attempt to compensate for a high CO
2
by retaining bicarbonate in the
kidneys.
493
34 Intensive Care: The Basics
(a) In a case of a metabolic acidemia, is the PaCO
2
<4.3 kPa? If so, there is evi-
dence of respiratory compensation.
(b) In a case of respiratory acidemia (PaCO
2
>6.5 kPa), is the BE >+2? If so,
there is evidence of metabolic compensation.
(c) In a case of metabolic alkalemia (BE >+2), a PaCO
2
>6.5 would indicate
respiratory compensation (unusual).
(d) Respiratory alkalemia is usually very short-lived , and there is rarely time for
compensation . If metabolic compensation did occur , it would be indicated by
a BE < − 2 .
34.5 Further Discussion on Acidosis
In any discussion about acid–base balance, the following are basic concepts that
must be remembered:
The acidity of a solution is determined by its hydrogen ion concentration: acidity •
is usually expressed as pH (pH = −log
10
[H
+
]). The greater the concentration of
hydrogen ions, the more acid the solution. Pure water has a pH of 7.0 at 25 and
is “neutral” in acid–base terms.
An acid is a proton donor (it generates hydrogen ions when in solution), and base •
is a proton acceptor.
Strong acids or bases dissociate completely when in solution, weak acids or •
bases only partially: the Henderson–Hasselbach equation can be used to calcu-
late the ratio of dissociated to undissociated ions for weak acids.
Although around a 1,000 mmol of hydrogen ions [H
+
] are produced each day, the
concentration of hydrogen ions in the body is normally controlled tightly at
40 nmol·L
−1
(pH 7.42) [ 1 ] .
Most of the [H •
+
] ions arise as a result of CO
2
production and can be excreted via
the lungs (volatile acids). Minute ventilation is stimulated by an increase in CO
2
and [H
+
], thus increasing excretion of volatile acids.
Additionally, around 1 mmol [H •
+
]·kg
−1
·24 h
−1
of nonvolatile acids are produced
(mainly sulfuric acid) as a result of metabolism on noncarbohydrate substrates.
Such nonvolatile acids are excreted by the kidney.
Changes in blood [H
+
] concentration can therefore result from changes in vola-
tile acids (PaCO
2
) and nonvolatile acids (hydrochloric, sulfuric, lactic, etc.). An
acidosis caused by changes in volatile acids is clinically referred to as a respiratory
acidosis, if due to changes in nonvolatile acids as a metabolic acidosis [ 2 ] .
At constant temperature, three factors determine [H
+
] in the plasma:
1. The partial pressure of CO
2
(PaCO
2
)
2. The quantity of weak acids present and their pK
a
values
3. Strong ion difference.
494
J.R. Goodall
34.5.1 Strong Ion Difference [ 3, 4 ]
Ions such as Na
+
and Cl
−
completely dissociate in aqueous solutions. These ions are
called “strong ions” to distinguish them from “weak ions” (e.g., albumin, phos-
phate, HCO
3
−
), which exist in both charged (dissociated) and uncharged forms.
Under normal physiological conditions, lactate is so nearly completely dissociated
that it can be considered a strong ion.
In a neutral salt solution containing only water and a salt (e.g., NaCl), the sum of
strong cations (Na
+
) minus the sum of strong anions (Cl
−
) is zero (i.e., Na
+
= Cl
−
).
In blood plasma, however, strong cations (Na
+
, K
+
, Mg
2+
, Ca
2+
) outnumber strong
anions (Cl
−
and lactate). The difference by which strong cations exceed strong
anions is known as the strong ion difference (SID).
SID has a powerful electrochemical effect on water dissociation and, hence, on
H
+
concentration. The blood cannot become electrically charged: in order to main-
tain electrical neutrality as SID decreases (e.g., when Cl
−
is allowed to rise), the SID
becomes less positive, [H
+
] rises, and pH falls. It is important to recognize that
metabolic acidosis is produced by a decrease in the SID, resulting in an increase in
free H
+
concentration.
34.6 Sepsis and the Systemic Infl ammatory
Response Syndrome
Sepsis and SIRS are common: most doctors working in an acute hospital setting will
encounter patients exhibiting signs of these conditions on a daily basis.
Increasing complexity of surgical procedures and the aging population are among
the reasons for a continued rise in the number of patients presenting with such con-
ditions. Despite recent medical advances, mortality from SIRS and sepsis remains
high: for surgical patients with severe sepsis or septic shock, mortality rates of 50%
are often quoted.
SIRS and sepsis describe a spectrum of illness, which ranges from the mild sys-
temic disturbances commonly seen in many postoperative patients to life-threaten-
ing conditions requiring organ support and intensive care. Although often used
synonymously and interchangeably, international consensus defi nitions have been
developed to reduce confusion, as outlined in Table 34.2 .
34.6.1 Causes of Sepsis and SIRS
Sepsis and SIRS are “mediator-driven” diseases: the signs and symptoms associated
with these conditions are caused by the release of endogenous mediators. The
production of such mediators (including cytokines, nitric oxide, histamine, and
495
34 Intensive Care: The Basics
prostaglandins) is part of the humoral response to trauma and infection: excessive
or prolonged production of such mechanisms, however, can lead to the vasodilata-
tion, myocardial depression, and capillary leak commonly seen in such patients.
SIRS and sepsis can be precipitated by a wide range of insults and disease
processes.
34.6.2 Treatment of SIRS/Sepsis
34.6.2.1 Immediate Care
Patients with major sepsis will be very unwell. They will need supplementary oxy-
gen and may need respiratory and cardiovascular support. Approaching such
patients with the “ABCs” as a priority is essential: using algorithms suggested in
life support courses such as “ALERT” and “CCrISP” is a sensible and pragmatic
approach.
Table 34.2 Consensus defi nitions
Consensus conference defi nitions of SIRS, sepsis, and septic shock
Systemic infl ammatory response syndrome (SIRS) :
Two or more of the following:
Temperature >38°C or <36°C
Heart rate >90 beats/min
Respiration >20/min or PaCO
2
<32 mmHg
Leukocyte count >12,000/mm
3
, <4,000/mm
3
, or >10% immature (band) cells
Sepsis :
SIRS resulting from a documented infection site (documented by positive culture for organisms
from that site). Blood cultures do NOT need to be positive
Severe sepsis :
Sepsis associated with organ dysfunction, hypoperfusion, or hypotension Hypoperfusion
abnormalities include but are not limited to:
Lactic acidosis
Oliguria
An acute alteration in mental status
Septic shock :
Sepsis-induced hypotension (systolic BP <90 mmHg or a reduction of >40 mmHg from
baseline) in the absence of other causes for the hypotension and despite adequate. (Patients
who are already receiving inotropes or vasopressors may not be hypotensive when perfusion
abnormalities are documented)
Refractory shock :
Shock unresponsive to conventional therapy (fl uid resuscitation, inotropes, or vasopressors)
within 1 h
Data from the American College of Chest Physicians: Society of Critical Care Medicine Consensus
Conference. Defi nitions for sepsis and organ failure and guidelines for the use of innovative thera-
pies in sepsis. Crit Care Med. 1992;20:864–75.
496
J.R. Goodall
In recent years, it has been shown that early, effective management of such patients
improves outcomes. In 2004, the “Surviving Sepsis Campaign” led to the development
of international guidelines which have been widely adopted and which were recently
updated [ 5 ] . They describe a structured approach to the management of such patients.
Initial Resuscitation
Resuscitation should begin as soon as the condition is recognized. In the fi rst 6 h, it
should include all of the following:
Central venous pressure 8–12 mmHg
Mean arterial pressure >65 mmHg
Urine output >0.5 mL·kg
−1
·h
−1
Central venous oxygen saturation (ScvO
2
) >70%
What Is ScvO
2
?
ScvO
2
is the saturation of blood in the central venous system. It refl ects the balance
between O
2
requirement and delivery. Samples are taken from the SVC via a CVC
line and are measured either intermittently (aspiration and gas analysis) or continu-
ously (infrared spectrophotometry) using a bedside monitor.
It can be used as a predictor of complications after major general surgery and
other conditions (e.g., after myocardial infarction) and has been shown to correlate
with blood loss after trauma (Table 34.3 ).
Diagnosis
Appropriate cultures should always be obtained before antimicrobial therapy, as
long as this does not delay treatment. At least two blood cultures should be taken,
including one from any IV device which has been in place for more than 48 h. Other
microbiological cultures, such as sputum or urine cultures, should be sent as appro-
priate. Imaging and other studies should be used to confi rm collections and help
with sampling.
Antibiotic Therapy
Antimicrobial therapy should be started as soon as possible and always within 1 h
of onset of severe sepsis. Initial empirical therapy should be broad spectrum, chosen
Table 34.3 Range of ScvO
2
ScvO
2
>75%
↓ O
2
utilization – e.g., sepsis, vasopressors
65–75% Healthy person at rest
50–65% Healthy during exercise, ↓CO or ↓Hb
<50% ↓ ↓ CO or ↓ ↓ Hb
497
34 Intensive Care: The Basics
to work against likely infective agents, and have good penetration of the presumed
site of infection. Once the results of cultures and sensitivities are known, the therapy
can be reassessed and should focused to ensure optimal treatment and to minimize
the development of antimicrobial resistance.
Source Control
Patients should be fully evaluated as soon as possible, and the presence of a focus of
infection amenable to “source control measures” must be considered. For example,
failure to drain an empyema of a gall bladder, relieve an obstructed, infected kidney,
or remove an infected central venous catheter will lead to loss of valuable time. The
appropriate means of source control will depend upon the clinical situation: sending
an unwell patient to the CT scanner is not always safe!
Fluid Therapy
Fluid resuscitation may consist of natural or artifi cial colloids or crystalloids. There
is no evidence-based support for one type of fl uid over another. Central venous
pressure should be used to guide fl uid therapy: although trends are always more
useful than absolute values, a CVP of 8 (or 12 in a mechanically ventilated patient)
can be used as a guide. Although the guidelines specify initial boluses of 500 mL
colloid or 100 mL crystalloid over 30 min, it must be remembered that much larger
volumes and more rapid infusion rates may be needed.
Vasopressors and Inotropes
It is recommended that a mean arterial pressure (MAP) of 65 mmHg is maintained.
Noradrenaline or dopamine can be used to support MAP if this is not achieved by
fl uid therapy alone. Adrenaline should only be used when these agents have been
found to be unsuccessful.
If the patient has myocardial dysfunction (with elevated cardiac fi lling pressures
and a low-cardiac-output state), the use of dobutamine should be considered to
improve cardiac output (but achieving supranormal output is not the goal of such
therapy). In all such cases, help from intensive care medicine specialists should be
sought, as these patients are very sick and are likely to deteriorate quickly.
Steroids
Hydrocortisone may be useful if the hypotension associated with septic shock
responds poorly to adequate fl uid resuscitation and vasopressors (100 mg three
times a day). This should be reduced once the situation improves, and steroids
should not be used to treat SIRS or sepsis in the absence of nonresponsive hypoten-
sion unless the patient is taking steroids long term.
498
J.R. Goodall
Recombinant Human Activated Protein C
Although outside the remit of this chapter, use of activated protein C should be
considered in adult patients with sepsis-induced organ dysfunction with clinical
assessment of high risk of death as long as there are no contraindications to its use.
If the initial assessment suggests a low risk of death, activated protein C should not
be used.
34.7 Brain Death in the ICU
Although outside the remit of clinical practice for surgical trainees, understanding
the concepts of brain death is important for all clinicians.
The concept of brain death was introduced in 1959, when two French clinicians
described a state they named “coma depasse” (“beyond coma”) [ 6 ] . An ad hoc
committee of Harvard Medical School introduced brain death to a much wider
audience [ 7 ] in a report published in 1968, which demanded “unreceptivity and
unresponsivity,” including no movements when the patient was observed for 1 h,
apnea when the ventilator was disconnected for 3 min, and the absence of excitable
refl exes. Harvard states that these tests must be repeated after a minimum of 24 h.
These early concepts have been refi ned and developed in the intervening years.
The widely recognized “Minnesota Criteria” introduced the notion of etiological
preconditions, reiterated the importance of apnea, and included a requirement for
absence of brain-stem refl exes.
Current UK guidance follows that outlined in Sections 4 and 5 in “Code of prac-
tice for the diagnosis and confi rmation of death,” published by the Academy of
Medical Royal Colleges in October 2008 [ 8 ] , which follows and refi nes the criteria
specifi ed by Conference of Medical Royal Colleges in the period 1976–1981 [ 9 ] .
The guidelines below are taken from this code of practice.
34.7.1 The Diagnosis of Death Following Irreversible Cessation
of Brain-Stem Function
34.7.1.1 Who Can Perform the Tests?
The diagnosis of death by brain-stem testing should be made by at least two doctors.
One must be a consultant, and both must have been registered for more than 5 years.
They should also be competent in the conduct and interpretation of brain-stem test-
ing. It is essential that those involved must not have, or be perceived to have, any
clinical confl ict of interest: they most defi nitely cannot be a member of the trans-
plant team.
499
34 Intensive Care: The Basics
34.7.1.2 How Many Times are the Tests Performed?
The nominated doctors should do the tests together. The tests must always be per-
formed on two separate occasions, and each time, a complete set of tests should be
performed. For example, doctor A may perform the fi rst set of tests while doctor B
observes, with the roles reversed on the second occasion. Each test (including the
apnea test) is therefore performed twice.
34.7.1.3 Criteria that Must be Fulfi lled Before Brain-Stem Testing
Before considering the diagnosis of death following irreversible cessation of brain-
stem function, the “preconditions” must be fulfi lled:
1 . Etiology of irreversible brain damage .
There must be no doubt that the patient has suffered irreversible brain damage
of recognized etiology. In cases such as severe brain trauma or spontaneous
intracranial hemorrhage, this may be easily recognized: following cardiac arrest
or periods of hypoxia diagnosis may take longer to establish.
2 . Potentially reversible causes of coma must be excluded .
The patient must be apneic and needing mechanical ventilation. They must be
deeply comatose and unresponsive. In particular, the following must be
excluded:
(a) That the state could be caused by depressant drugs
(b) That the state could be caused by primary hypothermia (core temperature of
>34°C at the time of testing)
(c) That the state could be caused by potentially reversible circulatory, endo-
crine, and metabolic disturbances (e.g., hypernatremia, hyper- or hypoglyce-
mia, hypotension, or hypercarbia)
3 . Potentially reversible causes of apnea are excluded .
The document makes particular reference to the exclusion of neuromuscular
blocking agents and the need to exclude cervical spine injury as a cause of respi-
ratory muscle dysfunction.
34.7.1.4 Testing for the Absence of Brain-Stem Refl exes
It is necessary to show that the brain stem is not functioning, so the tests are designed
to demonstrate a loss of brain-stem refl exes, including the response to a raised
PaCO
2
and the confi rmation of persistent apnea.
All of the following must be elicited:
The pupils are fi xed and do not respond to sharp changes in the intensity of inci-•
dent light.
There is no corneal refl ex. •
500
J.R. Goodall
There is absence of the oculovestibular refl ex. In this test, a minimum of 50 mL •
of ice-cold water is injected over at least 1 min into each ear in turn, having pre-
viously established that the tympanic membrane is clearly visible.
For each of the above, unilateral testing is acceptable if local injury or disease
prevents bilateral investigation.
There is no motor response within the cranial nerve distribution in response to •
adequate stimulation of any somatic area.
There is no cough refl ex in response to carinal/bronchial stimulation by a suction •
catheter in the trachea, or gag refl ex in response to stimulation of the posterior
pharyngeal wall.
34.7.1.5 Testing for Apnea (the Respiratory Response to Hypercarbia)
The apnea test should be tested last and should not be performed if any of the pre-
ceding tests have confi rmed active brain-stem refl exes. It is essential during this test
that signifi cant hypoxia, excessive hypercarbia, and potentially damaging changes
in arterial blood pressure are avoided.
Apnea is established by demonstrating the absence of any respiratory move-
ment during disconnection from the ventilator. The period of apnea should be
long enough to ensure that the arterial carbon dioxide tension (PaCO
2
) rises to a
level capable of stimulating the respiratory center (a minimum of PaCO
2
>6.0 kPa
and a pH <7.40, but not substantially higher is recommended in the guidelines:
excessive hypercarbia can infl uence conscious level. Ensuring the PaCO
2
rises to
a point where the pH <7.4 is required in a patient who is known to chronically
retain carbon dioxide). After 5 min, a presumption of no respiratory center activ-
ity can be made.
Hypoxia can usually be avoided by preoxygenating the patient, followed by
insuffl ation of oxygen down the tracheal tube via a suction catheter: if this proves
insuffi cient to prevent a fall in SaO
2
, additional measures, for example, the use of
CPAP (continuous positive airway pressure), may be needed.
34.8 Renal Replacement in Critical Care
Acute renal failure is not only very common in the critically ill surgical patient and,
if managed correctly, can often be avoided altogether.
Acute renal failure (ARF) is very common in the critically ill and appears to
be an independent risk factor for poor outcome [ 10 ] . The kidney has very high
metabolic activity and is therefore particularly susceptible to consequences of
low blood pressure and under perfusion. Although ARF is usually found in the
context of multiorgan dysfunction, occasionally a single identifi able event can
Соседние файлы в папке Библиотека им академика М.И. Перельмана