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_663_Библиотеки_им_академика_М_И_Перельмана
.pdf
15 Sepsis andSeptic Shock
https://t.me/medicina_free
137
• Septic shock is a specic subset of sepsis in which profound circulatory, cellular and metabolic abnormalities
are associated with a greater risk of mortality than sepsis
alone.
• Patients with penetrating trauma are at high risk for developing sepsis and its associated complications.
• Prompt identication and appropriate management are
vital to improve outcomes.
• Early appropriate antimicrobial therapy, restoration of
adequate cellular perfusion and timely source control are
the essential pillars in the management of patients with
sepsis and septic shock.
• Inability to achieve adequate source control despite rapid
resuscitation and initiation of appropriate antimicrobials
may result in failure to obtain clinical stability or sustained patient improvement.
• Multiple organ systems may be affected by sepsis and
septic shock and a multifaceted approach to the management including appropriate supportive measures and relevant post-sepsis care are integral components of the
complete care required in such patients.
Suggested Reading
Al Rawahi AN, Al Hinai FA, Doig CJ, et al. The prognostic value of
serum procalcitonin measurements in critically injured patients: a
systematic review. Crit Care. 2019;23:390.
Azuhata T, Kinoshita K, Kawano D, et al. Time from admission to
initiation of surgery for source control is a critical determinant of
survival in patients with gastrointestinal perforation with associated
septic shock. Crit Care. 2014;18:R87.
Bednarczyk JM, Fridnnson JA, Kumar A, etal. Incorporating dynamic
assessment of uid responsiveness into goal-directed therapy: a systematic review and meta-analysis. Crit Care Med. 2017;45:1538–45.
Berenholtz SM, Pham JC, Thompson DA, etal. Collaborative cohort
study of an intervention to reduce ventilator-associated pneumonia in the intensive care unit. Infect Control Hosp Epidemiol.
2011;32:305–14.
Blot K, Bergs J, Voelaers D, etal. Prevention of central line- associated
bloodstream infections through quality improvement interventions: a systematic review and meta-analysis. Clin Infect Dis.
2014;59:96–105.
Boyer A, Vargas F, Coste F, etal. Inuence of surgical treatment
timing on mortality from necrotizing soft tissue infections
requiring intensive care management. Intensive Care Med.
2009;35:847–53.
Brunauer A, Koköfer A, Bataar O, etal. Changes in peripheral perfu-
sion relate to visceral organ perfusion in early septic shock: a pilot
study. J Crit Care. 2016;35:105–9.
Buck DL, Vester-Andersen M, Moller MH. Surgical delay is a criti-
cal determinant of survival in perforated peptic ulcer. Br J Surg.
2013;100:1045–9.
Casciani F, Trudeau MT, Vollmer CM. Perioperative immunization
for splenectomy and the Surgeon’s responsibility: a review. JAMA
Surg. 2020;155:1068–77.
Cecconi M, Hernandez G, Dünser M, et al. Fluid administration for
acute circulatory dysfunction using basic monitoring: narrative
review and expert panel recommendations from an ESICM task
force. Intensive Care Med. 2019;45:21–32.
Cowley NJ, Owen A, Shiels SC.Safety and efcacy of antiviral therapy
for prevention of cytomegalovirus reactivation in immunocompetent critically ill patients: a randomized clinical trial. JAMA Intern
Med. 2017;177:774–83.
Dünser M, Mer M, Petros S, Dankl D.Clinical examination skills in
the adult critically ill patient. NewYork City: Springer International
Publishing; 2018.
Dünser MW, Takala J, Brunauer A, et al. Re-thinking resuscitation:
leaving blood pressure cosmetics behind and moving forward to
permissive hypotension and a tissue perfusion-based approach. Crit
Care. 2013;17:326.
Eriksson J, Lindström AC, Hellgren E, etal. Postinjury sepsis—asso-
ciations with risk factors, impact on clinical course, and mortality:
a retrospective observational study. Crit Care Explor. 2021;3:e0495.
Evans L, Rhodes A, Alhazzani W, et al. Surviving sepsis campaign:
international guidelines for management of sepsis and septic shock
2021. Intensive Care Med. 2021;47:1181–247.
Font MD, Thyagarajan B, Khanna AK.Sepsis and septic shock—basics
of diagnosis, pathophysiology and clinical decision making. Med
Clin North Am. 2020;104:573–85.
Fullen WD, Hunt J, Altemeier WA.Prophylactic antibiotics in penetrat-
ing wounds of the abdomen. J Trauma. 1972;12:282–9.
Goldberg SR, Anand RJ, Como JJ, etal. Prophylactic antibiotic use
in penetrating abdominal trauma: an Eastern Association for the
Surgery of trauma practice management guideline. J Trauma Acute
Care Surg. 2012;73(Suppl 4):S321–5.
Golger A, Ching S, Goldsmith CH, etal. Mortality in patients with nec-
rotizing fasciitis. Plast Reconst Surg. 2007;119(6):1803–7.
Heffernan AJ, Mohd Sazlly Lim S, Lipman J, et al. A personalised
approach to antibiotic pharmacokinetics and pharmacodynamics in
critically ill patients. Anaesth Crit Care Pain Med. 2021;40:100970.
Hernández G, Teboul JL. Is the macrocirculation really dissociated
from the microcirculation in septic shock? Intensive Care Med.
2016;42:1621–4.
Johnson MT, Reichley R, Hoppe-Bauer J, etal. Impact of previous anti-
biotic therapy on outcome of Gram-negative sepsis. Crit Care Med.
2011;39(8):1859–65.
Knox DB, Lanspa MJ, Kuttler KG, etal. Phenotypic clusters within
sepsis-associated multiple organ dysfunction syndrome. Intensive
Care Med. 2015;41:814–22.
Komori A, Iriyama H, Kainoh T, etal. The impact of infection compli-
cations after trauma differs according to trauma severity. Sci Rep.
2021;11:13803.
Kronen R, Liang SY, Bochiccio G, etal. Invasive fungal infections sec-
ondary to traumatic injury. Int J Infect Dis. 2017;62:102–11.
Kumar A, Ellis P, Arabi Y, etal. Initiation of inappropriate antimicrobial
therapy results in a vefold reduction of survival in human septic
shock. Chest. 2009;136(5):1237–48.
Lamoth F.Galactomannan and 1,3-β--glucan testing for the diagnosis
of invasive aspergillosis. J Fungi. 2016;2:22.
Liu TM, Chi CY, Ho MW, etal. Microbiology and factors affecting
mortality in necrotizing fasciitis. J Microbiol Immunol Infect.
2005;38(6):430–5.
Liu VX, Fielding-Singh V, Greene JD, etal. The timing of early antibi-
otics and hospital mortality in sepsis. Am J Respir Crit Care Med.
2017;196:856–63.
Ma XY, Tian LX, Liang HP.Early prevention of trauma-related infec-
tion/sepsis. Mil Med Res. 2016;3:33.
Manrique-Caballero CL, Del Rio-Pertuz G, Gomez H. Sepsis-
associated acute kidney injury. Crit Care Clin. 2021;37:279–301.
Martinez ML, Ferrer R, Torrents E, et al. Impact of source control
in patients with severe sepsis and septic shock. Crit Care Med.
2017;45:11–9.
138
https://t.me/medicina_free
M. Mer and M. W. Dünser
Martin-Loeches I, Antonelli M, Cuenca-Estrella M, et al. ESICM/
ESCMID task force on practical management of invasive candidiasis in critically ill patients. Intensive Care Med. 2019;45:789–805.
Mer M, Lipman J. Antibiotic administration in the critically ill—in
need of intensive care! S Afr Med J. 2015;105(5):357–9.
Mer M, Schultz MJ, Adhikari NK.European Society of Intensive Care
Medicine (ESICM) Global Intensive Care Working Group and
the Mahidol-Oxford research Unit (MORU), Bangkok, Thailand.
Core elements of general supportive care for patients with sepsis
and septic shock in resource-limited settings. Intensive Care Med.
2017;43(11):1690–4.
Miyamoto K, Shibata N, Ogawa A, et al. Prehospital and in-hospital
quick sequential organ failure assessment (qSOFA) scores to predict
in-hospital mortality among trauma patients: an analysis of nationwide registry data. Acute Med Surg. 2020;7:e532.
Montravers P, Gauzit R, Muller C, et al. Emergence of antibiotic-
resistant bacteria in cases of peritonitis after intraabdominal surgery
affects the efcacy of empirical antimicrobial therapy. Clin Infect
Dis. 1996;23(3):486–94.
Montravers P, Tubach F, Lescot T, etal. Short-course antibiotic therapy
for critically ill patients treated for postoperative intra-abdominal
infection: the DURAPOP randomised clinical trial. Intensive Care
Med. 2018;44(3):300–10.
Müller F, Christ-Crain M, Bregenzer T, etal. Procalcitonin levels pre-
dict bacteremia in patients with community-acquired pneumonia: a
prospective cohort trial. Chest. 2010;138:121–9.
Myburgh JA, Finfer S, Bellomo R, et al. Hydroxyethyl starch or
saline for uid resuscitation in intensive care. N Engl J Med.
2012;367:1901–11.
Osborn TM, Tracy JK, Dunne JR, et al. Epidemiology of sepsis in
patients with traumatic injury. Crit Care Med. 2004;32:2234–40.
Pugh R, Grant C, Cooke RPD, etal. Short-course versus prolonged-
course antibiotic therapy for hospital-acquired pneumonia in critically ill adults. Cochrane Database Syst Rev. 2015;2015:CD007577.
Roberts JA, Abdul-Aziz MH, Davis JS, etal. Continuous versus inter-
mittent β-lactam infusion in severe sepsis. A meta-analysis of individual patient data from randomized trials. Am J Respir Crit Care
Med. 2016;194:681–91.
Rudd KE, Johnson SC, Agesa KM, etal. Global, regional, and national
sepsis incidence and mortality, 1990–2017: analysis of the global
burden of disease study. Lancet. 2020;395:200–11.
Russel JA, Rush B, Boyd J.Pathophysiology of septic shock. Crit Care
Clin. 2018;34:43–61.
Sawyer RG, Claridge JA, Nathens AB, et al. Trial of short-course
antimicrobial therapy for intraabdominal infection. N Engl J Med.
2015;372:1996–2005.
Schmittinger CA, Torgersen C, Luckner G, etal. Adverse cardiac events
during catecholamine vasopressor therapy: a prospective observational study. Intensive Care Med. 2012;38:950–8.
Seymour CW, Gesten F, Prescott HC, etal. Time to treatment and mor-
tality during mandated emergency Care for Sepsis. N Engl J Med.
2017;376:2235–44.
Seymour CW, Liu VX, Iwashyna TJ, etal. Assessment of clinical cri-
teria for sepsis: for the third international consensus denitions for
sepsis and septic shock (Sepsis-3). JAMA. 2016;315:762–74.
Singer M, Deutschman CS, Seymour CW, etal. The third international
consensus denitions for sepsis and septic shock (Sepsis-3). JAMA.
2016;315:801–10.
Smith BJ, Heriot G, Buising K.Antibiotic treatment of common infec-
tions: more evidence to support shorter durations. Curr Opin Infect
Dis. 2020;33:433–40.
Thompson BT, Chambers RC, Liu KD.Acute respiratory distress syn-
drome. N Engl J Med. 2017;377:562–72.
Tokuda Y, Miyasato H, Stein GH, etal. The degree of chills for risk of
bacteremia in acute febrile illness. Am J Med. 2005;118:1417.
Vardakas KZ, Voulgaris GL, Maliaros A, etal. Prolonged versus short-
term intravenous infusion of antipseudomonal β-lactams for patients
with sepsis: a systematic review and meta-analysis of randomised
trials. Lancet Infect Dis. 2018;18:108–20.
Vincent JL, Moreno R, Takala J, etal. The SOFA (sepsis-related organ
failure assessment) score to describe organ dysfunction/failure.
On behalf of the working group on sepsis-related problems of the
European Society of Intensive Care Medicine. Intensive Care Med.
1996;22:707–10.
Wong CH, Chang HC, Pasupathy S, etal. Necrotising fasciitis: clinical
presentation, microbiology and determinants of mortality. J Bone
Joint Surg Am. 2003;85(8):1454–60.
Zampieri FG, Machado FR, Biondi RS, etal. Effect of intravenous uid
treatment with a balanced solution vs. 0.9% saline solution on mortality in critically ill patients: the BaSICS randomized clinical trial.
JAMA. 2021;326:1–12.
Zuercher P, Moret CS, Dziewas R, etal. Dysphagia in the intensive care
unit: epidemiology, mechanisms, and clinical management. Crit
Care. 2019;23:103.
Endpoints ofResuscitation
=× ×××
()
https://t.me/medicina_free
DavidMuckart
“Resuscitare” [Latin transitive verb] “to bring back to life”
If the aim of resuscitation is to restore life, as the above
denition implies, the underlying pathophysiology which
threatens existence must be understood. Whatever the mechanism of shock, the nal common denominators are tissue
ischaemia and anaerobic metabolism. The reason why this
pathophysiological state is lethal can be explained by basic
physiology. The human is an aerobic organism and 90% of
consumed oxygen is used to produce adenosine triphosphate
(ATP) via Kreb’s cycle. Manufactured by mitochondria
within the cell, ATP is virtually the sole energy source for the
myriad of energy requiring enzymatic reactions to maintain
homeostasis. The human consists of four quadrillion cells, in
each of which there are thousands of mitochondria. On average, only 100g of ATP exists at any one time and cells turn
over 107 molecules of ATP per second, with each molecule
being recycled every 20–30s. This results in an average daily
production of 100–150 kg of ATP per day. The molecular
weight of ATP, which therefore contains Avogadro’s number
or 6×1023 molecules, is 0.5kg, and therefore the daily minimum production is at least two hundred times this number,
namely, 12× 1025 molecules. How big is this number? It
amounts to the number of cupsful of water in 200 Pacic
Oceans. Little wonder then that shock, which disrupts oxygen delivery or utilisation at the cellular level, is a threat to
life. Even for only a short period, shock results in marked
depletion of ATP, and protracted episodes result in a profound physiological abyss from which there is no prospect of
recovery. Therefore, the ultimate goal of resuscitation is to
restore anaerobic metabolism as swiftly as possible.
In the absence of traumatic brain injury which accounts
for the majority of trauma deaths, there are three independent predictors of death in trauma, namely, hypoxia, hypo-
16
perfusion and hypothermia, a combination termed the “triple
H syndrome”. The presence of the lethal triad of acidosis,
coagulopathy and hypothermia is a late consequence of
shock, and the thrust of resuscitation must be to correct the
“triple H syndrome”. Hypoxia may be absolute when there is
a low PaO2, or relative which is reected by a lactic acidosis
indicating anaerobic metabolism and cellular hypoxia.
Hypoperfusion is manifest by hypotension but may be present even in the face of a normal mean arterial blood pressure
if vasopressors have been commenced. Hypothermia exists if
the core temperature is below 35°C.
Given the above physiological review and the independent
risk factors for death, the thrust of resuscitation must be to
restore oxygen delivery (DO2) and oxygen consumption (VO2)
and monitor the effect of interventions and reversal of the metabolic acidosis. The equation for DO2 is the product of cardiac
output and arterial oxygen content which translates into:
DO heart rate stroke volumeHbSaO
2 2
0 0031
+×
where SaO2=arterial oxygen saturation and PaO2=arterial
partial pressure of oxygen
Given the above equation and the need to reverse anaerobic metabolism, the two common areas of monitoring to
determine the endpoints of resuscitation involve the macrocirculation using haemodynamics and the microcirculation
assessing markers of tissue perfusion.
()
PaO
.
2
16.1 Haemodynamic Monitoring
16.1.1 Pulse Rate
134
.
D. Muckart (*)
Trauma and Trauma Intensive Care Units, Inkosi Albert Luthuli
Central Hospital, Nelson R.Mandela School of Clinical Medicine,
Durban, KZN, South Africa
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023
E. Degiannis et al. (eds.), Penetrating Trauma, https://doi.org/10.1007/978-3-031-47006-6_16
From ancient time, the character of the pulse has guided physicians. One of the early denitions of shock was a systolic
pressure < 100 mmHg and a pulse rate of >100beats per
minute. The endpoint of resuscitation was to reverse these
139
140
https://t.me/medicina_free
D. Muckar t
numbers. A reduction in pulse rate is uncommon for a number of reasons. Firstly, shock results in an altered level of
consciousness and failure to appreciate a noxious stimulus.
Restoration of cerebral perfusion results in pain and anxiety
with a resultant tachycardia. Secondly, the normal baroreceptor response is tonic and during shock baroreceptor
impulses decrease resulting in a rise in pulse rate. Despite
restoration of an adequate intravascular volume, the baroreceptor response lags behind and a tachycardia persists.
Thirdly, the systemic inammatory response syndrome
(SIRS) is dened by a tachycardia and is an almost constant
feature of trauma. For these reasons, relying on a fall in pulse
rate to signify an endpoint of resuscitation is not
recommended.
16.1.2 Arterial Saturation (SaO2)
A minimum SaO2 of 95% must be achieved during the initial
resuscitation, above this level there being minimal improvement in DO2. Anaerobic metabolism creates air hunger and
tachypnoea as a compensatory mechanism with the aim of
removing CO2 to eliminate acid. Even if SaO2 can be maintained by spontaneous ventilation, the work of breathing is
markedly increased resulting in an increase in oxygen consumption. In the presence of a moderate to severe metabolic
acidosis, this compensation should default to the clinician,
and patients with hypotension must be intubated and
mechanically ventilated, thereby eliminating unnecessary
wastage of DO2. Protective lung ventilation has been proposed as standard of care in the critically ill, but it is crucial
to understand that all data from these studies have been
extracted from critically ill patients in ICU with established
severe lung dysfunction. These results have no relevance
whatsoever to the emergency room and acute resuscitation,
and the use of low tidal volumes will not allow the effective
removal of CO2 nor will it recruit atelectatic lung segments,
a not uncommon problem in thoracic trauma as a result of
pulmonary contusions. Assuming similar effects, the misguided extrapolation of results from one phase of critical
care to a markedly different scenario and location is unjustiable and dangerous. The endpoint of ventilatory resuscitation is a SaO2 of >95% and a CO2 which allows the arterial
pH to remain above 7.2 until intravascular volume expansion
has been achieved and the metabolic acidosis improving.
The most effective method of reducing arterial PaCO2 is by
increasing the tidal volume and not the respiratory rate. The
benet of using larger tidal volumes during acute resuscitation far outweighs the potential long-term risk of ventilatorinduced lung injury. End-tidal CO2 closely reects arterial
PaCO2 and is the most practical method of monitoring and
obviates the need for frequent arterial blood gas sampling.
16.2 Mixed andCentral Venous Oxygen
Saturation
Mixed venous saturation (SvO2) is measured in blood sampled from the pulmonary artery and therefore requires the
insertion of a pulmonary artery catheter. Central venous
saturation (ScvO2) is obtained from a central venous catheter and is an acceptable substitute. The normal oxygen
extraction ratio (arterial saturation − venous saturation) is
25% and ScvO2 is therefore around 75%. Due to mixing of
venous blood from the coronary sinus which drains directly
into the right atrium, SvO2 is usually 5% lower than ScvO2,
although this difference may be reversed in septic shock.
In the presence of shock and a low ScvO2, the assumption
is that DO2 is inadequate with excessive oxygen extraction
at the cellular level. The aim therefore is to achieve a
ScvO2 of >70%. Although theoretically sound, there are
caveats. A high ScvO2 may be present but the acidosis fails
to improve and may even worsen. This suggests an unsalvageable situation where cellular hypoxia has resulted in
mitochondrial dysfunction and the inability to extract and
utilise delivered oxygen. There is no current evidence to
substantiate the application of ScvO2 in trauma
resuscitation.
16.3 Pressure andFlow
DO2 depends on adequate blood ow to the tissues but
despite attempts to quantify cardiac output, this has been elusive (vide infra). As a result, we use pressure as a surrogate
but this has certain pitfalls. The law of haemodynamics dictates that pressure is a product of ow and peripheral vascular resistance; there is no mention of volume.
16.4 Central Venous Pressure (CVP)
CVP has been used to reect right heart preload, dened as
the degree of ventricular stretch at end diastole. In the spontaneously breathing patient, this may have some merit but in
those undergoing mechanical ventilation, this is erroneous. It
is assumed that a high CVP indicates loss of vascular compliance and therefore an adequate intravascular volume.
There are many other compliance issues which impact on
CVP however, namely, pulmonary pressure during mechanical ventilation, right heart volume, chest wall anatomy and
intra-abdominal pressure. As such, in the critically injured
patient undergoing positive pressure ventilation, CVP is an
unreliable indicator of right heart preload and intravascular
volume and cannot be used as an indicator of uid
responsiveness.
16 Endpoints ofResuscitation
https://t.me/medicina_free
141
16.5 IVC Diameter
Although CVP has been shown to be unreliable, ultrasonic
measurement of IVC diameter may reect intravascular volume. In haemodynamically normal patients breathing spontaneously, when assessed by abdominal ultrasound, the IVC
diameter decreases by 50% during inspiration due to the
negative intrathoracic pressure allowing improved venous
return. The opposite occurs during positive pressure ventilation where increased intrathoracic pressure during inspiration reduces venous return and the IVC expands although the
volume change is much lower. Measurement is made during
mandatory inspiration using a tidal volume of 8mL/kg or
less. A change in IVC diameter of >15% from baseline expiration indicates increased compliance due to hypovolaemia.
16.6 Pulmonary Arterial Pressure
For many years, the pulmonary artery catheter (PAC) was
regarded as the gold standard for haemodynamic monitoring
with the assumption that a pulmonary artery wedge pressure
(PAWP) reects left ventricular volume. Swan and Ganz,
however, stated categorically that this held true only in
patients with no lung pathology. For some reason, this statement was ignored and the PAC became routine practice. It is
nonsensical to believe that if right atrial pressure measured
by a central venous catheter placed directly adjacent to that
chamber is inaccurate but that a catheter measuring a pressure across a diseased organ (the lung), another chamber (the
left atrium) and a valve (the mitral valve) is correct. The pulmonary artery occlusion pressure does not reect intravascular volume or uid responsiveness and there is no role for the
PAC in acute trauma resuscitation.
16.7 Peripheral Arterial Pressure
patients with a reduced intravascular volume may occlude
forward ow to the left side of the heart. The combined
effects are reduction of systolic blood pressure during inspiration and a fall in systolic pressure of >15mmHg during
inspiration which is a strong indicator of a suboptimal intravascular volume despite what would appear to be an adequate mean arterial pressure. If measuring systolic pressure
variation, certain criteria must be fullled, namely, that the
patient must be mechanically ventilated and take no spontaneous breaths. The patient must be pre-oxygenated and
briey hyperventilated to reduce the PaCO2 and therefore
eliminate triggered spontaneous breaths. Thereafter, the ventilator is placed on expiratory hold and the systolic pressure
determined during apnoea. This manoeuvre eliminates the
effect of inspiration while maintaining PEEP, and in virtually
all patients, the variation in systolic pressure will disappear.
Mechanical ventilation is then recommenced and the effect
on systolic blood pressure ascertained. A fall in systolic
blood pressure during inspiration indicates hypovolaemia,
whereas a rise suggests the need for inotropic support.
16.8 Cardiac Output Monitoring
With the decline of the PAC, less invasive methods of cardiac
output (CO) monitoring have evolved using a variety of techniques. Despite concerns about the accuracy of the PAC, this
is used as the comparator for these monitors. No method of
non-invasive CO monitoring has less than a 20% error rate or
greater than 90% concordance with the PAC, and the percentage error rises with the use of vasopressors, the very patients
in whom an accurate estimation of CO is desired. There are
few data demonstrating a survival advantage using these
monitors. CO monitoring simply generates a number and
does not indicate whether this meets tissue oxygen demands.
It should never be used in isolation but if CO is determined, it
must be combined with markers of peripheral perfusion.
Although more accurate than CVP as an indicator of intravascular volume, a normal mean arterial pressure may not
signify a successful endpoint of resuscitation. Peripheral
vasoconstriction may maintain arterial pressure despite
hypoperfusion. This is especially true in children who have
the ability to maintain their blood pressure by profound
vasoconstriction and their cardiac output by a signicant
tachycardia until sudden decompensation occurs.
A simple but reliable indicator of arterial volume is the
use of systolic or pulse pressure variation using invasive arterial monitoring. During the inspiratory phase of mechanical
ventilation, venous return is reduced by increased intrathoracic pressure resulting in a reduction in right ventricular
preload and therefore stroke volume. As the lungs expand,
alveolar expansion compresses pulmonary capillaries and in
16.9 Haemoglobin andCoagulation
More than two millennia ago, the Hindu doctrines of Sushruta
Samhita (circa 700BCE) dictated that the best treatment of
any lost substance is replacement by an identical expander.
For some inexplicable reason, it has taken us two and a half
thousand years to adopt his philosophy. Although stroke volume may be restored using either crystalloids or colloids,
these solutions do not carry oxygen, and in the presence of
severe haemorrhage, their use should be limited. The only
effective mechanism for oxygen transport is haemoglobin, and
a massive transfusion protocol which allows the rapid administration of blood must be in place in any health facility which
treats major trauma. The endpoint of PRBC transfusion is a
142
https://t.me/medicina_free
D. Muckar t
haemoglobin concentration of 10 g/dL. Based on rheology,
this is the optimal concentration for oxygen delivery. The initial haemoglobin concentration is articially high and misleading and should be repeated frequently during resuscitation.
On average, in the absence of major ongoing haemorrhage,
one unit of PRBC will raise the haemoglobin by 1g.
In addition to PRBCs, the acute coagulopathy of trauma
and shock (ACoTS) necessitates the administration of
plasma, platelets and possibly cryoprecipitate. Although this
must not be viewed as absolute, current evidence suggests
that the optimal ratio of packed red blood cells (PRBC) to
plasma and platelets is 1:1:1. A word of caution is in order
when blindly adopting such a policy. Firstly, PRBC and
component therapy are not cheap and over-zealous use
attracts both economic and physiological adverse consequences. Secondly, patients are unique individuals and the
need for ratios of unity is dependent on the physical and
physiological scenario. Although overlap is obvious, patients
may be broadly grouped into four categories as depicted
below, and this should dictate how aggressively blood and
component therapy is employed (Fig.16.1).
The broad divisions are the degree of physiological
derangement and whether source control is absolute. Patients
in whom total source control of haemorrhage can be achieved,
such as splenectomy, and who are not severely physiologically deranged may not require additional component therapy or the full ratios. In contrast, those with incomplete
source control such as liver or pelvic packing who are hypothermic and acidotic would undoubtedly benet. The optimal method of ascertaining the need for component therapy
is thromboelastometry. The standard laboratory tests for
coagulation are not representative of the trauma patient, are
performed at 37° centigrade, take 20–30 min, assess only
the initial phase of clot formation and give no information
regarding the quality or strength of clot formation, platelet
function or brinolysis. Thromboelastography (TEG) or
thromboelastometry (ROTEM©) has been proposed as the
gold standard, reecting as close to an invivo situation as
possible. We have used thromboelastometry for the last
10years and found it immensely helpful in not only identifying ACoTS but also dictating the need for, and the effect of,
administering specic component therapy. The main components of the graphic representation of coagulation are illustrated and described below with normal values (Fig.16.2).
• R time (reaction time from 0 to 2mm amplitude) is normally between 7 and 15min and represents the clotting
time until initial brin formation.
• K time (coagulation time) is normally between 3 and
6min and reects the rate of clot formation from the end
of R time at 2 to 20mm clot amplitude.
• α angle is normally between 45 and 55° and represents the
rate of clot formation by brin build-up and
cross-linking.
• MA is normally around 60mm and reects the maximum
clot strength.
Factors affecting measurements in thromboelastography:
• Prolonged R time: anticoagulants and reduced clotting
factor concentration
• Prolonged K time: reduced clotting factors, brinogen
deciency and thrombocytopaenia
• Low α angle: reduced clotting factors, brinogen deciency and thrombocytopaenia
• Reduced MA: platelet dysfunction
• Fibrinolysis: acute coagulopathy of trauma and shock
(ACoTS)
Fig. 16.1 Recommendations
for the use of blood, platelets,
plasma and cryoprecipitate
depending on whether source
control has been achieved and
the degree of hypothermia.
The ratios (eg 1 : 1) depict the
number of packs of plasma or
platelets per unit of blood
COMPLETE SOURCE CONTROL
Temperature > 35 BD <-5
PRBC PRBC
< 6No platelets : No plasma < 6Platelets 1 : 1 + TEG
6 –8 Platelets 1 : 1 Plasma 0.5 : 16 –8 Platelets 1 : 1 Plasma 0.75 : 1
>8 Platelets 1 : 1 Plasma 1 : 1> 8Platelets 1 : 1 Plasma 1 : 1
COMPLETE SOURCE CONTROL
Temperature < 35 BD >-5
PRBC PRBC
< 6Thromboelastography < 6Platelets 1 : 1 Plasma 0.5 : 1
6- 8Platelets 1 : 1 Plasma 0.75 : 16 –8 Platelets 1 : 1 Plasma 1 : 1
> 8Platelets 1 : 1 Plasma 1 : 1> 8Platelets 1 : 1 Plasma 1 : 1 + cryo
INCOMPLETE SOURCE CONTROL
Temperature > 35 BD <-5
INCOMPLETE SOURCE CONTROL
Temperature < 35 BD >-5
16 Endpoints ofResuscitation
https://t.me/medicina_free
Fig. 16.2 Normal
thromboelastogram tracing
(In Raj TD (eds) Data
Interpretation in Anesthesia
pp.160–66. Springer. Charm.
https://doi.
org/10.1007/978- 3- 31955862- 2_30)
143
α
R
K
MA
30 min
A
30 (LY 30)
16.10 Reversal ofAnaerobic Metabolism
16.10.1 Lactate
During normal aerobic metabolism of glucose, lactate is produced from pyruvate by lactate dehydrogenase and the normal pyruvate/lactate ratio is 1:10. During anaerobic
metabolism, pyruvate cannot enter Kreb’s cycle and lactate
levels increase, and this serves as a marker of anaerobic
metabolism and oxygen debt. The normal lactate concentration is <2.5mmol/L, and there is no substantial difference
between arterial and central venous lactate concentrations,
therefore allowing either to sufce for monitoring. Although
liver and renal dysfunction may result in delayed metabolism
of lactate, this is uncommon, and serial estimations of lactate
indicate the success or otherwise of resuscitation. The initial
lactate concentrations do not necessarily correlate with outcome, and the time to lactate clearance is a more accurate
and independent predictor of survival. Complete elimination
within 24h is associated with high survival rates, whereas
failure to normalise lactate after 48 h increases mortality
substantially. A distinction must be made between oxygen
decit and oxygen debt. Normal haemodynamic parameters
are an indication that there is no decit in DO2 and by extrapolation VO2, but the presence of a persistently elevated lactate suggests that an oxygen debt remains and is a marker of
occult tissue hypoxia. This oxygen debt has to be repaid
before physiology is normalised and is a useful indicator to
decide when elective fracture xation is safe. Despite similar
fracture xation techniques and operative times, patients in
whom surgery is undertaken when the lactate is within normal limits fare better postoperatively compared to their
abnormal counterparts.
common complications as a result of a shock episode and
worsen outcome. Base decit is unaffected by acute respiratory conditions, is a pure metabolic marker for both aerobic
and anaerobic pathologies and as such more accurately
reects the global metabolic dysfunction and the severity of
the underlying physiological disruption. Base decit correlates with injury severity, the need for urgent blood transfusion and outcome. As with lactate, rapid clearance indicates
successful resuscitation and a protracted base decit a poor
prognosis.
16.11 Supranormal Resuscitation
andPermissive Hypotension
16.11.1 Supranormal Resuscitation
If a subnormal DO2 is the underlying pathophysiology in
shock, then in theory, rapid correction of this state and driving haemodynamics to supranormal levels should improve
survival. The initial chosen endpoints were a DO2 of
>600mL/m2 and VO2 of >170mL/m2 using a combination of
intravenous uids, inotropes and vasopressors. Unfortunately,
this theory has been disproven and deliberate attempts to
achieve predetermined goals of DO2 and VO2 do not reduce
mortality. Survival is determined by the individual’s physiological reserve and the capability of spontaneous restoration
of adequate perfusion. It is independent of the endpoints of
resuscitation or method of monitoring. Patients who achieve
the predetermine goals have a far better prognosis but
attempting to drive patients to these endpoints is of no
benet.
16.10.2 Base Decit
Lactate is a measure only of anaerobic metabolism and does
not assess metabolic acidoses from aerobic causes such as
acute kidney injury or hyperchloraemia, both of which are
16.11.2 Permissive Hypotension
There is a concern that rapid restoration of blood pressure
may destroy tenuous early clot formation and precipitate further haemorrhage or aggravate blood loss and coagulopathy
in patients who have not achieved spontaneous haemostasis.
144
https://t.me/medicina_free
D. Muckar t
In patients who are transient or non-responders to resuscitation, surgery must be undertaken as part of the resuscitation
process. Mean arterial pressure should be maintained at
50–60mmHg until surgical control of haemorrhage has been
obtained. Hypoperfusion of this magnitude may be tolerated
for 60 min, but beyond that physiological reserve will be
exhausted, multiple organ dysfunction is the rule and mortality is extremely high.
16.12 Conclusion
There is no one monitoring tool which guarantees the endpoint of resuscitation. Although intuitive, the normalisation
of haemodynamic parameters does not necessarily signify
success, and these must be combined with tissue perfusion
techniques to allow a global assessment of perfusion and satisfactory restoration of aerobic metabolism.
Important Points
• Anaerobic metabolism is lethal and must be rapidly
reversed.
• Hypoxia, hypoperfusion and hypothermia are independent predictors of death.
• No single haemodynamic monitoring tool is reliable as an
endpoint.
• Lactate clearance is proportional to survival.
• A massive transfusion protocol improves outcome.
• Ratios of blood/plasma/platelets are dictated by ease of
source control and physiology.
• Thromboelastometry is essential to determine the need
for component therapy.
Suggested Reading
Abu-Zidan FM.Optimizing the value of measuring inferior vena caval
diameter in shocked patients. World J Crit Care. 2016;5:7–11.
Barbee RW, Reynolds PS, Ward KR. Assessing shock resuscitation
strategies by oxygen debt repayment. Shock. 2010;33:113–22.
Brohi K, Cohen MJ, Ganter MT, etal. Acute coagulopathy of trauma:
hypoperfusion induces systemic anticoagulation and hyperbrinolysis. J Trauma. 2008;64:1211–7.
Cestero RF, Dent DL.Endpoints of resuscitation. Surg Clin North Am.
2015;95:319–36.
Grey BC, Rodseth R, Muckart DJJ.Early fracture xation in the pres-
ence of subclinical hypoperfusion. Injury. 2013;44:217–20.
Hardcastle TC, Muckart DJJ, Maier RV. Ventilation in the trauma
patients: the rst 24h is different. World J Surg. 2017;41:1153–8.
Johannson PI, Stissing P, Boschen L, etal. Thromboelastography and
thromboelastomotry in assessing coagulation in trauma. Scand J
Trauma Resusc Emerg Med. 2009;17:45–53.
Maddirala S, Khan A. Optimizing haemodynamic support in septic
shock using central and mixed venous oxygen saturation. Crit Care
Clin. 2010;26:323–33.
Marik PE. Non-invasive cardiac output monitors: a state of the art
review. J Cardiothorac Vasc Anaesth. 2013;1:121–34.
Marik PE, Lemson J.Fluid responsiveness: an evolution of our under-
standing. Br J Anaesth. 2014;112:617–20.
Michard F, Teboul JL.Predicting uid responsiveness in ICU patients:
a critical analysis of the evidence. Chest. 2002;121:2000–8.
Monnet X, Teboul J-L. Assessment of volume responsiveness during
mechanical ventilation: recent advances. Crit Care. 2013;17:217.
http:// ccforum. com/ content/ 17/ 2/ 217
Muckart DJJ, Bhagwanjee S, Gous E.Validation of an outcome predic-
tion model for critically ill trauma patients without head injury. J
Trauma. 1997;43:934–8.
Muckart DJJ, Malbrain MLNG. A whiter shade of pale. The ongo-
ing challenge of haemorrhagic shock. Anaesthesiol Intensive Ther.
2018;50:1–6.
Mutschler M, Nienaber U, Brockamp T, et al. Renaissance of base
decit for the initial assessment of trauma patients: a base decitbased classication for hypovolaemic shock developed on data from
16,305 patients derived from the TraumaRegister DGU®. Crit Care.
2013;17:R42. http://ccforum.com/content/17/2/R42
Odom SR, Howell MD, Silva GS, etal. Lactate clearance as a pre-
dictor of mortality in trauma patients. J Trauma Acute Care Surg.
2013;74:999–1004.
Okorie ON, Dellinger P.Lactate: biomarker and potential therapeutic
target. Crit Care Clin. 2011;27:299–326.
Paxian M, Bauer I, Rensing H, etal. Recovery of hepatocellular ATP
and “pericentral apoptosis” after haemorrhage and resuscitation.
FASEB J. 2003;17:993–1002.
Reminiac F, Saint-Etienne C, Runge I, etal. Are central venous lactate
and arterial lactate interchangeable? A human retrospective study.
Anesth Analg. 2012;115:605–10.
Riskin DJ, Tsai TC, Riskin L, etal. Massive transfusion protocols: the
role of aggressive resuscitation versus product ratio in mortality
reduction. J Am Coll Surg. 2009;209:198–205.
Rixen D, Siegel JH.Bench-to-bedside review: oxygen debt and its met-
abolic correlates as quantiers of the severity of haemorrhagic and
post-traumatic shock. Crit Care. 2005;9:441–53.
Tisherman SA, Barie P, Bokhari F, etal. Clinical practice guideline:
endpoints of resuscitation. J Trauma. 2004;57:898–912.
Velmahos GC, Demetriades D, Shoemaker WC, et al. Endpoints of
resuscitation of critically injured patients: normal or supranormal?
Ann Surg. 2000;232:409–18.
Plain X-Rays forPenetrating Trauma
https://t.me/medicina_free
SimengWang, DonaldJ.Green, MarkBernstein,
andMarkoBukur
17
17.1 Plain X-Rays forPenetrating Trauma
Plain X-rays have long been used in assessing traumatic injuries and comprise an integral part of the Advanced Trauma
Life Support (ATLS) approach to the care of traumatic
patients. Meanwhile, rapid, multi-detector computed tomography (CT) has become readily available and steps away from
the resuscitation bay. The routine use of CT has been adopted
as protocol in many centers, including our own. Though there
is no question that advanced imaging provides superior resolution and diagnostic capability, there is still great utility in using
plain X-rays for rapid assessment of penetrating injuries.
17.2 Rationale forthe“Plain Film”
There are a multitude of reasons that a trauma surgeon should
become procient in interpreting plain X-rays. Advanced
imaging studies may be subject to resource availability and
technical failures, especially in non-US civilian centers.
Additionally, patients with penetrating injury in critical condition may not be suitable for leaving the resuscitation bay that
can lead to the infamous “death in CT scan”; thus plain lms
in conjunction with bedside ultrasound may be the only feasible studies in certain circumstances. Furthermore, screening
of asymptomatic patients with diagnostic X-rays has been
shown to decrease time spent in the emergency department,
provide substantial cost savings, and avoid unnecessary radiation exposure to those who do not require further workup.
17.3 Limitations of“Plain Film” Imaging
There are several limitations intrinsic to using conventional
X-rays in assessing penetrating trauma. Portable, single- view
plain lms are readily acquired and often immediately available for review in the resuscitation bay. The capability of evaluating anatomic structures is often limited. For example,
pseudocardiomegaly, mediastinal enlargement, or increased
pulmonary vascularity is often seen in the anteroposterior (AP)
view chest X-ray. In abdominal images, the AP view cannot
distinguish superimposed soft tissue or bony structures from
underlying viscera. Additionally, without additional dimensions, X-rays do not always provide adequate information to
delineate the relative location of the injury to anatomic structures. Lastly, the sensitivity of demonstrating air-uid level,
pneumothorax, or free intraperitoneal air is largely undermined
by supine or semirecumbent patient positioning during resuscitation. Despite these limitations, when analyzed appropriately
by experienced clinicians, plain lms can be invaluable with
respect to the information they readily provide.
17.4 Chest Radiography
S. Wang · M. Bukur (*)
Department of Surgery, New York University Grossman School of
Medicine, NYC Health + Hospitals/Bellevue, New York, NY, USA
e-mail: simeng.wang@nyulangone.org;
marko.bukur@nyulangone.org
D. J. Green
Trauma and Emergency Surgery, HonorHealth,
Scottsdale, AZ, USA
M. Bernstein
Department of Radiology, New York University Grossman School
of Medicine, NYC Health + Hospitals/Bellevue,
New York, NY, USA
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023
E. Degiannis et al. (eds.), Penetrating Trauma, https://doi.org/10.1007/978-3-031-47006-6_17
Thoracic injuries account for a signicant proportion of traumatic deaths. Penetrating injuries to the thorax account for
4–15% of admissions to major civilian trauma centers. A
high percentage of these patients will have injuries involving
the chest wall, pleura, or lungs that are identiable on chest
X-ray. The portable chest radiograph is the initial screening
test for the majority of patients with penetrating thoracic
trauma. It allows for detection of major life-threatening thoracic injuries and assists in triage of these patients. We will
discuss the utility of thoracic plain lms and imaging ndings of specic injuries in the sections that follow.
145
146
https://t.me/medicina_free
17.4.1 Soft Tissues andBony Thorax
Subcutaneous hematomas present as nonspecic radiodensity overlying the chest wall due to blood accumulation in
the soft tissues. This can result from damage to muscular
structures, underlying rib fractures, or injury to vessels of the
chest wall. Radiodense foreign bodies dislodged in the soft
tissue such as a missile or a penetrating object can be identied on plain lms.
Rib fractures are the most common injury identied on
X-rays (Fig. 17.1) and may signify associated pleural and
parenchymal injuries. Once a rib fracture is found in the penetrating setting, it is important to vigilantly look for a possible hemothorax, pneumothorax, or pulmonary contusion as a
result of the penetrating objects or the sharp rib fractured
edges.
Soft tissue emphysema is another commonly identied
abnormality on radiographic imaging of penetrating trauma
(Figs.17.1 and 17.2). Similarly, the presence of subcutaneous air should alert one to look for associated ipsilateral rib
fractures and intrathoracic pathology. This nding should be
presumed from an underlying pneumothorax, even if not
readily identiable on the radiograph.
S. Wang et al.
Fig. 17.2 Subcutaneous emphysema (red arrowheads) in a patient
with small left pneumothorax (white arrows) conrmed on a later CT
chest
17.4.2 Pleura andLung Parenchyma
Pneumothoraces are common complications from penetrating thoracic injury and occur secondary to disruption of
lung parenchyma that leads to air accumulation in the intrapleural space. The most typical radiographic nding is the
“visceral- pleural line” in the apical-lateral lung eld repre-
Fig. 17.1 Image of a gunshot wound to the left chest with rst rib
fracture (red asterisk) and associated subcutaneous emphysema of the
neck (red arrow heads). The white arrows dene the underlying
hemopneumothorax
Fig. 17.3 Subtle left anterior pneumothorax in anteromedial (red
arrowheads) recess following left chest stab injury with abundant sub-
cutaneous emphysema
senting separation of the normally apposed visceral and
parietal pleura. However, this nding may not be visualized
in up to 30% of the cases when chest X-rays are taken in
supine or semirecumbent positions, as commonly done in
trauma settings. Instead, pneumothoraces may be seen in
the anteromedial and subpulmonic recesses (Fig. 17.3).
Other less common X-ray ndings also include a hyperlucent upper abdomen, sharply demarcated diaphragm,
demarcation of the inferior surface of the lung, and the
“deep sulcus sign” (Fig.17.4).
Соседние файлы в папке Библиотека им академика М.И. Перельмана