Добавил:
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 / @xirurgi_2025 / @xirurgi_2025 - 318 - файл

.pdf
Скачиваний:
0
Добавлен:
28.08.2026
Размер:
58 Мб
Скачать
116
https://t.me/medicina_free
G. A. Richards et al.
• End-tidal CO2, especially if there is a concomitant trau­matic brain injury
• Optimal endotracheal or tracheostomy tube positioning and cuff pressure
13.8 Longer-Term ICU Airway Management
13.8.1 Tracheostomy
There are two main indications for tracheostomy, long-term airway support as is the case with facial fractures, severe traumatic brain (TBI), and laryngeal injury and prolonged requirement for ventilatory support. Essentially a tracheos­tomy is performed to facilitate nursing care and oral hygiene, as there is controversy surrounding the overall benet, with some suggesting that there might be reduced ventilator­associated pneumonia (VAP) and a shortened ICU stay.
Either a percutaneous or an open procedure (with difcult
neck anatomy or need for other operative procedures) may be performed, either primarily or around day 3 for patients with compromised airways or neuromuscular dysfunction.
A tracheostomy for cardiopulmonary dysfunction is com-
monly performed at around day 10, depending on the degree of persistent pulmonary compromise and as to whether extu­bation is likely in the near future.
ble, as this leads to loss of PEEP and actually increases the work of breathing, risking higher failure rates and loss of recruitment.
When all reversible issues have been addressed and the patient remains persistently ventilator dependent, the approach will depend on available resources. A heart and/or lung transplant may be considered where resources are avail­able, but with limited resources, a family meeting, including the patient where possible, should frankly discuss the situa­tion with the likely transition from curative to palliative care.
Important Points
• Airway and ventilation go hand in hand but should be
independently assessed.
• Early resuscitative ventilation is different from ICU ven-
tilation as the goals differ.
• Hypercarbia is to be avoided in the TBI patient.
• Tracheostomy should be considered on an individual
patient basis.
• Weaning should be performed when the patient pathology
is reversed and the ventilator requirements have been
reduced to minimal levels.
• Remove chest tubes as soon as reasonable.
Suggested Reading
13.8.2 Weaning
Weaning is facilitated by early mobilization and reduced use of sedation.
There are three main causes of weaning failure:
• Weakness (ICU-associated weakness, cord injury, tho­racic cage injury, low GCS)
• Persistent hypoxemia due to due to unresolved or irre­versible pulmonary injury
• Myocardial dysfunction (myocardial brosis after a con­tusion or infarct or a preexisting cardiomyopathy)
As described above, early conversion to spontaneous ven-
tilation with pressure support is suggested with a gradual reduction of PSV rst and thereafter PEEP to a predened baseline such as 6–8cmH2O for both. If the patient tolerates this without elevation of RSBI above 80, hypoxemia (satura­tion<90%), and hypercarbia (with acidosis) with no signs of distress (sweating, agitation) and is awake, then the patient should be extubated. If the patient is fully conscious but is considered to be high risk for failure or still requires PSV, one may extubate to a noninvasive PSV mode, avoiding the risks of prolonged intubation, while simultaneously optimiz­ing oxygenation. A T-piece trial should be avoided if possi-
Alhazzani W, Belley-Cote E, Moeller MH, etal. Neuromuscular block-
ade in patients with ARDS: a rapid practice guideline. Intensive Care Med. 2020;46:1977–86.
Amato MB, Meade MO, Slutsky AS, etal. Driving pressure and sur-
vival in the acute respiratory distress syndrome. N Engl J Med. 2015;372:747–55. https://doi.org/10.1056/NEJMsa1410639.
Aslakson RA, Bridges JFP.Assessing the impact of palliative care in
the intensive care unit through the lens of patient-centered outcomes research. Curr Opin Crit Care. 2013;19:504–10.
Brain Trauma Foundation. Guidelines for the management of severe
traumatic brain injury. Hyperventilation, 3rd edition. J Neurotrauma. 2007;24(Suppl 1):S87–95.
Cinotti R, Lascarrou J-B, Azais M-A, etal. Diuretics decrease uid bal-
ance in patients on invasive mechanical ventilation: the randomized­controlled single blind. IRIHS Study Crit Care. 2021;25:98. https://
doi.org/10.1186/s13054- 021- 03509- 5.
Coppola S, Froio S, Chiumello D. Protective lung ventilation during
general anaesthesia: is there any evidence? In: Vincent JL, editor. Annual update in intensive care and emergency medicine, 2014. Switzerland: Springer; 2014.
Cornillon A, Balbo J, Cofnet J, etal. The ROX index as a predictor
of standard oxygen therapy outcomes in thoracic trauma. Scand J Trauma Resusc Emerg Med. 2021;29:81. https://doi.org/10.1186/
s13049- 021- 00876- 4.
Desai NR, Myers L, Simeone F. Comparison of 3 different methods
used to measure the rapid shallow breathing index. J Crit Care. 2012;27(4):418–24.
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(11):1181–247. https://doi.
org/10.1007/s00134- 021- 06506- y.
13 Ventilation intheTrauma Patient: APractical Approach
https://t.me/medicina_free
117
Gattinoni L, Chiumello D, Carlesso E, etal. Bench to bedside review:
chest wall elastance in acute lung injury/acute respiratory distress syndrome patients. Crit Care. 2004;8(5):3505.
Gattinoni L, Cressoni M, Brazzic L. Fluids in ARDS: from onset
through recovery. Curr Opin Crit Care. 2014;20:373–7. https://doi.
org/10.1097/MCC.0000000000000105.
Gattinoni L, Pesenti A.The concept of “baby lung”. Intensive Care
Med. 2005;31(6):776–84.
Hardcastle TC, Maier R, Muckart DJJ.Ventilation in trauma patients—
the rst 24 h is different! World J Surg. 2017;41(5):1153–8. https://
doi.org/10.1007/s00268- 016- 3530- 1.
Haut ER, Kalish BT, Efron DT, etal. Spine immobilization in penetrat-
ing trauma: more harm than good? J Trauma. 2010;68(1):115–21.
https://doi.org/10.1097/TA.0b013e3181c9ee58.
Hickman CE, Montecinos-Munoz NR, Castanares-Zapatero D, et al.
Acute effects of sitting out of bed and exercise on lung aeration and oxygenation in critically ill subjects. Respir Care. 2020;66(2):253–
62. https://doi.org/10.4187/respcare.07487.
Hraiech S, Yoshida T, Annane D, etal. Myorelaxants in ARDS patients.
Intensive Care Med. 2020;46:2357–72. https://doi.org/10.1007/
s00134- 020- 06297- 8.
Jackson JC, Girard TD, Gordon SM, et al. Long-term cognitive and
psychological outcomes in the awakening and breathing controlled trial. Am J Respir Crit Care Med. 2010;182:183–91. https://doi.
org/10.1164/rccm.200903- 0442OC.
Kovacs G, Law JA, editors. Airway management in emergencies. 2nd
ed. Connecticut, USA: Peoples Publishing House; 2011.
Lachmann B.Open up the lung and keep the lung open. Intensive Care
Med. 1992;18:319–22.
Lou M, Xue F, Chen L, et al. Is high PEEP ventilation strategy safe
for acute respiratory distress syndrome after severe traumatic brain injury? Brain Inj. 2012;26:887–90. https://doi.org/10.3109/026990
52.2012.660514.
Lowe GL, Ferguson ND.Lung-protective ventilation in neurosurgical
patients. Curr Opin Crit Care. 2006;12:3–7.
Meng L, Wang C, Li J, Zhang J.Early vs late tracheostomy in critically
ill patients: a systematic review and meta-analysis. Clin Respir J. 2015;10(6):684–92. https://doi.org/10.1111/crj.12286.
Mireles-Cabodevila E, Siuba MT, Chatburn RL. A taxonomy for
patient-ventilator interactions and a method to read ventilator wave­forms. Respir Care. 2021;67(1):129–48. https://doi.org/10.4187/
respcare.09316.
Papazian L, Aubron C, Brochard L, etal. Formal guidelines: manage-
ment of acute respiratory distress syndrome. Ann. Intensive Care. 2019;9:69. https://doi.org/10.1186/s13613- 019- 0540- 9.
Papazian L, Forel J-M, Gacouin A, et al. Neuromuscular block-
ers in early acute respiratory distress syndrome. N Engl J Med. 2010;363:1107–16. https://doi.org/10.1056/NEJMoa1005372.
Penuelasa O, Thillec AW, Esteban A. Discontinuation of ventilatory
support: new solutions to old dilemmas. Curr Opin Crit Care. 2015;21:74–81. https://doi.org/10.1097/MCC.0000000000000169.
Pipeling MR, Fan E.Therapies for refractory hypoxemia in acute respi-
ratory distress syndrome. JAMA. 2010;304(22):2521–7. https://doi.
org/10.1001/jama.2010.1752.
Richards GA, White H, Hopley M. Rapid reduction in oxygenation
index by employment of a recruitment technique in patients with severe ARDS.J Intensive Care Med. 2001;16:193–9.
Roberts JR, Spadafora M, Cone DC.Proper depth of placement of oral
endotracheal tubes in adults prior to radiographic conrmation. Acad Emerg Med. 1995;2:20–4.
Siddiqui UT, Tahir MZ, Shamim MS, Enam SA. Clinical outcome
and cost effectiveness of early tracheostomy in isolated severe head injury patients. Surg Neurol Int. 2015;6:65. https://doi.
org/10.4103/2152- 7806.155757.
Sutherasan Y, Vargas M, Pelosi P.Protective mechanical ventilation in
the non-injured lung: review and meta-analysis. In: Vincent JL, edi­tor. Annual update in intensive care and emergency medicine, 2014. Switzerland: Springer; 2014.
The Acute Respiratory Distress Syndrome Network. Ventilation
with lower tidal volumes as compared with traditional tidal vol­umes for acute lung injury and the acute respiratory distress syn­drome. N Engl J Med. 2000;342:1301–8. https://doi.org/10.1056/
NEJM200005043421801.
Turner DA, Rehder KJ, Bonadonna D, et al. Ambulatory ECMO as a
bridge to lung transplant in a previously well pediatric patient with ARDS.Pediatrics. 2014;134(2):583–5.
Wade D, Hardy R, Howell D, etal. Identifying clinical and acute psy-
chological risk factors for PTSD after critical care: a systematic review. Minerva Anestesiol. 2013;79(8):944–63. PMID 2355861
Weingart SD, Levitan RM. Preoxygenation and prevention of
desaturation during emergency airway management. Ann Emerg Med. 2012;59:165–75. https://doi.org/10.1016/j.
annemergmed.2011.10.002.
Wongtangman K, Grabitz SD, Hammer M, et al. Optimal sedation in
patients who receive neuromuscular blocking agent infusions for treatment of acute respiratory distress syndrome—a retrospective cohort study from a New England health care network. Crit Care Med. 2021;49(7):1137–48.
ECMO intheTrauma Patient: APractical
https://t.me/medicina_free
Approach
JeromeCrowley
14
14.1 Introduction
This chapter will provide the trauma surgeon with an over­view of extracorporeal membrane oxygenation (ECMO). Indications for ECMO will be discussed as well as the basics of cannulation strategies. Troubleshooting of common ECMO scenarios will be discussed as well as the basics of weaning from ECMO.
14.2 Background onECMO
ECMO is fundamentally the provision of gas exchange for the blood outside the body. There are three main types of ECMO of interest to the acute trauma population: venoarte­rial (V-A), veno-pulmonary arterial (V-P), and veno-venous (V-V) ECMO.By convention, letters listed before the hyphen refer to cannula draining blood from the patient to the ECMO circuit, and letters listed after the hyphen refer to cannula returning blood from the ECMO circuit to the patient. The three subtypes of ECMO support differ what type of support is provided to the patient. V-V ECMO is indicated for respi­ratory failure, either hypoxic, hypercapnic, or mixed. V-V ECMO does not provide any signicant hemodynamic sup­port, but by correcting the respiratory acidosis and reversing the hypoxemia, there may be improvement in myocardial function, particularly on the right side of the heart. V-P ECMO is indicated for the scenario of signicant isolated right ventricular dysfunction and is able to provide respira­tory as well as right ventricular support. Finally, V-A ECMO is primarily indicated to provide hemodynamic support to the systemic circulation in the setting of cardiac pump fail­ure. As discussed in a later section, the amount of respiratory support provided by V-A ECMO is variable and depends on native lung function and cannulation strategy.
J. Crowley (*) Anesthesia, Critical Care, and Pain Medicine, Massachusetts General Hospital, Boston, MA, USA e-mail: jccrowley@mgh.harvard.edu
An ECMO circuit consists of four main components: a drainage cannula removing blood from a large central vein, a pump to move blood through the circuit, an oxygenator to provide gas exchange, and a return cannula that is placed in the patient to return oxygenated blood. The amount of ECMO support a patient is on is described by three variables: the ow through the circuit, the percentage of oxygen in the gas in the oxygenator known as the delivered oxygen frac­tion (FdO2), and the ow rate of the gas in the oxygenator known as the sweep ow. The FdO2 is analogous to the frac­tion of inspired oxygen on the ventilator and is one of the determinants of the oxygenation of blood. The sweep ow rate determines the rate of carbon dioxide removal and is analogous to the minute ventilation. The ow through the circuit is determined by several factors: the rotations per minute of the centrifugal pump (RPMs), the resistance to drainage through the venous cannula, and the resistance to return through the return cannula. Increasing the RPMs will increase the ow to a point; however it is always important to remember that the ECMO pump is both preload dependent and afterload sensitive, so the ow may vary at the same RPMs due to different loading conditions.
Oxygenation of the blood via the ECMO circuit is related to two factors: the fraction of delivered gas that is oxygen and the total ow of the ECMO circuit. Approximately 70% of blood must participate in efcient gas exchange to main­tain an arterial saturation of 90–94%, so assuming 1.0 FdO2, then the ECMO circuit ow must be 70% of the cardiac output to achieve this goal. This is particularly relevant for veno-venous ECMO when deciding the goal ow rates.
14.3 Veno-venous ECMO
V-V ECMO is indicated for respiratory failure refractory to maximal medical management. The trauma patient presents a unique challenge as all available medical therapies may not be appropriate (proning may be contraindicated, for exam­ple, or due to a traumatic bronchopleural stula, lung-
© 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_14
119
120
https://t.me/medicina_free
J. Crowley
protective ventilation may not be feasible). Common indications that are encountered in the trauma population include severe acute respiratory distress syndrome, severe pneumonia or aspiration, pulmonary contusions, inhalational injuries, refractory status asthmaticus, airway obstruction, severe air leak syndrome, or intraprocedural need for lung isolation that is tolerated by conventional means. Most con­traindications to veno-venous ECMO are relative, but care should be taken in patients with severe cardiogenic shock (may need venoarterial ECMO), patients with signicantly elevated body mass index (>40–45) as this will be challeng­ing to support due to the high ow rates needed, as well as patients with signicant underlying comorbidities (end-stage renal disease, cirrhosis, chronic lung disease, severe intracra­nial pathology) as it is unlikely that these patients will sur­vive an ECMO course.
14.4 Cannulation forVeno-venous ECMO
V-V ECMO cannulation is almost always done peripherally (not directly in the thorax). There are multiple congurations available; the most important concept to keep in mind is that blood must be drained from a large central vein (usually the inferior vena cava) and returned to a large central vein (usu­ally the superior vena cava or the right atrium). Dictating the positioning of the cannula for V-V ECMO is a balance between obtaining adequate drainage to obtain the goal ow rate (for V-V ECMO, the drainage is almost always the limit­ing factor unless the return cannula is grossly undersized) and avoiding the phenomenon of recirculation. Recirculation is when blood passes directly from the return cannula back to the drainage cannula rather than through the circulation of the patient. This reduces both the efciency of the ECMO circuit and the percentage of oxygenated blood available to the patient. In order to minimize this phenomenon, it is ideal to position the tip of the return cannula 10cm or greater from the tip of the drainage cannula.
Cannulation for V-V ECMO is most commonly accom­plished percutaneously, ideally using ultrasound guidance to identify a safe location to access the vein. Options for can­nulation include femoral/internal jugular, femoral/femoral, femoral/subclavian, or dual-lumen single-site cannulation. Common to all forms of cannulation is meticulous avoidance of air in the ECMO circuit using “wet to wet” connections and robust securing of cannula with multiple sutures to pre­vent inadvertent dislodgement.
Femoral/internal jugular and femoral/subclavian are simi­lar. Under ultrasound guidance, the common femoral vein is identied (preferentially the right as this is a straighter path to the inferior vena cava although anatomic conditions may dictate choice of the left) and access in the standard fashion, and a small sheath is placed. Via this sheath a long (180cm or 260cm) wire is passed to the right atrium. This is ideally
accomplished under imaging guidance: uoroscopy, trans­esophageal echocardiography, or transthoracic echocardiog­raphy; if not available a plain X-ray may sufce to conrm appropriate wire placement. In the busy setting of an acute trauma patient, a 180cm wire may be preferred as this can reduce redundant wire and compromise of sterility. Over this wire, using serial dilation and Seldinger technique, a venous drainage cannula is placed. For adult patients, a 25Fr cannula is usually sufcient in any patient over 40 kg. In smaller patients a 23Fr cannula may be sufcient but will limit drain­age. The tip of this cannula is ideally placed close to the right atrial/IVC junction. If imaging guidance is available, it is often advantageous to place a stiff wire from the femoral location to act as a more stable access rail for the long venous cannula. The benets of a stiff wire need to be balanced with an increased risk of vascular perforation if imaging is not available and providers are not experienced with endovascu­lar procedures. If possible, it is desirable to place the tip at least past the hepatic vein so the proximal drainage ports are in the intrahepatic IVC which is more resistance to collapse from intra-abdominal factors than the more distal IVC and will provide more reliable drainage without needing exces­sive uid administration. If traumatic injury precludes such placement, then shorter cannula can be used. In order to compensate for less ideal positioning of the femoral cannula, it may be necessary to place two femoral drainage cannula and connect them together to ensure adequate drainage for the ECMO circuit. The return cannula is a shorter arterial/ jugular cannula that in most adults is a 19 or 21Fr (allowing for ows >5LPM if needed). The easiest location for the return cannula is the right internal jugular vein where place­ment is analogous to normal central venous cannulation. The right internal jugular vein is identied under ultrasound and accessed in the normal fashion. This access is used to place a wire to the right atrium over which the cannula is placed with tip in the superior vena cava after serially dilating the tract. If the right internal jugular vein is not feasible, then the left subclavian vein is another option with placement being simi­lar. The left internal jugular vein and right subclavian vein are only recommended if uoroscopic guidance is available due to the higher risk for cannula malposition with these locations.
Femoral/femoral cannulation is an attractive cannulation strategy in patients with potential neck trauma or traumatic brain injury as it does not affect cerebral venous drainage signicantly and allows for cannulation to be performed away from the airway. Access of the femoral vessels is as described above. A long wire is passed from the left femoral vein to the right atrium; this is either a standard stiffness wire or a stiff wire, or if a stiff wire does not pass easily, a soft wire is placed and then exchanged over a pigtail catheter for a stiff wire. Next a wire is advanced from the right femoral vein to the right atrium. It is preferred to place the left-sided cannula rst as the right-sided cannula will straighten the
14 ECMO intheTrauma Patient: APractical Approach
https://t.me/medicina_free
121
vena cava and may make the left-sided access more acute in angle increasing the risk of vascular perforation. The left femoral cannula is a 25Fr drainage cannula and the right femoral cannula is a long (55cm) 19 or 21Fr return cannula (tip placed in the right atrium). Based on patient anatomy, smaller cannula may be needed which will reduce maximal ows. This represents one of the limitations of femoral/fem­oral V-V ECMO: lower maximal ow than other cannulation strategies. The other drawbacks include a higher rate of recirculation (due to proximity of cannula) and a high rate of deep venous thrombosis around the cannula.
Dual-lumen cannulation represents an attractive option as it allows for single-site access and as it is supradiaphrag­matic allows for easier patient mobilization. It is also appro­priate for patients who cannot have a femoral cannula placed (severe pelvic trauma, presence of an IVC lter, signicant caval distortion from injury). Drawbacks are that it is more time-consuming and prone to malposition necessitating repositioning which requires echocardiography. Dual-lumen cannulation is not recommended as rst line for an emergent cannulation due to more nesse required for appropriate positioning. The dual-lumen cannula has drainage holes in both the SVC and IVC and returns blood to the right atrium ideally directed at the tricuspid valve. It is most commonly placed via the right internal jugular vein but can be placed from either jugular vein or subclavian if anatomy is favor­able. Positioning of the cannula is determined by both uo­roscopy and transesophageal echocardiography. Attempts to place the cannula without image guidance run a high risk of right ventricular perforation and are not recommended.
After cannulation, the ECMO circuit is appropriately con­nected ensuring no air in the lines. It is recommended that an “ECMO Initiation Checklist” be performed in order to ensure appropriate direction of tubing, adequate fresh gas supply, and appropriate levels of oxygen are conrmed. Support should be initiated slowly in order to minimize abrupt tem­perature shifts (exercise extreme caution using a circuit that has not been warmed as rapid infusion of cold uid can cause the heart to brillate) and to ensure appropriate stability. Cannulation can trigger a vasodilatory response, so vaso­pressors should be available to support the blood pressure. Conversely, correction of the respiratory acidosis/hypoxia may lead to rapid improvement in vasomotor tone and car­diac function, so close monitoring is essential. Once ECMO support is established satisfactorily, ventilatory support should be weaned to lung-protective settings in order to min­imize further lung injury.
14.5 Veno-pulmonary Arterial ECMO
V-P ECMO is indicated to support the failing right ventricle as well as providing veno-venous ECMO support. This con­guration is not commonly used, but due to the availability
of percutaneous dual lumen, cannula is not becoming more prevalent. Advantages include a low rate of recirculation (drainage is in the right atrium and return in the pulmonary artery; the tricuspid and pulmonic valves serve to minimize mixing) and the ability to support a failing right heart as well as potentially help decongest the liver and kidneys in the set­ting of right ventricular failure. It is important to remember that this conguration is not ideal in the setting of any degree of left ventricular dysfunction as the independent right-sided support will rapidly overwhelm the failing left ventricle leading to severe pulmonary edema.
Placement is almost always via the right internal jugular vein. Under uoroscopic guidance, a balloon-tipped, ow­directed catheter is placed into the pulmonary artery and exchanged for a stiff wire. Over this wire, using serial dila­tion, the cannula is advanced and appropriately positioned. It cannot be emphasized enough that placement cannot be readily adjusted once the wire is removed, so all efforts should be made to ensure satisfactory location before leaving the uoroscopy suite.
ECMO support is initiated as above with additional atten­tion paid to the left ventricular function to avoid overloading the pulmonary circulation. In the setting of isolated right ventricular dysfunction, improvement in cardiac output should be noted with a reduced need for inotropic support.
14.6 Venoarterial ECMO
V-A ECMO is indicated in patients with hemodynamic compromise related to inadequate cardiac function. The most common indications are acute myocardial infarction, myocarditis, massive pulmonary embolism, or decompen­sated heart failure. Trauma patients may benet from V-A ECMO if they show evidence of impaired myocardial func­tion due to contusions, severe acidosis, volume overload, overdoses, or electrolyte abnormalities. Anatomic contrain­dications to V-A ECMO include signicant aortic insuf­ciency and aortic dissection. Similar contraindications exist as related to V-V ECMO with the additional caveat that patients on V-A ECMO can “live” on ECMO for a pro­longed period of time even with no reasonable chance of recovery. This can be incredibly distressing on both health care providers and patient’s families, and early discussion of feasibility of recovery is critical. Exit strategies from V-A ECMO include recovery, durable left ventricular sup­port devices, heart transplant, or additional mechanical support devices designed to act as a further bridge to inter­vention. The candidacy of most trauma patients for these advanced therapies will be unknown, so best practice would be to choose patients likely to recover as most patients suf­fering traumatic injury would need to have signicant recovery before being considered for advanced cardiac therapies.
122
https://t.me/medicina_free
J. Crowley
Cannulation for V-A ECMO is dened as either central (in the thorax) or peripheral. Central ECMO has been described for trauma patients; however it is most commonly only due in the cardiac surgical operating room, and tech­niques are beyond the scope of this text. Focus will be made on peripheral V-A ECMO which is the most common can­nulation strategy in an emergency. Peripheral cannulation is accomplished via the femoral vessels by either an open or percutaneous technique. Open techniques have the advan­tages of a higher success rate, easier method of ensuring limb perfusion, and potentially easier removal of cannula. Drawbacks include higher rates of bleeding, infection, and slower cannulation times. Ultrasound-guided percutaneous cannulation is rapidly becoming the standard of care. In either strategy, the common femoral artery is identied below the inguinal ligament but above the bifurcation of the supercial and deep femoral arteries. A small sheath is placed and used to introduce a J-wire into the descending aorta over which serial dilation is used to place an appropri­ately sized cannula. Cannula size is determined by the vessel size and by the goal ow. Goal ow on V-A ECMO is tar­geted to a cardiac index of 2.4 (so goal ow is body surface area multiplied by 2.4). In an acute trauma situation this is not often known, so a rough guide is to use a 17Fr cannula in most adult patients (capable of 4.5LPM of ow). A 19Fr cannula can be chosen in larger patients who are >180cm (allowing for 5.5LPM of ow), and a 15Fr cannula can be chosen in smaller patients (allowing for 3.5LPM of ow). The venous cannula is placed analogous to the method described in the V-V ECMO section, with most adult patients accommodating a 25Fr cannula (and smaller patients tolerat­ing a 23Fr cannula). It is critical to ensure that the venous cannula is in the vein and not the artery as the large venous cannula has a high likelihood of causing catastrophic vessel injury if misplaced.
After cannulation, the ECMO circuit is appropriately con­nected ensuring no air in the lines. It is recommended that an “ECMO Initiation Checklist” be performed in order to ensure appropriate direction of tubing, adequate fresh gas supply, and appropriate levels of oxygen are conrmed. Support should be initiated slowly in order to minimize abrupt tem­perature shifts (exercise extreme caution using a circuit that has not been warmed as rapid infusion of cold uid can cause the heart to brillate) and to ensure appropriate stability. Cannulation can trigger a vasodilatory response, so vaso­pressors should be available to support the blood pressure. Conversely, correction of the low-output state may allow for rapid weaning of vasopressors, and close monitoring of blood pressure is critical.
Other considerations unique to peripheral V-A ECMO are north/south syndrome (or differential hypoxia) and left ventricular venting. Due to the retrograde nature of the ow on V-A ECMO (ECMO ow owing retrograde up the aorta
from the femoral arterial cannula), there is a location of mixing in the aorta where “ECMO blood” meets “native blood” that has been ejected from the heart and has been oxygenated via the lungs. If the patient’s native lung func­tion is severely compromised, then this blood has the poten­tial to be signicantly hypoxic. This is problematic as the coronaries and the cerebral circulation are more likely to see native blood and consequently will suffer hypoxic injury despite adequate performance of the ECMO circuit. Close vigilance for this phenomenon is critical and includes arte­rial blood gas sampling from the right upper extremity as this will reect the blood entering the cerebral circulation and will give warning of differential hypoxia in a patient on peripheral V-A ECMO. An additional complication on peripheral V-A ECMO is left ventricular distension. Due to the retrograde ow on ECMO, the left ventricle will see increased afterload which in the setting of impaired left ven­tricular function may lead to distension. This distension of the left ventricle will lead to further left ventricular stress in the setting of increased wall tension as well as the potential for signicant pulmonary edema which will reduce the like­lihood of liberation from ECMO.Monitoring for left ven­tricular distension includes frequent echocardiography to assess for aortic insufciency, left ventricular function, mitral regurgitation, and left ventricular size, chest X-rays to look for pulmonary edema progression, and consider­ation of a pulmonary artery catheter to monitor left ventricu­lar lling pressures.
In all forms of ECMO, it is optimal to maintain a reason­able degree of anticoagulation to reduce the risk of thrombo­sis in the circuit and thrombotic complications in the patient. Targeted levels vary by institution and usually involve target­ing an aPTT range, a Xa range, or an activated clotting time. Trauma patients may not tolerate heparinization and this becomes a risk-benet discussion. One possibility is that anticoagulation is felt to be safe and standard protocols can be followed (usually a bolus of 100units/kg of heparin or a similar efcacy bolus of bivalirudin followed by an infusion to maintain a therapeutic level). If the risk of bleeding is felt to be too high, then either just a bolus dose for cannulation (likely the highest initial risk portion due to stasis in the can­nula) or anticoagulation can be avoided all together. There are multiple reports of ECMO cannulation and circuits run­ning without anticoagulation, so in the appropriate patient, this is reasonable acknowledging the likely increased risk of thrombotic complications. In order to mitigate these risks in a trauma patient, it is reasonable to consider a strategy to reduce any periods of blood stasis. This may include prefer­entially owing the circuit at higher rates, having two pro­viders perform cannulation simultaneously to avoid prolonged periods where a cannula is left clamped with no ow, and ushing of cannulas with saline to avoid any blood sitting in them while ECMO is being prepared.
14 ECMO intheTrauma Patient: APractical Approach
https://t.me/medicina_free
123
14.7 Troubleshooting
14.7.1 Recirculation onV-V ECMO
Recirculation is the phenomenon where blood that has been oxygenated via the ECMO circuit passes back into the ECMO circuit rather than through the systemic circulation. This can be suspected when the patient’s arterial saturation remains low despite what should be adequate ECMO ow. In order to diagnose this, the saturation of the blood on the drainage limb should be checked. The closer this to the arte­rial saturation, the more likely that recirculation is occurring (assuming the oxygenator is functioning well). Another hall­mark of this phenomena is that increasing the ECMO ow has minimal effect on the oxygen saturation. In order to rec­tify this situation, the cannula likely need to be adjusted. Ideally, under imaging guidance, the cannula can be retracted slightly so that a separation of at least 10 cm is obtained. Remember, the initial goal location of the drainage cannula is in the IVC just below the right atrium, and the return can­nula is in the SVC just above the right atrium. If the patient has a single-site dual-lumen catheter, a transesophageal echocardiogram is likely indicated to ensure appropriate positioning. Plain lm radiographs may also be helpful to determine if there has been cannula migration since catheter placement.
14.7.2 Progressive Hypoxemia onV-V ECMO
One of the most common complications of ECMO is sepsis (also a common fear in trauma patients). As sepsis com­monly presents with elevated cardiac output, the required V-V ECMO ow rates will increase as the patient becomes more hyperdynamic. This will manifest as worsening of hypoxemia despite stable ECMO ows and no change in recirculation. The treatment is to increase ECMO ows; however this may require the placement of additional drain­age cannula, and it is important to note that most adult ECMO oxygenators are not capable of oxygenating blood at a rate greater than 7LPM.Vigilance for sepsis is critical and early antibiotic therapy is important.
14.7.3 Dierential Hypoxia
As described above, differential hypoxia results from com­peting native cardiac ejection and ECMO ow in the setting of impaired lung function. This is seen in trauma patients who have recovery of their cardiac function faster than their lung function. Diagnosis is made by sampling blood from the right upper extremity arterial system. Management of this depends on the severity of the lung injury. As a rst
maneuver, ventilatory support can be optimized in order to improve native blood oxygenation. This is not ideal however if it results in injurious settings that can potentiate further lung injury and reduce the likelihood of recovery. A second option is to create a hybrid circuit, known as veno­arteriovenous ECMO (V-AV). Here, an additional return cannula is placed in one of the jugular or subclavian veins and y-connected to the femoral arterial cannula so that some oxygenated blood is returned to the venous system, “pre­oxygenating” the blood before it passes into the native lungs. In effect the patient is now on both V-V and V-A ECMO.This conguration can be challenging to maintain as it requires higher total drainage to support the ows needed as well as a partial occluding clamp in order to adjust the relative venous vs arterial ow.
14.7.4 Left Ventricular Distension
Left ventricular distension results from an impaired left ven­tricle facing the elevated afterload resulting from retrograde ECMO ow. If left untreated this can lead to irreversible left ventricular injury, pulmonary edema, and stasis in the left ventricle leading to thrombotic complications. An initial maneuver can be to increase inotropic support to encourage left ventricular contraction. In addition, ECMO ow can be increased further to decrease blood returning to the left ven­tricle. It should be noted, however, that this is not ideal in a trauma patient who is not on anticoagulation as a noncon­tractile left ventricle will quickly develop thrombosis with a high likelihood of stroke. Additional methods of decom­pressing the left ventricle are more invasive: placement of an intra-aortic balloon pump (less likely to efcacious in younger patients with compliant aortas), placement of a per­cutaneous left ventricular assist device, atrial septostomy, or placement of a surgical vent via the left ventricular apex or the left upper pulmonary vein.
14.7.5 ECMO Flow Issues
Commonly referred to as “chatter,” this refers to intermittent uctuations in ECMO ow that can lead to cut outs and poor circuit performance. This is usually due to problems with venous drainage. If the drainage pressure is being measured, commonly it will be dropping to 100 mmHg or greater implying insufcient drainage. The problem can often be temporized with volume resuscitation. The next step is to check cannula position. If the cannula is adequately posi­tioned, then causes of hypovolemia should be addressed (gastrointestinal bleeding, over diuresis, etc.). If volume sta­tus is adequate and the cannula is adequately positioned, then the problem may be that the drainage cannula cannot
124
https://t.me/medicina_free
J. Crowley
support the goal ow rates in which case an additional drain­age cannula may be needed.
14.7.6 Weaning
Weaning from V-V ECMO can be prolonged, but the concept is relatively straight forward. The patient must have sufcient recovery of native lung function in order to liberate from the ECMO circuit. This can be detected by improvements in imaging, lung compliance, and resolution of the underlying disease process. As the patient’s native lung function improves, the required sweep gas ow and FdO2 will decrease. Once these are minimal, then the patient can be placed on standard ventilatory settings, and the sweep gas turned to 0LPM.This effectively means the patient is off ECMO.Flow is maintained in the ECMO circuit in order to prevent throm­bosis; however no gas exchange is occurring. If the patient tolerates this for a prescribed period of time (6–24h depend­ing on the fragility of their respiratory status), then they can be decannulated. Decannulation from V-V ECMO can usu­ally be performed at the bedside with cannula removed and hemostasis obtained with sutures at the skin site and manual pressure. Patients who do not show signs of lung recovery should be considered for referral to a lung transplant center that has experience with prolonged ECMO weans and the possibility of lung transplant if the patient fails to wean.
Weaning for V-A ECMO is more complicated as the sweep ow can never be reduced to zero (this would create a large shunt) and that even at lower ow rates some hemo­dynamic support is maintained. For some patients, cardiac recovery is obvious. For others a more deliberate approach is needed. Once a patient can tolerate anticoagulation, a ramp trial can be attempted if there are signs of myocardial recovery. The ECMO ows are slowly decremented to 2LPM over a period of 12–24h, and an echocardiogram is obtained. If this study is promising, then the patient can be further anticoagulated and the ows further reduced until the circuit is clamped and the patient is observed off of ECMO.Caution must be taken in the setting of right ven­tricular failure as often the right ventricle only needs partial unloading and failure to wean may not be apparent imme­diately. If the wean is successful, the patient can be decan­nulated from V-A ECMO which is commonly done via surgical cut down and direct repair of the femoral artery.
14.8 Final Thoughts
ECMO can be a life-saving intervention in appropriate patients, and comparative reviews of trauma patients have shown similar outcomes to non-trauma patients. The most important piece of developing an ECMO program is to rec­ognize that it is a team-based system. Attempting to imple­ment an ECMO service without having the appropriate support will not be successful. In addition, it is recommended that frequent review of ECMO patients is undertaken to determine appropriateness of candidacy, management, and complication rates. This is important as ECMO is often an expensive and limited resource that should be used appropriately.
Suggested Reading
Akoumianaki E, Jonkman A, Sklar MC, etal. A rational approach on
the use of extracorporeal membrane oxygenation in severe hypox­emia: advanced technology is not a panacea. Ann Intensive Care. 2021;11:107.
Mazzef MA, Rao VK, Dodd-O J, Del Rio JM, Hernandez A, Chung M,
Bardia A, Bauer RM, Meltzer JS, Satyapriya S, Rector R, Ramsay JG, Gutsche J. Intraoperative Management of Adult Patients on extracorporeal membrane oxygenation: an expert consensus state­ment from the Society of Cardiovascular Anesthesiologists-Part I, technical aspects of extracorporeal membrane oxygenation. Anesth Analg. 2021;133(6):1459–77.
Mazzef MA, Rao VK, Dodd-O J, Del Rio JM, Hernandez A, Chung M,
Bardia A, Bauer RM, Meltzer JS, Satyapriya S, Rector R, Ramsay JG, Gutsche J. Intraoperative Management of Adult Patients on extracorporeal membrane oxygenation: an expert consensus state­ment from the Society of Cardiovascular Anesthesiologists-Part II, Intraoperative Management and Troubleshooting. Anesth Analg. 2021;133(6):1478–93.
Rao P, Khalpey Z, Smith R, Burkhoff D, Kociol RD.Venoarterial extra-
corporeal membrane oxygenation for cardiogenic shock and cardiac arrest. Circ Heart Fail. 2018;11(9):e004905.
Sidebotham D.Troubleshooting adult ECMO.J Extra Corpor Technol.
2011;43(1):P27–32.
Squiers JJ, Lima B, DiMaio JM.Contemporary extracorporeal mem-
brane oxygenation therapy in adults: fundamental principles and systematic review of the evidence. J Thorac Cardiovasc Surg. 2016;152(1):20–32.
Wang C, Zhang L, Qin T, et al. Extracorporeal membrane oxygen-
ation in trauma patients: a systematic review. World J Emerg Surg. 2020;15:51.
Zonies D, Codner P, Park P, Martin ND, Lissauer M, Evans S,
Cocanour C, Brasel K. AAST critical care committee clini­cal consensus: ECMO, nutrition. Trauma Surg Acute Care Open. 2019;4(1):e000304.
Sepsis andSeptic Shock
https://t.me/medicina_free
MervynMer andMartinW.Dünser
15
15.1 Introduction andDenitions
Sepsis is dened as life-threatening organ dysfunction caused by a dysregulated host response to infection. Septic shock is a specic subset of sepsis in which profound circu­latory, cellular and metabolic abnormalities are associated with a greater risk of mortality than sepsis alone. With mor­tality rates ranging from 10% to 50%, sepsis makes up one of the major disease burdens worldwide accounting for almost one fth of all global deaths. Notably, the highest age­standardised incidence of sepsis occurred in regions with low socio-demographic indices, such as sub-Saharan Africa, Oceania, South Asia, East Asia and Southeast Asia. The short- and long-term morbidity as well as the social and eco­nomic burden caused by sepsis remain to be fully elucidated but are likely to be substantial.
Trauma patients are one of the populations at the highest risk of developing sepsis. Sepsis is also the most frequent cause of delayed death following severe trauma. The inci­dence of post-traumatic sepsis has been estimated to be as high as 22%, with higher rates seen in patients with greater injury severities. Sepsis following trauma does not only result in a signicantly increased mortality but also pro­longed intensive care unit and hospital lengths of stay. Age, premorbid conditions, injury severity, spinal and chest injury, shock, need for blood transfusion and a low Glasgow Coma Scale score and positive alcohol concentrations at admission are independent risk factors for the development of post­traumatic sepsis. Of note, the risk of sepsis increases in a
M. Mer (*) Divisions of Critical Care and Pulmonology, Department of Medicine, Charlotte Maxeke Johannesburg Academic Hospital and Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa e-mail: mervyn.mer@wits.ac.za
M. W. Dünser Department of Anesthesiology and Intensive Care Medicine, Kepler University Hospital and Johannes Kepler University Linz, Linz, Austria e-mail: martin.duenser@kepleruniklinikum.at
dose- dependent manner, with the number of blood transfu­sions received. Patients with penetrating trauma appear to be at a particularly high risk for sepsis as these types of injuries are commonly associated with a high injury severity, major blood loss, direct inoculation of bacteria into deep tissue structures and intestinal or hollow organ perforation.
15.2 Pathogenesis ofPosttraumatic Infection andSepsis
Infectious complications in patients sustaining penetrating injuries follow a biphasic pattern. A small peak occurs dur­ing the rst week after trauma, with a second and larger peak encountered during later stages of the disease course. Early infections typically include primary bacteremia, pleural or mediastinal infection, meningitis or secondary peritonitis due to gastrointestinal or other hollow organ injuries. Infections occurring after the rst week mostly follow a sim­ilar pattern to that seen in a general critically ill population. The respiratory tract is a frequent focus of infection. Device­related infections (e.g. central line-associated bloodstream infections, urinary catheter-associated infections or ventricu­lar drain-associated ventriculitis), surgical site infections and deep tissue abscess formations (e.g. abdominal) are other common sources of infections during this time frame. Early infections following penetrating trauma are often the conse­quence of direct inoculation of pathogens into deep tissue structures at the time of injury or during emergency surgery (e.g. pleural infection, meningitis, secondary peritonitis) or result from bacterial translocation in the gastrointestinal tract during periods of severe systemic hypoperfusion (e.g. pri­mary bacteremia). Immunosuppression due to a compensa­tory anti-inammatory response to severe injury makes trauma patients highly susceptible to hospital-acquired and device-associated infections at later stages. Unlike in community- acquired infections, infections in penetrating trauma victims are mostly due to bacterial pathogens. Particularly, during the second peak of infectious complica-
© 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_15
125
126
https://t.me/medicina_free
M. Mer and M. W. Dünser
tions, extensively or multidrug-resistant bacteria (e.g.
Pseudomonas spp., Acinetobacter spp., methicillin-resistant Staphylococcus aureus) are common pathogens causing infections. Fungal infections (e.g. Candida albicans and non-albicans) are on the increase and typically arise during
the second week or later. Re-activations of latent viral infec­tions (e.g. cytomegalo-, herpes or Epstein-Barr virus) are also encountered in trauma patients, but their pathogenic role remains unknown, and therapy is generally not recommended.
The exact reasons why infectious complications induce a dysregulated host response, acute organ dysfunction and thereby sepsis in some trauma patients while not in others remain incompletely understood. Genetic factors, injury severity, site and timing of infection all appear to play a role. The pathogenesis of the dysregulated host response to infec­tion is complex and does not only involve the immune sys­tem. Figure15.1 simplies pathways currently believed to be involved in the dysregulated host response to infection and which nally result in acute organ dysfunction and sepsis. An interesting recent observation is that organ dysfunction in sepsis appears to occur in four distinct clusters (i.e. shock
with acute kidney injury, minimal multi-organ dysfunction, shock with acute lung injury and altered mental state, and hepatic disease and thrombocytopenia). These clusters may reect underlying pathophysiological differences and could potentially dictate different therapeutic approaches in the future. In addition to acute organ dysfunctions in patients with sepsis, other body functions such as the endocrine and metabolic systems are also compromised.
15.3 Diagnosis andInvestigations
In line with the denition of sepsis, the diagnosis of post­traumatic sepsis relies on recognition of both the underlying infection and acute organ dysfunction.
15.3.1 Diagnosis oftheUnderlying Infection
Clinical signs are usually the rst to draw the physician’s attention to the potential presence of a post-traumatic infec­tion. While fever is a highly non-specic indicator of infec-
Fig. 15.1 Simplied pathogenetic pathway from infection to sepsis. ARDS acute respiratory distress syndrome, CNS central nervous system, GFR glomerular ltration rate, LOC level of consciousness, PAMP pathogen-associated molecular pattern. Icons by Flaticom.com