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Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_999_Библиотеки_им_академика_М_И_Перельмана

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believe that the amount of nutritional support proposed by the Brain Trauma Foundation, to provide more than 50% of resting energy expenditure (REE) for 2 weeks, is too conservative. It is not uncommon to observe 25% or more of increase in measured resting energy expenditure (mREE), conrming substantial energy loss. According to some studies, not only length of stay in the hospital and immune function can be negatively inuenced by insufcient alimentation, but also mortal­ity [53, 54].
We prefer jejunal tubes along with a peptide formula, for easier absorption. Gastric feeding with a nasogastric tube using conventional diets is an alternative; however, metoclopramide 10mg IV qid eventually complemented by erythromycin 250mg IV qid should be considered in circumstances of intolerance. The CORTRAK 2 Enteral Access System (EAS), endowed with an electromagnetic sensing device, can be convenient for optimal tube positioning in comatose patients, especially in the jejunum.
C. P. Marini et al.
Multimodality Monitoring andGoal-Directed Therapy Protocol (MM&GDTP)
The pillars of our proposal are normothermia (37°±0.2° C) along with ICP, PbtO2, CPP, and rSO2 control. Hourly cerebral microdialysis (CMD) data (lactate, glucose, pyruvate, glutamate, and derived lactate/pyruvate ratio [LPR]) supplies metabolic information, and continuous EEG with BS should be considered as well. These measures are started 2–4h after admission, or promptly after immediate craniot­omy/craniectomy, if that was necessary, and maintained for 3–5days.
Despite lack of consensus in the literature and increased hospital expenditures, gathering such physiologic data is justied by the ability to predict outcomes bet­ter than intermittent data [52, 55]. They should be added to early and effective nutritional therapy for more favorable survival and long-term functional end points [56]. As MM&GDTP has not been tested yet in controlled trials, it should still be classied as investigational. The suggested therapeutic algorithm is out­lined in Table12.6.
Rehabilitation
Given the immediate, intermediate, and late functional repercussions of sTBI, this population demands rehabilitation protocols starting in the trauma unit, proceeding to the subsequent hospitalization phase, and continuing after discharge. Experienced trauma and neuroplasticity teams are adept at dealing with coma and arousal states, weaning off mechanical ventilation, and early mobilization. Although late rehabili­tation is an option for enhancing functional recovery, the earlier it is started the best [57, 58].
12 Severe Traumatic Brain Injury: AReview fortheGeneral andTrauma Surgeon
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Table 12.6
Treatment algorithm
Type A ICP20mmHg; CPP70mmHg; NIRS >55%; PbtO
20mmHg; CMD L/P<40
2
No further therapy needed Type B Sustained ICP>20mmHg; CPP70mmHg; NIRS >55%; PbtO
20mmHg, CMD L/P<40
2
Therapy aimed at decreasing ICP Tier 1 Elevated head of bed to 30° Maintain normothermia (37°C) Drain CSF Adjust sedation with midazolam/propofol 3% Normal saline to serum Na 155–160mEq/L Mannitol 0.25–0.50g/kg IV bolus to serum osmolality 320mOsm/kg/H
O or Osm gap <20
2
Tier 2: ICP>20mmHg for >15min for 1 h during rst 72h despite tier 1 therapy Increase respiratory rate to keep PCO
32–35mmHg
2
High dose mannitol 1.0–1.5g/kg IV bolus if Osm<320 mOSm/L BS (2–4 burst/min on cEEG) with midazolam to 10–15mg/h and propofol to 75–100μg/kg/min Repeat CT scan head to assess mass lesion progression If ICP refractory, and there is increased mass effect, decompressive craniectomy Type C ICP<20mmHg; CPP70mmHg; NIRS <55%; PbtO
<20mmHg; CMD L/P>40 with glucose
2
<0.8mmol/L and pyruvate <120μmol/L Therapy aimed at increasing PbtO
and decreasing LPR
2
Tier 1 Increase CPP up to 100mmHg in increments of 10mmHg with infusion NE, if ICP decreases
3mmHg with increasing CPP.Do not proceed if ICP does not decrease or rises with increasing CPP
Optimize sedation Increase FiO Increase PEEP to 10cm H Do not increase PaO
100 then keep at 60%
2
O
2
>150mmHg for sustained periods of time
2
Tier 2 Increase midazolam to 10–15mg/h and propofol to 75–100μg/kg/min Setup cEEG to BS 2–4 bursts/minute Drain CSF <15mmHg If Hg<7g/dL transfuse 3units PRBCs less than 7days old
ICP intracranial pressure, CPP cerebral perfusion pressure, NIRS near infrared spectroscopy, PbtO
brain tissue oximetry, CMD L/P cerebral microdialysis lactate/pyruvate ratio, CSF cerebro-
2
spinal uid, PCO
partial pressure of CO2, BS burst suppression, NE norepinephrine, PEEP posi-
2
tive end expiratory pressure
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C. P. Marini et al.
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20. Marmarou A, Signoretti S, Fatouros PP, Portella G, Aygok GA, Bullock MR.Predominance of cellular edema in traumatic brain swelling in patients with severe head injuries. J Neurosurg. 2006;104(5):720–30.
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25. Marshall LF, Marshall SB, Klauber MR, etal. A new classication of head injury based on computerized tomography. J Neurosurg. 1991;75(Suppl):S14–20.
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30. Rowell SE, Fair KA, Barbosa RR, etal. The impact of pre-hospital Administration of Lactated Ringer’s solution versus normal saline in patients with traumatic brain injury. J Neurotrauma. 2016;33(11):1054–9.
31. Stocchetti N, Penny KI, Dearden M, et al. Intensive care management of head-injured patients in Europe: a survey from the European brain injury consortium. Intensive Care Med. 2001;27(2):400–6.
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35. Asgari S, Vespa P, Bergsneider M, Hu X.Lack of consistent intracranial pressure pulse mor­phological changes during episodes of microdialysis lactate/pyruvate ratio increase. Physiol Meas. 2011;32(10):1639–51.
36. Carney N, Totten AM, O’Reilly C, etal. Guidelines for the management of severe traumatic brain injury. Neurosurgery. 2017;80(1):6–15.
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38. Stiefel MF, Gracias VH, Bloom S.Conventional neurocritical care and cerebral oxygenation after traumatic brain injury. J Neurosurg. 2006;105:8.
39. Okonkwo DO, Shutter LA, Moore C, etal. Brain tissue oxygen monitoring and Management in Severe Traumatic Brain Injury (BOOST-II): a phase II randomized trial. Crit Care Med. 2017;45(11):1907–14.
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43. Bayir H, Adelson PD, Wisniewski SR, et al. Therapeutic hypothermia preserves antioxi­dant defenses after severe traumatic brain injury in infants and children. Crit Care Med. 2009;37(2):689–95.
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45. Cooper DJ, Nichol AD, Bailey M, etal. Effect of early sustained prophylactic hypothermia on neurologic outcomes among patients with severe traumatic brain injury: the POLAR random­ized clinical trial. JAMA. 2018;320(21):2211.
46. Olson DM, Grissom JL, Williamson RA, Bennett SN, Bellows ST, James ML.Interrater reli­ability of the bedside shivering assessment scale. Am J Crit Care. 2013;22(1):70–4.
47. Sadaka F, Krause K, Tow M, Wilcox M, O’Brien J.Induced normothermia after severe trau­matic brain injury: a prospective observational pilot safety and feasibility study. J Neurol Res. 2015;4(5–6):127–31.
48. Kilpatrick MM, Lowry DW, Firlik AD, Yonas H, Marion DW.Hyperthermia in the neurosurgi­cal intensive care unit. Neurosurgery. 2000;47(4):850–6.
49. Yokobori S, Yokota H.Targeted temperature management in traumatic brain injury. J Intensive Care. 2016;4(1):28.
50. Frankeneld DC, Ashcraft CM. Estimating energy needs in nutrition support patients. J Parenter Enter Nutr. 2011;35(5):563–70.
51. Pavlidou E, Petridis D, Tolia M, etal. Estimating the agreement between the metabolic rate calculated from prediction equations and from a portable indirect calorimetry device: an effort to develop a new equation for predicting resting metabolic rate. Nutr Metab. 2018;15:41.
52. Krakau K, Omne-Pontén M, Karlsson T, Borg J. Metabolism and nutrition in patients with moderate and severe traumatic brain injury: a systematic review. Brain Inj. 2006;20(4):345–67.
53. Härtl R, Gerber LM, Ni Q, Ghajar J.Effect of early nutrition on deaths due to severe traumatic brain injury. J Neurosurg. 2008;109(1):50–6.
54. Maxwell J, Gwardschaladse C, Lombardo G, etal. The impact of measurement of respiratory quotient by indirect calorimetry on the achievement of nitrogen balance in patients with severe traumatic brain injury. Eur J Trauma Emerg Surg. 2017;43(6):775–82.
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58. Johnston MV.Plasticity in the developing brain: implications for rehabilitation. Dev Disabil Res Rev. 2009;15(2):94–101.
C. P. Marini et al.
Chapter 13
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Current Management ofPost-operative Mesenteric Ischemia
RohanN.Kulkarni andMohammadH.Eslami
Acute Mesenteric Ischemia
Acute mesenteric ischemia (AMI) is a sudden, severe decrease in blood ow to the intestines due to thrombosis or embolism and is considered a medical emergency requiring urgent intervention. If left untreated, acute mesenteric ischemia can prog­ress to bowel infarction, perforation, and sepsis. Globally, the incidence of AMI is rare, estimated to be 0.1–0.2% of all hospital admissions; however, certain surgical procedures especially with prolonged hypotension are precipitating mechanisms, of the non-occlusive modality however encompassing thrombosis as well. Mortality rate depends on many factors, ranging from 10 to 50% [16]. Classic acute mesen­teric ischemia can result from various causes including thrombosis of the mesen­teric arteries due to atherosclerosis, embolism of cardiac or aortic origin, and arterial dissection. Vasospasm can be a contributing phenomenon. The most common cause of AMI is embolic occlusion usually from cardiac sources such as atrial brillation, myocardial infarction, or endocarditis [7, 8]. Thrombotic occlusion of the mesen­teric arteries can also cause AMI, usually in patients with underlying atherosclerosis or hypercoagulable states [9].
The clinical presentation of acute mesenteric ischemia is often abrupt, with patients experiencing some or all of the following: severe abdominal pain, nausea, vomiting, diarrhea, and bloody stools. The pain is usually out of proportion to the physical exam and is often described as cramping, colicky, or diffuse with associ­ated abdominal tenderness, rebound tenderness, and/or absent bowel sounds [10,
11]. Patients with acute mesenteric ischemia may also have signs of systemic
inammation such as fever, leukocytosis, and metabolic acidosis [12]. Imaging
R. N. Kulkarni (*) · M. H. Eslami Division of Vascular Surgery, Department of Surgery, UPMC Heart and Vascular Institute, UPMC Presbyterian Hospital, Pittsburgh, PA, USA e-mail: kulkarnirn@upmc.edu; mohammad.eslami@vandaliahealth.org
Switzerland AG 2024 J. Faintuch, S. Faintuch (eds.), Recent Strategies in High Risk Surgery,
https://doi.org/10.1007/978-3-031-56270-9_13
209© The Author(s), under exclusive license to Springer Nature
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studies such as computed tomography angiography (CTA), magnetic resonance angiography (MRA), or duplex ultrasonography may conrm the diagnosis of AMI.
The management of acute mesenteric ischemia starts with infusion of uids, anti­coagulants, and antibiotics. It involves as well emergent revascularization to restore blood ow to the affected mesenteric arteries. Options for revascularization include surgical intervention such as thromboembolectomy, bypass grafting, or endarterec­tomy, or endovascular intervention such as catheter-directed thrombolysis or angio­plasty with stenting. Typically, open or laparoscopic surgical exploration is required alongside revascularization to assess the viability of the bowel and may involve bowel resection. Old age, chronic renal disease, patient dependency, arrhythmias, cardiac failure, hypotension, large bowel involvement, acidosis (lactate), delay to surgery and inotropes are all ominous markers as concerns mortality. Bowel wall thickening and notably timely anticoagulation and revascularization seem to improve survival [1].
R. N. Kulkarni and M. H. Eslami
Chronic Mesenteric Ischemia
Chronic mesenteric ischemia (CMI) is a gradual, progressive decrease in blood ow to the intestines due to atherosclerotic narrowing of the mesenteric arteries [8]. CMI is a rare condition that accounts for less than 5% of all cases of mesenteric ischemia, typi­cally affects patients over the age of 60 with a history of atherosclerotic disease, and can be associated with other systemic manifestations of atherosclerosis [13]. Other causes of CMI include vasculitis, bromuscular dysplasia, and radiation- induced vasculopathy.
The clinical presentation of chronic mesenteric ischemia is often insidious and may include post-prandial abdominal pain, weight loss, food fear, and diarrhea [14]. The pain is usually located in the epigastric or periumbilical region and may be relieved by fasting or lying down. Patients with chronic mesenteric ischemia may also have signs of malnu­trition, such as hypoalbuminemia, anemia, or vitamin deciencies [15].
The management of chronic mesenteric ischemia involves revascularization to restore blood ow to the affected mesenteric arteries [8]. The choice of treatment depends on the severity and location of the arterial stenosis or occlusion. Endovascular interventions, such as percutaneous transluminal angioplasty (PTA) and stenting, are considered rst-line treatment for chronic mesenteric ischemia [16]. In patients with extensive atherosclerosis or multiple arterial stenoses, open surgical revascularization such as mesenteric artery bypass or endarterectomy may be preferred over endovascular intervention or may be necessary in cases where endovascular interventions have failed [17, 18].
Non-occlusive Mesenteric Ischemia (NOMI)
NOMI is also known as mesenteric vasoconstriction syndrome. NOMI is a type of mesenteric ischemia that occurs when blood ow to the intestines is reduced due to high doses or prolonged use of vasopressors in critically ill patients, notably with
13 Current Management ofPost-operative Mesenteric Ischemia
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refractory shock. These patients typically have underlying medical conditions such as heart failure, liver cirrhosis, or sepsis [19, 20]. This then leads to vasoconstriction in the mesenteric circulation resulting in reduced blood ow and oxygen delivery to the intestines [21]. The pathophysiology of vasopressor-induced NOMI is complex and not fully understood. It is thought to involve multiple factors, including the direct effects of vasoconstrictive medications on the mesenteric vessels, impaired autoregulation of mesenteric blood ow, and the effects of systemic hypoperfusion and hypoxia in critically ill patients [22].
The diagnosis of NOMI can be challenging as imaging studies may not show a clear obstruction in the mesenteric vessels [23]. Diagnosis is typically based on a high index of clinical suspicion, along with imaging ndings such as thickened bowel walls, decreased contrast enhancement, or pneumatosis intestinalis on CT scans [24].
Management of vasopressor-induced NOMI involves maintaining hemodynamic support despite sharp reduction or discontinuation of vasopressors and providing adequate oxygenation and uid resuscitation. This is not an easy challenge for hypotensive patients with severe derangements of the macro and micro circulation. Additional treatments may include pharmacologic vasodilators, such as direct pros­taglandin infusion in the superior mesenteric artery (Alprostadil/prostaglandin E1, UCB Pharma, Monheim, Germany) or endovascular interventions such as angio­plasty or stenting [3, 25]. With irreversible ischemia, surgery will be necessary to remove damaged or necrotic bowel.
211
Mesenteric Venous Ischemia
Mesenteric venous ischemia is a condition in which a blood clot forms in one of the primary veins draining the intestines resulting in massive congestion within the mesenteric circulation. The superior mesenteric vein (SMV) is the most commonly affected vein in mesenteric venous thrombosis (MVT), accounting for approxi­mately two-thirds of cases; however, the portal vein is also commonly involved, either alone or in combination with the SMV [26]. The exact cause of MVT is often not clear, but risk factors can include hypercoagulable states, abdominal surgeries, inammatory bowel disease, pregnancy and the post-partum period, liver disease, pancreatitis, and certain medications [2628].
Venous mesenteric ischemia can either present suddenly with severe diffuse abdominal pain or insidiously over the course of days to weeks [29]. Diagnosis requires a high index of suspicion given the patients history and physical exam, and typically requires a CTA with a dedicated venous phase, although a duplex ultra­sound scan can be performed in those that cannot undergo CTA [30].
The treatment of venous mesenteric ischemia involves anticoagulation therapy, initially with heparin or low-molecular-weight heparin to prevent the progression of thrombosis, followed by bowel rest, and supportive care for complications such as sepsis, dehydration, and electrolyte imbalance [31, 32]. This is followed by
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long- term anticoagulation with warfarin or direct oral anticoagulants (DOACs) to prevent recurrence.
Depending on the severity of bowel ischemia, surgery may be indicated. Surgical treatment includes both open and endovascular options with or without bowel resection. In the most severe cases, an intestinal transplant may be necessary.
R. N. Kulkarni and M. H. Eslami
Initial Post-operative Assessment andMonitoring
After surgery, patients with mesenteric ischemia require close monitoring to assess their condition and ensure that they are recovering properly. Post-operative monitor­ing is critical to ensure adequate blood ow to the intestines and prevent further complications, as many of the described syndromes can be progressive or with delayed repercussions. Close observation and prompt recognition of any signs of complications are necessary to facilitate early reintervention and minimize morbid­ity and mortality.
Vascular Procedures
After revascularization with or without bowel resection, patients are typically moni­tored in the intensive care unit (ICU) to ensure stable hemodynamics and adequate organ perfusion.
Secondary Embolism, Thrombosis, Non-occlusive Ischemia
For patients experiencing AMI secondary to an embolic source, the pre- and post-op exams should be identical to rule out any new emboli. Patients with CMI may also have peripheral vascular disease in multiple distributions and are at risk of non­occlusive mesenteric ischemia in the event of post-operative hypotension or vaso­pressor support [33, 34]. In either case an early thorough vascular exam can help signicantly in identifying post-operative complications and determining the nature of its cause.
Blood pressure monitoring is essential in the post-operative period to assess the patient’s hemodynamic stability [34]. Multi-lumen central lines are maintained for resuscitation and medication administration along with invasive monitoring via arterial lines to provide accurate and continuous blood pressure readings. Persistent post-operative hypotension should raise concerns for hypovolemia, bleeding, car­diac dysfunction, or sepsis and should be monitored in conjunction with serial phys­ical exams, urine output, and laboratory values.
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213
Ongoing/Recurrent Abdominal Pain
Patients who experience new or worsening abdominal pain and distension or signs of bleeding may require additional imaging studies to monitor the patency of the revascularized arteries and evaluate intestinal perfusion. Post-operative imaging modalities may include computed tomography angiography (CTA), magnetic reso­nance angiography (MRA), or duplex ultrasound [3537]. CTA is typically pre­ferred for imaging mesenteric vessels as compared to MRA as it provides faster imaging and higher spatial resolution for the detection and localization of vascular stenoses, is more widely available, allows better visualization of calcication, and is more resistant to patient motion [3840]. Additionally, when ordered along with a venous phase, CTA allows for interrogation of bowel ischemia. These studies can be performed within the rst 24–48h after revascularization and may be repeated as needed.
Laboratory Work Up
1. Coagulation studies: Coagulation studies such as prothrombin time (PT), acti-
vated partial thromboplastin time (aPTT), and international normalized ratio (INR) help in monitoring coagulation status and can be used in conjunction with the CBC.A thromboelastogram (TEG) may also be utilized to identify any spe­cic deciencies in the patient’s ability to form clot. Disseminated intravascular coagulation (DIC) is not a common nding, with an incidence between 5 and 20% for acute mesenteric ischemia and less than 5% for chronic; however, the development of DIC in mesenteric ischemia is associated with worse outcomes, including higher mortality rates [6, 4144].
2. Serial post-operative serum lactate levels are often utilized to monitor bowel
perfusion recovery and aid in detecting any signs of continued hypoxia or hypo­perfusion. Persistently elevated serum lactate levels after revascularization should prompt concerns for continued tissue ischemia and is associated with worse patient outcomes [45].
Medical Management
Medical management of mesenteric ischemia may involve several measures to sup­port the patient’s hemodynamic status and address underlying comorbidities. These measures include uids and electrolytes, antibiotics, pain medication, and paren­teral/enteral feeding, depending on gastrointestinal tolerance [4648].
Anticoagulation therapy: Heparin, low-molecular-weight heparin, or direct oral anticoagulants (DOACs) may be used. Many patients experience acute mesenteric