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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), conrming substantial energy
loss. According to some studies, not only length of stay in the hospital and immune
function can be negatively inuenced by insufcient 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 10mg IV qid eventually complemented by erythromycin
250mg 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 andGoal-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 2–4h after admission, or promptly after immediate craniotomy/craniectomy, if that was necessary, and maintained for 3–5days.
Despite lack of consensus in the literature and increased hospital expenditures,
gathering such physiologic data is justied 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 classied as investigational. The suggested therapeutic algorithm is outlined in Table12.6.
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: AReview fortheGeneral andTrauma Surgeon
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205
Table 12.6
Treatment algorithm
Type A
ICP≤20mmHg; CPP≥70mmHg; NIRS >55%; PbtO
≥20mmHg; CMD L/P<40
2
No further therapy needed
Type B
Sustained ICP>20mmHg; CPP≥70mmHg; NIRS >55%; PbtO
≥20mmHg, 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 155–160mEq/L
Mannitol 0.25–0.50g/kg IV bolus to serum osmolality 320mOsm/kg/H
O or Osm gap <20
2
Tier 2: ICP>20mmHg for >15min for 1 h during rst 72h despite tier 1 therapy
Increase respiratory rate to keep PCO
32–35mmHg
2
High dose mannitol 1.0–1.5g/kg IV bolus if Osm<320 mOSm/L
BS (2–4 burst/min on cEEG) with midazolam to 10–15mg/h and propofol to 75–100μg/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<20mmHg; CPP≥70mmHg; NIRS <55%; PbtO
<20mmHg; CMD L/P>40 with glucose
2
<0.8mmol/L and pyruvate <120μmol/L
Therapy aimed at increasing PbtO
and decreasing LPR
2
Tier 1
Increase CPP up to 100mmHg in increments of 10mmHg with infusion NE, if ICP decreases
≥3mmHg with increasing CPP.Do not proceed if ICP does not decrease or rises with increasing
CPP
Optimize sedation
Increase FiO
Increase PEEP to 10cm H
Do not increase PaO
100 then keep at 60%
2
O
2
>150mmHg for sustained periods of time
2
Tier 2
Increase midazolam to 10–15mg/h and propofol to 75–100μg/kg/min
Setup cEEG to BS 2–4 bursts/minute
Drain CSF <15mmHg
If Hg<7g/dL transfuse 3units PRBCs less than 7days 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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C. P. Marini et al.

Chapter 13
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Current Management ofPost-operative
Mesenteric Ischemia
RohanN.Kulkarni andMohammadH.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% [1–6]. 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
inammation 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 conrm 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 deciencies [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 ofPost-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,
inammatory bowel disease, pregnancy and the post-partum period, liver disease,
pancreatitis, and certain medications [26–28].
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 andMonitoring
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
signicantly 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 [35–37]. 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 calcication, and
is more resistant to patient motion [38–40]. Additionally, when ordered along with
a venous phase, CTA allows for interrogation of bowel ischemia. These studies can
be performed within the rst 24–48h 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 specic deciencies 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, 41–44].
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 [46–48].
Anticoagulation therapy: Heparin, low-molecular-weight heparin, or direct oral
anticoagulants (DOACs) may be used. Many patients experience acute mesenteric
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