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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_901_Библиотеки_им_академика_М_И_Перельмана
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12 Surgical Intensive Care
Delirium
Management
Non-pharmacological approaches to prevention and treatment of delirium
Nursing-based protocols: Reorientation, early mobilization, proper hydration and
nutrition
Multimodal pain management
Avoiding antipsychotics and benzodiazepines for treatment of hypoactive delirium
Renal dosing for patients with renal failure
Avoid polypharmacy
Intraoperative: Use regional anesthesia instead of general anesthesia when possible,
limit operative time when possible, avoid intraoperative blood pressure uctuations,
limit intraoperative blood transfusion, monitor depth of anesthesia (bispectral
index-BIS)
Pharmacological management of delirium
Condition Treatment
Agitation associated with
sedative-hypnotic
withdrawal (alcohol,
benzodiazepine)
Benzodiazepine
413
Hyperactive delirium Antipsychotics
Medication Dose
Haloperidol 0.5–1mg PO or IV or 2mg IM
Risperidone 0.5mg PO twice daily
Olanzapine 5mg PO daily; (2.5mg once daily in patients
>60years)
Quetiapine 12.5mg PO daily
Increasing sedative effects: Haloperidol > risperidone > olanzapine > quetiapine
Worsening extrapyramidal symptoms: Haloperidol < risperidone <olanzapine <
quetiapine
Outcomes Delirium is associated with an increase in mortality, complications (aspiration
pneumonia), length of stay, cost of care, readmission rates, falls, bladder catheter use,
and cognitive decline
Delirium is associated with a decrease in patient satisfaction, functional status,
increased rates of institutionalization

414
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Antipsychotics
Medication Advantages Disadvantages
A. H. Sohail et al.
Haloperidol Moderately sedating
Dopamine antagonist
Used for control of positive symptoms
of delirium and ICU psychoses
Minimal cardiorespiratory effects
No denite dose limit
Olanzapine Availability of short-acting IM
formulation
Less risk of extrapyramidal symptoms
and QT prolongation than haloperidol
Quetiapine Less risk of extrapyramidal symptoms
and QT prolongation than haloperidol
Ziprasidone Less risk of extrapyramidal symptoms
than haloperidol
Not FDA approved for sedation
Half-life becomes prolonged with
repeated administration
Dose-dependent QT interval
prolongation
Extrapyramidal symptoms and
neuroleptic malignant syndrome
(more common when administered
IM as compared to IV)
Orthostatic hypotension,
hyperglycemia, somnolence
QT interval prolongation
Anticholinergic effects
Enteral route of administration
Slow onset of action
Sedation, orthostatic hypotension,
and QT interval prolongation
Orthostatic hypotension,
hyperglycemia, QT prolongation
Research
Reference Conclusion
Constantin JM, Momon A, Mantz J, etal.
Efcacy and safety of sedation with
dexmedetomidine in critical care
patients: A meta- analysis of randomized
controlled trials. Anaesth Crit Care Pain
Med. 2016;35(1):7–15
IM formulation contains cyclodextrin
(nephrotoxin)
IV formulation is not available
In 3 meta-analyses related to intensive care unit patients,
dexmedetomidine was associated with a reduced incidence of
delirium, intensive care unit length of stay, and mechanical ventilation
duration, despite a signicant heterogeneity among studies
Benzodiazepines, propofol, and ketamine have a higher risk of
intensive care unit delirium
Dexmedetomidine (Precedex) is associated with an increase in
bradycardia and hypotension

12 Surgical Intensive Care
Research
Reference Conclusion
415
Hshieh TT, Yue J, Oh E, etal.
Effectiveness of multicomponent
nonpharmacological delirium
interventions: A meta-analysis [published
correction appears in JAMA Intern Med.
2015;175(4):659.]. JAMA Intern Med.
2015;175(4):512–520
Mahanna-Gabrielli E, Schenning KJ,
Ericsson LI, etal. State of the clinical
science of perioperative brain health:
report from the American Society of
Anesthesiologists Brain Health Initiative
Summit 2018. Br J Anaesth.
2019;123(4):464-478
This meta-analysis showed that non- pharmacologic interventions for
delirium tends to reduce overall length of hospital stay
An intraoperative blood transfusion of >1000mL, American Society
of Anesthesiologists (ASA) risk classication of ≥4, and BMI<18
are also a risk factors for delirium
Age is also a risk factor, but an age of >70years presents the highest
risk for development of delirium
Cognitive impairment is a risk factor if the score on the mini-mental
state examination is less than 25
Sedatives
Drug Advantage Disadvantage
A potent amnestic and anxiolytic agent
Midazolam
(versed)
Lorazepam
(Ativan)
Immediate onset of action and a short
duration of effect
Short acting
Sedative, amnestic, potent anxiolysis with
anticonvulsant properties
No active metabolites
Risk of delirium
Contraindicated in pregnancy
Slow onset ➔ risk of over-sedation when
titrating due to delayed response and
accumulation in peripheral tissues
Propylene glycol solvent may accumulate with
prolonged use or high dosing ➔metabolic
acidosis and end-organ dysfunction
Long half-life, with signicant risk of
accumulation in older adults or in patients with
signicant renal or hepatic impairment
Diazepam
(valium)
Rapid onset with potent sedative and
muscle- relaxant effects
Useful for critically ill patients at risk of
alcohol withdrawal or seizures due to drug
overdose or poisoning
Half-life may be prolonged in critically ill
patients with hepatic or renal impairment
Risk of delirium
Interacts with drugs used in the ICU that alter
CYP metabolism
Injection solution contains propylene glycol
solvent and cannot be delivered as a continuous
infusion
Multiple active metabolites

416
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A. H. Sohail et al.
Post cardiac arrest care
• Patients admitted to the intensive care unit after out-of-hospital cardiac arrest have a high risk of death and
neurologic decit
• Targeted temperature management (TTM) is an intervention that has both short- and long-term survival and
neurologic recovery advantages
➔TTM with urgent coronary angiography as initial steps in management of these patients
• The TTM trial showed that the benets of 36°C were similar to a TTM of 33°C.Current recommendations have
a target of 33–36°C for at least 24h
Research
Kirkegaard H, Søreide E,
de Haas I, etal. Targeted
temperature management
for 48 vs 24 hours and
neurologic outcome after
out-of-hospital cardiac
arrest: a randomized
clinical trial. JAMA.
2017;318(4):341–350
The time-differentiated therapeutic hypothermia trial studied the difference in duration
of hypothermia (24 vs. 48h). This study conrmed no difference in 6-month
neurologic outcomes or mortality in 355 patients randomized to TTM (33±1°C) for
48h or 24h. Based on these results, current recommendations are TTM to 33–36°C
for 24h
Endocrine Dysfunction
Adrenal insufciency
Characteristics
Presentation
Diagnosis
ACTH stimulation test
Manifestations of adrenal insufciency in the critically ill patient are nonspecic ➔
clinicians should have a high index of suspicion
Hyponatremia, hyperkalemia, and hypotension (Addison crisis), that is refractory to
uids and vasopressors without any clear causation
Most commonly used test in the intensive care unit is the ACTH stimulation test
The low-dose ACTH stimulation test ➔ more sensitive and specic than the high-dose
test but has not been validated in critically ill patients➔high-dose test should be used
• Sample baseline blood sample
• Cosyntropin (a synthetic peptide that consists of the rst 24 amino acids of human
ACTH) is given any time of the day at a dose of 1μg (low dose) or at a high dose of
250μg (high dose)➔to stimulate adrenocortical steroidogenesis
Cortisol blood samples are drawn at time 0 (baseline), 30, 60, and 90min
Diagnostic criteria for adrenal insufciency are a post-ACTH serum cortisol increment
of <9μg/dL

12 Surgical Intensive Care
Adrenal insufciency
The Surviving Sepsis Guidelines 2012 recommendations regarding steroid use are as
follows:
• IV hydrocortisone should not be used to treat adult septic shock patients if adequate
uid resuscitation and vasopressor therapy are able to restore hemodynamic stability.
In case this is not achievable, it is suggested that IV hydrocortisone at a dose of
200mg per day (grade 2C) be administered
Management
• ACTH stimulation test should not be used to identify adults with septic shock who
should receive hydrocortisone (grade 2B)
• In treated patients, hydrocortisone should be tapered when vasopressors are no
longer required (grade 2D)
• Corticosteroids should not be administered for the treatment of sepsis in the absence
of shock (grade 1D)
• When hydrocortisone is given, continuous ow should be used (grade 2D)
Thyroid dysfunction
Euthyroid sick syndrome Low triiodothyronine(T3)
• High endogenous serum cortisol concentrations
• Glucocorticoid therapy
417
Mechanism for euthyroid sick
syndrome
Management Thyroid function tests should not be measured in critically ill patients except if
• Circulating inhibitors of deiodinase activity
• Drugs that inhibit 5’-monodeiodinase activity (amiodarone and high doses of
propranolol)
• Circulating cytokines (tumor necrosis factor, interferon-α, NF-kB)
there is a strong suspicion of hypothyroidism
Case Management
Critically ill patient with low T3 or
low T4 and no clinical signs of
hypothyroidism
Critically ill patients undergoing
coronary artery bypass grafting
Critically ill patient with low T3 or
low T4 with symptoms of
hypothyroidism
Critically ill patient with myxedema
coma
No treatment
Do not treat in the postoperative period if
patient was previously euthyroid
Cautious repletion of thyroid hormone
Aggressive repletion of thyroid hormone

418
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Insulin resistance
Pathophysiology Due to increased ACTH and cortisol secretion
Maintain blood glucose concentration between 140 and 180mg/dL
A. H. Sohail et al.
Management
Outcomes
Hyperglycemia in the intensive care unit ➔ best managed with IV insulin therapy
Insulin infusions are preferred ➔ can be easily adjusted based on changes in patients’ clinical
status (nutritional status)
Transient hypoglycemia is associated with adverse outcomes in critically ill patients
Stress hyperglycemia is associated with increased risk of the critical illness polyneuropathy
and myopathy
Research
Reference Findings
Jacobi J, Bircher N, Krinsley J, etal. Guidelines for the
use of an insulin infusion for the management of
hyperglycemia in critically ill patients. Crit Care Med.
2012;40(12):3251–3276
American Diabetes Association. Diabetes care in the
hospital. Sec. 13. In Standards of Medical Care in
Diabetes—2016. Diabetes Care 2016; 39 (Suppl.
1):S99–S104
The initial method of glucose control should be an
intravenous insulin infusion. This allows for close
monitoring and adjustments of the insulin infusion until
a stable nutritional regimen can be initiated
For intensive care unit patients, the American Diabetes
Association’s standards of medical Care in
Diabetes—2016 recommends target glucose levels
between 140 and 180mg/dL
Diabetic ketoacidosis versus hyperosmolar hyperglycemia
Diabetic ketoacidosis (DKA) Hyperosmolar hyperglycemia state (HHS)
Epidemiology
Features
Ketoacids
Diagnosis
Often in diabetics Type I
Very common
High blood glucose and metabolic acidosis
Increased anion gap
Increased serum ketones
Present (ß-hydroxybutryic acid, Acetoacetic acid, and Acetone)
Hyperglycemia with metabolic acidosis
and the presence of ketones (serum or
urine)
Often in diabetics type II
Relatively rare
Altered level of consciousness
Severe hyperglycemia
Serum osmolality >320mOsm
No ketoacid detected
• Serum glucose levels >600mg/dL
• Serum osmolality >320mOsm/kg
• pH>7.40
• Bicarbonate greater than 15mEq/L
• Minimal ketones

12 Surgical Intensive Care
Diabetic ketoacidosis versus hyperosmolar hyperglycemia
Diabetic ketoacidosis (DKA) Hyperosmolar hyperglycemia state (HHS)
419
Low-dose IV insulin if K>3.3mEq/L
If K<3.3mEq/L ➔ insulin therapy should
be delayed until potassium replacement
has begun and the serum potassium
concentration has increased
Management
Infusion of isotonic saline to expand
extracellular volume
Insulin treatment will result in correction
of hyperglycemia prior to correction of
ketonemia➔ after correction of
hyperglycemia, insulin should be
continued but dextrose is given to avoid
hypoglycemia
Nutrition andMetabolism
Malnutrition
Risk Factors
Signs of malnutrition
Patients on ventilators, those with altered sensorium, those in the intensive care unit
(ICU), and those with preoperative weight loss
• Muscle wasting
• Patients with signicant weight loss over a 6-month period
• History of intolerance of oral intake
• Absorption disorders
• Malignancy
Intravenous uid to reestablish tissue perfusion (HHS
patients usually dehydrated by 8–12L)
Attempts to correct this usually take place over 24h,
with initial rates of normal saline often in the range of
1L/h for the rst few hours or until the condition
stabilizes
Insulin is given but K>3.3mEq/L ➔ then an insulin
infusion of 0.1units/kg/h
Metrics for malnutrition
Serum markers of
malnutrition
Metrics to assist with the diagnosis of malnutrition
• Percentage body weight loss
• Physical exam
• Serum markers: albumin, transferrin, prealbumin, and retinol-binding protein
• Indirect calorimetry
Marker t
Albumin 21days Most accurate marker in stable
Transferrin 8days Negative acute-phase reactant
Prealbumin 3days Negative acute-phase reactant
Retinol-binding protein 12h Negative acute-phase reactant
½
Characteristics
patients; use is limited in
acutely ill patients secondary to
prolonged t½
Value drops in inammatory
conditions
Value drops in inammatory
conditions

420
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Malnutrition
A. H. Sohail et al.
Preferred modality for determining a patient’s nutritional needs by calculating his or
her oxygen (O2) consumption and carbon dioxide (CO2) production
Indirect calorimetry
Respiratory quotient (RQ)
Nitrogen balance
Limitations of indirect calorimetry:
• Expensive
• Limited in ventilated patients on a high fraction of inspired oxygen
• Static measurement, does not give objective data as patient condition uctuates
RQ is the ratio of CO2 produced to O2 consumed while food is being metabolized
RQ=CO
A characteristic RQ exists for each fuel metabolized:
• Glucose RQ=1.0
• Protein RQ=0.8
• Fat RQ=0.7
If the RQ of a patient is >1, then it is a strong indicator of overfeeding
Nitrogen balance: Total protein intake (g)/6.25– UUN+4g
UUN=urinary urea nitrogen=nitrogen lost in urine in 24h
4=non-urinary losses of nitrogen (“insensible losses” via the skin and
6.25=grams of protein per gram of nitrogen
• If the nitrogen balance is 0 ➔ patient is consuming the same amount of protein that
• If the nitrogen balance is negative ➔the protein intake should be increased
• If the goal is repletion ➔ protein intake should be increased to more than what
Requirements of well-nourished patients
2 eliminated/O2 consumed
gastrointestinal tract)
they are using
would result in nitrogen equilibrium
Protein: 0.8g/kg/day
Daily requirements
• Glucose: 7.2g/kg/day
• Fat: 1g/kg/day
➔these requirements will increase during critical illness
Research
Reference Conclusion
McClave SA, Martindale RG, Vanek VW,
etal. Guidelines for the provision and
assessment of nutrition support therapy in
the adult critically ill patient: Society of
Critical Care Medicine (SCCM) and
American Society for Parenteral and Enteral
Nutrition (A.S.P.E.N.) JPEN J Parenter
Enteral Nutr. 2009;33(3):277–316
Current recommendations from nutrition and critical care societies
state that appropriate caloric / protein needs outweigh the
theoretical increases in azotemia with protein supplementation in
the critically ill

12 Surgical Intensive Care
Enteral nutrition
421
• Results in better substrate utilization than parenteral nutrition
Benets of enteral nutrition
Timing
Absolute contraindications
Gastric vs duodenal feedings
Methods
• Trophic effects on the liver, maintenance of gut integrity, decreased septic
• Reduced infectious complications in comparison with parenteral feeds
• The presence of bowel sounds is not required to initiate enteral feeds
• Enteral feeds should be started within 24–48h of admission to the ICU to
• Early institution of enteral feeds➔ fewer septic complications; shorter
• Complete bowel obstruction
• Bowel ischemia, ileus
• Circulatory shock with high-dose vasopressor requirements
• No difference in the risk of aspiration with gastric versus duodenal
• Duodenal placement may be necessary in patients who regurgitate
• Bolus feeds are more physiologic, can only be given via gastric methods
• Continuous feeds are more likely to be used in the ICU.Pauses in
Complications of enteral feeding
complications, and a stabilized glycemic prole
take advantage of the protective effects of tube feedings
hospital stay
feedings
intragastric feedings
(not tolerated via jejunostomy access)
delivery can result in decreased nutritional intake
Complication Description Management
Refeeding syndrome Metabolic disturbances as a result of reinstitution
of nutrition in starved patients
Azotemia Excessive protein leads to azotemia, hypertonic
dehydration, hyperammonemia, and metabolic
acidosis
Hyperglycemia Excessive carbohydrate leads to in
hyperglycemia, hypercapnia, and fatty liver
Hyperlipidemia Excessive fat has caused hyperlipidemia and
fat-overload syndrome
Undernutrition Enteral feeding is more frequently associated
with undernutrition
Total parenteral nutrition (TPN) is more likely to
result in a patient’s being overfed
Overfeeding Patients who are very small, very large, or very
old are particularly vulnerable to overfeeding
Replete phosphate
Adequately hydrate
Increase caloric supply from fat
Treat hyperglycemia
Avoid discontinuing enteral nutrition
haphazardly
Provide correct amount of calories,
protein, and carbohydrate

422
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A. H. Sohail et al.
Access methods Benets/indications Disadvantages/contraindications
Nasogastric tube
Naso-jejunal tube
Gastrostomy tube
(percutaneous,
laparoscopic, open)
Jejunostomy tube
(percutaneous,
laparoscopic, open)
Short-term enteral access
Physiologic
Primarily used in patients with
delayed gastric emptying or
intolerance of gastric feeds
Long-term access
Physiologic
Long-term access
Used primarily if the patient has
contraindication to gastric feeds
• Short term use only
• High risk of aspiration
• Nasopharyngeal trauma/irritation
• Difcult to place and maintain in the correct
location
• Cannot provide bolus feedings
• Cannot provide hyperosmolar formulas
• Contraindicated after gastrectomy
• Massive ascites and severe malnutrition are
likely to result in ongoing uid leaks
• Need to ensure no viscera are between the
stomach and the abdominal wall
• Cannot provide bolus feeding
• Cannot provide hyperosmolar formula
• More difcult to replace than a gastrostomy
Complications of enteral access techniques and their treatment
Complication Description Management
Perforation Patients present with classic signs of
peritonitis
Dislodgment of the feeding tube away from
Leak
Obstruction
the abdominal wall before the tract has
matured
Feeding tubes with balloons when the
balloons migrate
Jejunal feeding tubes when the balloon
obstructs the lumen
Exploration in the operating room
If the tube has been in place >7days Bedside replacement
If the tube cannot be replaced because the ostomy
is too small ➔ can place a wire into the stomach ➔
consult an interventional radiologist
Dislodgment
If this occurs early postoperatively this is
usually difcult and requires interventional
radiology or surgical intervention
Attempt to replace the tube into the intestinal
lumen immediately➔ conrmation of correct tube
positioning and absence of tube site leak with a
contrast study
If the tube cannot be replaced ➔ emergent
reoperation to prevent potential intraperitoneal
contamination
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