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2/20/2018 1 Anesthesie voor Abdominale Heelkunde M. Verhaegen Anesthesie voor Abdominale Heelkunde 1. Algemene aandachtspunten Beknopt overzicht aandachtspunten pre-, per- en postoperatief 2. Rapid sequence inductie en intubatie 3. Laparoscopie met een CO 2 -pneumoperitoneum Insufflatiegas Pathofysiologische effecten Verwikkelingen Contra-indicaties Anesthesie-specifieke aandachtspunten 1. ALGEMENE AANDACHTSPUNTEN Anesthesie voor Abdominale Heelkunde Abdominal Surgery: Preoperative Attention Points Routine preoperative evaluation: “Preoperatieve screening en medicatie” (les E. Vandermeulen) Specific attention points in patients planned for abdominal surgery Weight loss, malnutrition, anemia E.g. Hypoalbuminemia Hepatobiliary pathology: (severe) hepatic dysfunction is possible Assessment of intravascular volume status Diagnosis of electrolyte or acid-base disturbances “Zuur-base stoornissen” (les M. Verhaegen) Assess risk of pulmonary aspiration of gastric contents Discuss anesthetic technique: general anesthesia +/- epidural anesthesia/analgesia Surgical procedure Contraindication for a specific technique Patient preference / objection

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2/20/2018

1

Anesthesie voor Abdominale Heelkunde

M. Verhaegen

Anesthesie voor Abdominale Heelkunde

1. Algemene aandachtspunten

– Beknopt overzicht aandachtspunten pre-, per- en postoperatief

2. Rapid sequence inductie en intubatie

3. Laparoscopie met een CO2-pneumoperitoneum

– Insufflatiegas– Pathofysiologische effecten

– Verwikkelingen

– Contra-indicaties

– Anesthesie-specifieke aandachtspunten

1. ALGEMENE AANDACHTSPUNTEN

Anesthesie voor Abdominale Heelkunde

Abdominal Surgery: Preoperative Attention Points

• Routine preoperative evaluation:

• “Preoperatieve screening en medicatie” (les E. Vandermeulen)

• Specific attention points in patients planned for abdominal surgery

– Weight loss, malnutrition, anemia• E.g. Hypoalbuminemia

– Hepatobiliary pathology: (severe) hepatic dysfunction is possible

– Assessment of intravascular volume status– Diagnosis of electrolyte or acid-base disturbances

• “Zuur-base stoornissen” (les M. Verhaegen)

– Assess risk of pulmonary aspiration of gastric contents

• Discuss anesthetic technique: general anesthesia +/- epidural anesthesia/analgesia– Surgical procedure

– Contraindication for a specific technique

– Patient preference / objection

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Abdominal Surgery: Intraoperative Attention Points

• Monitoring

– Routine monitoring

– Invasive monitoring (e.g. arterial catheter) depends on

• Surgical procedure• Co-morbidity

• Temperature: take measures to prevent hypothermia as soon as the patient enters the operating room

– Warm room at induction– Intravenous fluid warmer (before induction of anesthesia)

– Hot air warming device or warming mattress

– Cover the patient as much as possible

• Antibiotic prophylaxis– Before incision

– Repeat dose

– UZ Leuven guidelines (“Antibioticagids”)

Abdominal Surgery: Intraoperative Attention Points

• Muscle relaxation and neuromuscular monitoring

“Neuromusculaire blokkers”(les J. Lauwerijns)

– Intraoperatively

– Quantitative neuromuscular monitoring is absolutely necessary before emergence from anesthesia and extubation

• TOF ≥ 2 before reversal with neostigmine should be attempted• TOF ratio > 0.9 at adductor pollicis muscle

• Fluid management

“Vochtbeleid: krystalloïden, colloïden, transfusie en hemodilutie” (les L. Veeckman)• Prevention of postoperative nausea and vomiting

“Preventie en behandeling van (acute) complicaties” (les T. Dewinter)

• Analgesia resulting in painfree arrival in the PACU

“Postoperatieve pijntherapie en epidurale anesthesie” (les J. De Coster)

Abdominal Surgery: Postoperative Attention Points

• Postoperative fluid management

• Postoperative analgesia

• Thrombosis prophylaxis

• Prevention of stress ulcers• Postoperative nausea and vomiting

• Postoperative continuation of preoperative medication

2. RAPID SEQUENCE INDUCTIE EN INTUBATIE

Anesthesie voor Abdominale Heelkunde

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Anesthesia: Regurgitation and Aspiration

• Incidence of aspiration during induction

– Adults: 0.014 – 0.1 %

– Higher incidence

• Children• Emergency surgery

• Repeated intubation attempts

• Presence of risk factors• Morbidity may be severe

– Prolonged stay at intensive care unit

• Mortality: rare

– Aspiration is one of the most common causes of anesthesia-related death

Risk Factors for Pulmonary Aspiration of Gastric Co ntents

• Increased aspiration risk with emergent surgery and

– Nil per os (npo) < 6 hrs• Clear liquids < 2 hrs

• Breast milk < 4 hrs

– Acute trauma immediately after eating (delayed gastric emptying), even if surgery is scheduled after > 6 hrs npo• Pathology associated with increased risk of significant gastric contents or increased intragastric pressure

– Slow or delayed gastric emptying (e.g. diabetes mellitus, medication)

– Gastric outlet obstruction– Bowel obstruction

– Paralytic ileus

– Pregnancy

– Morbid obesity– Excessive ascites

• Severe gastro-esophageal reflux disease

� Determine if a rapid sequence intubation (RSI) is indicated

“Seven P’s” of RSI in Adults

1. Preparation

2. Preoxygenation

3. Pretreatment

4. Paralysis following induction5. Protection and positioning

6. Placement with proof

7. Postintubation management

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1. Preparation (1)

• Exclude contra-indications to RSI

– Anticipated difficult intubation

– Allergy to rapid onset muscle relaxants� Consider awake fiberoptic intubation

• Check and prepare equipment

– Endotracheal tube

• Appropriate size• Cuff free of leaks (tested)

– Stylet (+/- placed in the tube)

– Laryngoscope

• Tested• Different blades should be readily available

– Suction device, checked and ready

– Oral airway• If mask ventilation is unexpectedly needed

1. Preparation (2)

• Drugs

– Selection of induction agent and neuromuscular blocking agent (NMBA)

– Determination of the doses

– Drawn up in labeled syringes• Patient installation

– Fast-running IV line

– Monitoring• ECG, pulse oximetry, blood pressure monitoring in place

• Capnography available and ready for immediate use

– Optimal positioning for intubation

• “Sniffing position”

Mace, Emergency Medicine Clinics of North America 2008; 26: 977–1000

2. Preoxygenation (1)

Goal: Increasing apnea period with O2 saturation > 90% by increasing O2 stores in lungs, blood and tissues, thus avoiding mask ventilation before intubation• Washout of alveolar nitrogen: denitrogenation = replacing N2 with O2 in the lungs (in the FRC)

– The lungs serve as a large O2 reservoir during apnea

– When breathing room air (79% N2) ~ 450 mL of O2 is present in the lungs of an average healthy adult

– When a patient breathes 100% O2, this washes out the nitrogen, increasing the O2 in the lungs to ~3000 mL• Increasing oxyhemoglobin saturation

• (Oxygenation of plasma)

� Target: EtO2 concentration ≈ 90 %, EtN2 concentration ≈ 5 %

Nimmagadda et al., Anesth Analg 2017; 124: 507-17

Variation in the volume of O2 stored in the functional residual capacity ( ),blood (▲), tissue (○), and whole body (◼) with the duration of preoxygenation. Published with permission from Campbell and Beatty (Br J Anaesth 1994)

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2. Preoxygenation (2)

Goal: Increasing apnea period with O2 saturation > 90% by increasing O2 stores in lungs, blood and tissues, thus avoiding mask ventilation before intubation• Washout of alveolar nitrogen (denitrogenation)

• Target: EtO2 concentration ≈ 90 %, EtN2 concentration ≈ 5 %

Nimmagadda et al., Anesth Analg 2017; 124: 507-17

Comparison of mean end-tidal O2 and N2 concentration obtained at 30 second intervals during 5-minute period of spontaneous tidal volume oxygenation using the circle absorber and NasOral systems in 20 volunteers. Data are mean ± SD. Published with permission from Nimmagadda et al.(Anesthesiology 2000)

2. Preoxygenation (3)

• Efficacy assessment• FAO2 increase• PAN2 decrease• PaO2 increase

• Efficiency assessment• SaO2 decrease during apnea

Nimmagadda et al., Anesth Analg 2017; 124: 507-17

2. Preoxygenation (3)

Nimmagadda et al., Anesth Analg 2017; 124: 507-17

• Inspired O 2 concentration• Potential risks of high FiO2

• Absorption atelectasis• (Production of reactive O2 species)• (Cardiovascular responses)

Absorption Atelectasis

• Small airway closure and absorption of O2 (solubility in plasma: O2 >>> N2)

– FRC decrease (supine position, anesthesia)

– Compression of the lungs (supine position, increased intraabdominal pressure)

• Prevention– FiO2 decrease

– Recruitment maneuvers: CPAP, PEEP, reexpansion maneuvers

Nimmagadda et al., Anesth Analg 2017; 124: 507-17

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2. Preoxygenation (3)

Nimmagadda et al., Anesth Analg 2017; 124: 507-17

• Duration of breathing• A healthy adult generally reaches a

target EtO2 > 90 % within 3 – 5 min of breathing FiO2 ≈ 1.0

• VA/FRC ratio• Hyperventilation reduces time required

to increase O2 stores in the lungs

• Inspired O 2 concentration• Potential risks of high FiO2

2. Preoxygenation (4)

Nimmagadda et al., Anesth Analg 2017; 124: 507-17

• Target: EtO2 concentration ≈ 90 %, EtN2 concentration ≈ 5 %

• Specific patient populations

– Target EtO2 concentration ≈ 90 %, EtN2 concentration ≈ 5 % may be difficult / impossible to reach

– Not all techniques of preoxygenation are equally effective for these patients– Pregnant patients, morbidly obese patients, children and elderly patients, patients with pulmonary disease,

patients at high altitude

2. Preoxygenation (5)

Time to desaturation, even after preoxygenation, depends on efficacy of preoxygenation, patient characteristics and clinical situation (capacity for O2 loading, VO2)

Benumof et al, Anesthesiology 1997; 87: 979 - 82

Time to hemoglobin desaturation with initial FAO2 = 0.87

• SaO2 ≈ 90% marks the upper inflection point on the oxygen-haemoglobin dissociation curve beyond which further decreasesin PaO2 leads to a rapid decline in SaO2 (~ 30% every minute)

• In a healthy preoxygenated patient the safe apnea time is up to8 minutes, compared to ~1 min if they were breathing room air

• In some critically ill patients critical desaturation may occurimmediately despite attempts at preoxygenation

• Patient factors causing inadequate preoxygenation• Non cooperative or agitated patient• Poor respiratory reserve (e.g. low FRC)• Airway obstruction• Shunt physiology with shunt fraction > 30 %• Increased metabolic rate

2. Preoxygenation (6)

Time to desaturation, even after preoxygenation, depends on efficacy of preoxygenation, patient characteristics and clinical situation (capacity for O2 loading, VO2)

Benumof et al, Anesthesiology 1997; 87: 979 - 82

Time to hemoglobin desaturation with initial FAO2 = 0.87

Morbid obesity• More rapid oxyhemoglobin desaturation

• Lower FRC• Increased VO2

• Head-up positioning prolongs time to desaturation (≈ 50 sec)

Children• More rapid maximal preoxygenation

• Lower FRC• 2 min of TV breathing: maximum benefit

• More rapid oxyhemoglobin desaturation• Lower FRC• Increased VO2

• The younger the child, the faster the onset of desaturation

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3. Pretreatment

Goal: prevention of potentially adverse consequences of the physiologic responses to RSI

Drugs used for pretreatment vary with clinical circumstances

• Opioid

– To blunt increases in heart rate and blood pressure during laryngoscopy and intubation– E.g.: fentanyl, sufentanil

• Lidocaine

– 1.5 mg/kg iv 2 - 3 min before intubation – Suppression of cough reflex and attenuation of increased airway resistance following intubation?

– Attenuation of ICP rise upon intubation in patients at risk of adverse effects of an increase in ICP?

4. Paralysis following Induction (1)

Goal: rapid induction, immediately followed by paralysis

• Selection of appropriate agents

– Precalculated dosage, adequate to provide prompt loss of consciousness and muscle relaxation

– Problem: hemodynamically unstable patients• Intubation 45 - 60 sec after the administration of the NMBA

1. Induction: Rapidly acting intravenous induction agent– Propofol (1.5 – 2.5 mg/kg)

• Advantage: bronchodilation

• Disadvantage: hypotension (reduction of cerebral perfusion pressure)

– Etomidate (0.3 mg/kg)• Advantage: hemodynamic stability

• Disadvantage: suppression of adrenal cortisol production

4. Paralysis following Induction (2)

2. Paralysis: Rapidly acting NMBA immediately following induction

– Succinylcholine

• Depolarizing NMBA

• Dosage: 1 – 1.5 mg/kg– Rapid onset (45 - 60 sec), short half-life (6 - 10 min)

• Contraindications– Significant (acute) hyperkalemia (ECG changes)

– Risk of malignant hyperthermia

» Personal or family history

» Specific diseases

– Rhabdomyolysis

– Acetylcholine receptor upregulation

» Denervating diseases» Myopathies

» Prolonged total body immobilization

» Extensive burn injuries ≥ 72 hrs old

» Crush injuries ≥ 72 hrs old

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4. Paralysis following Induction (3)

2. Paralysis: Rapidly acting NMBA immediately following induction

– Rocuronium

• Non-depolarizing NMBA

• RSI dosage: 0.9 – 1.3 mg/kg– Rapid onset (45 - 60 sec)

• Longer duration of action than succinylcholine– Duration of action of approximately 60 min after 1 mg/kg (may be much longer in older patients)

– Reversal is possible

» Neostigmine

• Only after sufficient spontaneous reversal (at least 2 and preferably 3 responses with TOF monitoring)

• No use in acute situations

» Suggamadex

» 16 mg/kg immediately after administration of RSI dose of rocuronium (unexpected cannot intubate, cannot ventilate situation)

» 4 mg/kg: PTC at least 1 – 2

» 2 mg/kg: TOF count ≥ 2

» Ac

5. Protection and Positioning

Goal: Protection of the airway against aspiration of gastric contents prior to intubation

• Avoid mask ventilation and insufflation in the stomach

– Maximal preoxygenation– O2-saturation < 90 % � gentle mask ventilation (with cricoid pressure?)

• Cricoid pressure (Sellick’s maneuver) during induction?

– Prevention of regurgitation of gastric contents into the pharynx by temporary occlusion of the esophagus

– Discussion about effectiveness and safety

Cricoid Pressure (1)

• Effectiveness of CP has been questioned

– Evidence supporting effectiveness of CP

• Cadaver studies demonstrating inhibition or regurgitation into the pharynx

• MRI, videolaryngoscopy: compression of the postcricoid hypopharynx (esophageal entrance)– Evidence against effectiveness of CP

• Reports of regurgitation and aspiration in spite of CP– Retrospective studies, case reports, closed malpractice claims

– Correctly performed RSI and application of CP?

• MRI: CP often causes lateral displacement of esophagus– But: occlusion of hypopharynx is relevant

• Decreased lower esophageal sphincter tone during CP– Unchanged intragastric pressure � potentially increased risk of regurgitation

– Reflex mechanism induced by stimulation of pharyngeal mechanoreceptors

Fig. 2. A typical tracing showing lower esophageal sphincterpressure (LESP) and intragastric pressure (IGP) recordingsbefore application of cricoid pressure (A), during application of cricoid pressure (B), after release of cricoid pressure (new baseline; C), after administration of 0.15 mg/kg metoclopramide (D), during application of cricoid pressure (E), andafter release of cricoid pressure (F). Paper speed = 1 mm/s.

Reproduced with permission from Salem MR, Bruninga KW,Dodlapatii J, Joseph NJ: Metoclopramide does not attenuate cricoid pressure-induced relaxation of the lower esophageal sphincter in awake volunteers. ANESTHESIOLOGY 2008;109:806–10. Wolters Kluwer Health.

Salem et al, Anesthesiology 2017; 126: 738-52

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Cricoid Pressure (2)

• Problems caused by CP

– Discomfort while the patient is awake

– Obstruction of the airway and difficulty to pass an endotracheal tube• Force dependent

– Trauma (uncommon)• Esophageal rupture (due to vomiting during CP � importance of correct RSI)

• Laryngeal trauma, fracture of cricoid cartilage

– Displacement of unstable cervical spine

• There is a lack of RCTs– Ethically unfeasible

– Very large number of patients would be required

– Standardization of variables is difficult• E.g. positioning for intubation, CP force, presence or absence of nasogastric tubes

� Currently there is insufficient evidence to support or to abandon the use of CP during RSI

Cricoid Pressure (3): Technique

Downward pressure on cricoid cartilage (adult patients only)

• Sniffing position

• Exert pressure on cricoid cartilage with thumb and index vinger

– Avoid exerting pressure on thyroid cartilage– Pressure of 30 N (after loss of consciousness)

• Prevents regurgitation up to 40 mmHg

• 10 N before loss of consciousness

– (Bimanual technique)• Release CP only after endotracheal tube placement has been confirmed

Bimanual technique of CP

6. Placement with Proof

• Laryngoscopy after sufficient muscle relaxation has been achieved (45 – 60 s after NMBA administration)

• Placement of endotracheal tube (+/- stylet)

• Confirmation of endotracheal tube placement

– End-tidal CO2-measurement– Auscultation over both sides of the chest and the stomach

– (Visualization of the endotracheal tube between the vocal cords)

– (Misting of the tube with ventilation)• Check the depth of the tube

– Auscultation is equal over both lungs

7. Postintubation Management

• Secure the properly placed endotracheal tube

• Start mechanical ventilation

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3. LAPAROSCOPIE MET CO 2-PNEUMOPERITONEUM

Anesthesie voor Abdominale Heelkunde

Laparoscopic Surgery with CO 2-Pneumoperitoneum: Topics

• Insufflation gas

• Pathophysiology

• Complications

• Contraindications• Anesthesia

Laparoscopic Procedures for Gastrointesinal Surgery

• Diagnostic surgery• Cholecystectomy• Nissen fundiplication• Bowel surgery• Gastrectomy• Bariatric surgery• Pyloromyotomy• Pancreatic surgery (Whipple)• Partial hepatectomy• Splenectomy• Lymphadenectomy• Inguinal hernia• Appendectomy• …

Laparoscopic Surgery: Potential Benefits

• Less tissue trauma• Reduced surgical stress response• Pulmonary function less impaired postoperatively • Less postoperative ileus• Reduced postoperative pain • Faster postoperative recovery and ambulation• Shorter hospital stay• Better cosmetic results• High patient satisfaction • Cost savings

� Mainly postoperative advantages� Every benefit has not been demonstrated for every procedure

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Laparoscopic Surgery: Technical Aspects

• Creation of working space

– Pneumoperitoneum

– Gasless lifting system

– Combination of both techniques• Gravity as a retractor � extreme positioning

– Upper abdominal: reverse Trendelenburg positioning

– Lower abdominal: Trendelenburg positioning • Robot-assisted laparoscopic surgery

Pneumoperitoneum: Ideal Insufflation Gas

• Nonflammable

• Metabolically and chemically inert

• Highly soluble in blood

• Nontoxic• Odorless

• Colorless

• Readily available • Inexpensive

� Insufflation gas of choice: carbon dioxide (CO2) Wolf, Seminars in Surgical Oncology 12 (1996)

Pneumoperitoneum: Insufflation Gas

• Carbon dioxide

� Highly soluble in blood

� Non-flammable

� Hypercapnia� Irritation of diaphragma and peritoneum (� shoulder pain)

� Used for the vast majority of laparoscopic cases

• Nitrous oxide

� Highly soluble in blood (but less soluble than CO2)

� No irritation of diaphragm or peritoneum

• Surgery under local anesthesia� Supports combustion

• No major surgery possible

� Used occasionally for minor procedures

CO2 – PP: Pathophysiologic Changes

• Absorption of insufflated CO2

– Extraperitoneal > intraperitoneal insufflation

• Increased intra-abdominal pressure (IAP)

– Intraperitoneal > extraperitoneal insufflation

� Cardiovascular effects

� Pulmonary effects

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CO2 - PP: Absorption of Insufflated CO 2 (1)

Parameters affecting absorption of CO2

• Approach: extraperitoneal vs intraperitoneal insufflation

• Site of surgery: upper vs lower abdominal surgery

• Intra-abdominal pressure• Duration of pneumoperitoneum

• Subcutaneous emphysema

Figure 2. PaCO2 values after induction of

pneumo(pre)peritoneum.

Mean PaCO2 values at 5-min intervals after

insufflation for all patients undergoing either

pneumopreperitoneum (squares) or

pneumoperitoneum (triangles).

Error bars indicate SD.

Liem et al., Anesth Analg 1995; 81 (6): 1243 – 1249

P = 0.02

Extraperitoneal insufflation

Intraperitoneal insufflation

CO2 - PP: Absorption of Insufflated CO 2 (2)

Extraperitoneal vs intraperitoneal insufflation

• Intraperitoneal insufflation of CO2

– CO2-filled space lined by a membrane

– Limited expansion (→ absorption is self-limiting)• PaCO2 increase reaches plateau after 15 – 30 min

– Subcutaneous emphysema < 2 %

• Extraperitoneal insufflation of CO2

– CO2 migrates into tissues not confined by a membrane

– CO2 progressively dissects tissues (absorption ≈ unlimited)

• PaCO2 increase continues for much longer than 30 min

– High incidence of subcutaneous CO2 emphysema

CO2 - PP: Absorption of Insufflated CO 2 (3)

Upper vs lower abdominal surgery

• Upper abdominal surgery: intraperitoneal insufflation

• PaCO2 increase of 20 – 30 % from baseline (plateau after 15 – 30 min)

• Lower abdominal surgery– Intraperitoneal insufflation

• PaCO2 of 10 – 15 % from baseline (plateau after 15 – 30 min)

– Extraperitoneal insufflation• PaCO2 increase is generally > 30 % from baseline

• PaCO2 increase continues (> 30 min)

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CO2 - PP: Absorption of Insufflated CO 2 (4)

• Approach: extraperitoneal vs intraperitoneal insufflation

• Site of surgery: upper vs lower abdominal surgery

• Intra-abdominal pressure

– Intraperitoneal insufflation: IAP has a some effect at low pressures– Extraperitoneal insufflation: IAP has a greater effect

• Increasing contact surface with increasing pressure

• Duration of pneumoperitoneum– Important during extraperitoneal insufflation

• Subcutaneous emphysema

– Complication

– May result in severe hypercarbia– Incidence: extraperitoneal >>> intraperitoneal insufflation

CO2 – PP: Cardiovascular Effects

• Cardiac arrhythmias

• Systemic hemodynamic effects

• Regional hemodynamic effects

– Renal effects– Splanchnic perfusion

– Venous stasis

CO2 – PP: Cardiac Arrhythmias (1)

• Reflex increase of vagal tonus � bradycardia, asystole

– Eliciting factors

• Stretching of the peritoneum during insufflation

• Electrocoagulation of the fallopian tubes– Accentuated in case of

• Superficial level of anesthesia

• Patients on β – blocking drugs– Treatment

• Immediately interrupt insufflation

• Atropine

• Deepening of anesthesia after recovery of heart rate• Gas embolism may cause cardiac arrhythmias

• (Increased PaCO2)

– Arrhythmias also occur without a high PaCO2

– Arrhythmias do not correlate with magnitude of PaCO2

CO2 – PP Initiation (IAP > 10 mmHg): Systemic Hemodynamic Effects

Mean arterial blood pressure ⇑⇑⇑⇑

Heart rate ⇔⇔⇔⇔ ⇑⇑⇑⇑

Central venous pressure ⇑⇑⇑⇑ ⇓⇓⇓⇓

Pulm. cap. wedge pressure ⇑⇑⇑⇑ ⇓⇓⇓⇓

Cardiac output ⇓⇓⇓⇓ ⇔⇔⇔⇔ ⇑⇑⇑⇑

Systemic vascular resistance ⇑⇑⇑⇑

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CO2 – PP: Systemic Hemodynamic Effects (1)

Pathophysiologic mechanism: Multifactorial

• Increased systemic vascular resistance

– Mechanical mechanism

– Release of neurohumoral factors• Vasopressin

• Autotransfusion effect

– Compression of splanchnic blood vessels• Reduced venous return

– Compression of vena cava inferior

– Increased intrathoracic pressure

– Pooling of blood in the legs

CO2 – PP: Systemic Hemodynamic Effects (2)

Parameters affecting balance between mechanisms

• Intra-abdominal pressure

• Intravascular volume status

• Patient positioning• PaCO2

• Associated cardiac disease

• Anesthesia

Pneumoperitoneum: IAP ≤ 10 mmHg

Cardiopulmonary healthy normovolemic person

Compression of splanchnic vessels

Venous return (autotransfusion)

Preload

CO

Cardiac output

Neurohumoral effects

Afterload

CO

SVR

Pneumoperitoneum: IAP > 15 mmHg

Compression of v. cavaPooling of blood in legs

Cardiac output

Venous return

Preload

ITP Neurohumoral effects

SVR

Afterload

Cardiopulmonary healthy normovolemic person

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CO2 – PP: Systemic Hemodynamic Effects (3)

• Intravascular volume status

– Hypovolemia increases the negative hemodynamic effects of an increased IAP

• No splanchnic recruitment

• Aggravates SVR increase• Patient positioning

– Trendelenburg positioning

• Attenuates SVR increase– Reverse Trendelenburg positioning

• Pooling of blood in the lower limbs

• Aggravates SVR increase

• Avoid insufflation with the patient in reverse Trendelenburg positionFigure 68-5 Changes in the cardiac index and systemic vascular resistance during laparoscopy in two groups of patients. For group 1 (controls, n = 10, yellow bars), pneumoperitoneum was induced with patients in a 10-degree head-up position. Group 2 (volume loaded, n = 10, blue bars) patients received 500 mL of lactated Ringer's solution before anesthesia induction and were insufflated in the supine position. Data are presented as the mean ± SEM.

Jean J. Joris in Miller’ Anesthesia, 7th edition, p. 2190

CO2 – PP: Systemic Hemodynamic Effects (4)

• PaCO2

– Moderate hypercarbia

• Slight myocardial stimulation

• Decreased systemic vascular resistance– Severe hypercarbia

• Decreased myocardial contractility

• Decreased arrhythmia threshold• Associated cardiac disease

– More severe hemodynamic changes?

• Anesthesia

– Vasodilatation reduces SVR increase– Negative inotropic effects of anesthetics

CO2 – PP: Renal Effects

• Decreased diuresis, glomerular filtration rate, renal blood flow

– < 50 % of baseline values

– Normalization after deflation

• Mechanisms– Direct renal parenchymal compression

– Venous congestion (reduced flow in v. cava inferior)

• Clinical consequences?– Recuperation after release of pneumoperitoneum

– Postoperative renal dysfunction in specific patient populations?

• Pre-existing renal dysfunction?

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CO2 – PP: Effects on Splanchnic Perfusion

• Mechanisms with opposing effects � variable effect on splanchnic perfusion

– Mechanical compression: splanchnic blood flow decrease

• Abdominal organ microcirculation

• Abdominal blood vessels– Direct effect of CO2 from the PP: splanchnic vasodilation

• Hepatoportal circulation

– Decreased blood flow– Postoperative liver dysfunction?

• Patients with pre-existing liver disease?

• Gastrointestinal circulation

– Effects on blood flow depend on IAP• IAP < 12 mmHg: moderate splanchnic hyperemia

• IAP > 15 mmHg: pressure-induced blood flow decrease

– Risk of splanchnic ischemia and bacterial translocation?

CO2 – PP: Venous Stasis (1)

• Venous stasis in the lower limbs

– Increased femoral venous pressure

– Decreased femoral peak velocity

• Mechanisms

– Increased IAP and compression of v. cava inferior– Reverse Trendelenburg positioning

• Pooling of blood in lower limbs

0

5

10

15

20

0

5

10

15

20

25

30

PP PP

BeforePP

After PP

BeforePP

After PP

* * * *

Femoral venous pressure(mmHg)

Peak velocity(cm/sec)

Beebe et al., Surg Gynecol Obstet 1993; 176: 443 - 7

CO2 – PP: Venous Stasis (2)

Increased risk of postoperative venous thrombosis?

• Factors increasing risk vs open procedures

– Venous stasis in the legs

– Longer lasting procedures• Factors reducing risk vs open procedures

– Earlier ambulation

– Less surgery-induced hypercoagulability• Less tissue trauma

� Adequate thrombosis prevention: no increased risk

– Low molecular weight heparins

– Compressive stockings

CO2-PP: Pulmonary Effects

CO2 – PP has significant pulmonary effects due to

• Increased intra-abdominal pressure

• CO2 – absorption and PaCO2 increase

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CO2-PP: Intra-Operative Pulmonary Effects (1)

Increased intra-abdominal pressure

• Cranial displacement of diaphragm

• Increased airway pressure

• V/Q mismatch

� Functional residual capacity: decrease

� Thoracopulmonary compliance: decrease– 30 – 50 % decrease in healthy persons

� (Micro)Atelectasis

� Impaired oxygenation and hypoxemia

– Generally no problem in healthy persons– Obese patients, patients with pre-existing pulmonary disease

Eichenberger et al., Anesth Analg 2002; 95: 1788 - 92

* P < 0.05 vs before induction

# P < 0,05 vs control

Lapsc. Gastroplasty Lapsc. CCE

CO2-PP: Intra-Operative Pulmonary Effects (2)

PaCO2 increase

• Absorption of CO2 from the pneumoperitoneum

– Intraperitoneal CO2 insufflation

• 10 – 30 % PetCO2 increase (with constant minute volume)• Plateau after 15 – 30 min

– Subcutaneous emphysema

• Intraperitoneal insufflation and no plateau• Very large PetCO2 increase

• Mechanical factors

– V/Q mismatching

• Abdominal distension• Patient positioning (Trendelenburg)

– These mechanical factors contribute more to PaCO2 increase in patients with cardiorespiratory disease than in healthy patients

Extraperitoneal insufflation

Intraperitoneal insufflation

Liem et al., Anesth Analg 1995; 81 (6): 1243 – 1249

CO2-PP: Intra-Operative Pulmonary Effects (3)

Monitoring of PaCO2 changes during CO2 - PP

• Capnometry (PetCO2) is reliable in healthy patients

• ASA III and IV patients: PaCO2 and arterial-end tidal PCO2 gradient increase more than in ASA I - II

– Decreased cardiac output – Increased V/Q mismatch

� Hypercapnia may develop in the absence of an abnormal PetCO2

Wittgen et al. Arch Surg 1991

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CO2-PP: Postoperative Respiratory Effects (1)

• Increased minute ventilation to eliminate absorbed CO2

– Increased respiratory rate

– Increased PetCO2

– Up to 2 hours postoperatively– Increased work of breathing may be a problem in patients with serious cardiopulmonary disease

CO2-PP: Postoperative Respiratory Effects (2)

• Postoperative pulmonary function is better preserved after laparoscopy than after laparotomy

– Postoperative pulmonary dysfunction is less severe after laparoscopy

• 75 % of preoperative values (vs 50 % after laparotomy)

– Pulmonary function recovers faster after laparoscopy: within 1 - 2 d (vs 3 - 5 d after laparotomy)

Frazee et al., Ann Surg 1991; 213: 651-3

Joris et al., Br J Anaesth 1992; 69: 341 - 45

Preop 4 h Day 2 Preop 4 h Day 20

500

10001500

2000

2500

3000

3500

Forced vital capacity(ml)

Forced expiratory volume in 1 sec(ml / s)

*

* P < 0.05

*

*

*

Laparoscopy Laparotomy

CO2-PP: Postoperative Respiratory Effects (3)

• Postoperative pulmonary function is better preserved after laparoscopy than after laparotomy

– Postoperative pulmonary dysfunction is less severe after laparoscopy

• 75 % of preoperative values (vs 50 % after laparotomy)

– Pulmonary function recovers faster after laparoscopy: within 1 - 2 d (vs 3 - 5 d after laparotomy)– Pulmonary dysfunction is less severe after gynecologic than after upper abdominal laparoscopy

Joris et al., Br J Anaesth 1997; 79: 422 - 26

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CO2-PP: Postoperative Respiratory Effects (3)

• Postoperative pulmonary function is better preserved after laparoscopy than after laparotomy

– Postoperative pulmonary dysfunction is less severe after laparoscopy

• 75 % of preoperative values (vs 50 % after laparotomy)

– Pulmonary function recovers faster after laparoscopy: within 1 - 2 d (vs 3 - 5 d after laparotomy)– Pulmonary dysfunction is less severe after gynecologic than after upper abdominal laparoscopy

– Pulmonary dysfunction after laparoscopy is more severe and recovers slower in older patients, obese patients, smokers and COPD patients

• But also in these patients pulmonary function is better preserved after laparoscopy than after laparotomy

• Diaphragm dysfunction following upper abdominal laparoscopic surgery– Inhibition of phrenic discharge by visceral afferents from the gallbladder area or somatic afferents from the

abdominal wall

Laparoscopy with CO 2-PP: Complications (1)

• Veress needle / trocar trauma

• Subcutaneous emphysema

• Pneumothorax

PneumomediastinumPneumopericardium

• Gas embolism

• Endobronchial intubation• Peripheral nerve damage

� Incidence: no precise data

� Consequences may be severe

Laparoscopy with CO 2-PP: Complications (2)

• Anesthesiologist may be the first to notice signs of a complication, even if the event is surgery related

• Diagnosis may be difficult and delayed

– E.g. Significant retroperitoneal hematoma may develop insidiously

– Differential diagnosis of complications with pulmonary effects• Endobronchial intubation

• Subcutaneous emphysema

• Capnothorax• Pneumothorax

• Massive CO2 embolism

Veress Needle / Trocar Trauma

• Injury to large blood vessels

– Aorta, inferior v. cava, iliac vessels

• Injury to abdominal wall vasculature

• Retroperitoneal hematoma– Concealed bleeding � difficult diagnosis

• Abdominal organ perforation

– Small / large bowel, liver, spleen– Avoid gastric distension (mask ventilation)

• Diafragm, pleura, pericard perforation

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CO2 – PP: Subcutaneous Emphysema (1)

• Severe hypercapnia– Persisting in spite of increasing minute ventilation

• Mechanism– Accidental extraperitoneal CO2 insufflation– Side-effect of intentional extraperitoneal CO2 - PP

• Diagnosis– Sudden large increase in PETCO2 after PetCO2 had reached a plateau

• PETCO2 increase larger than 30 % from baseline• PETCO2 increase later than 30 min after beginning of insufflation

– Crepitus: abdominal wall, chest wall• Sometimes there is ocular and/or pharyngeal emphysema

CO2 – PP: Subcutaneous Emphysema (2)

• Intraoperative management

– Increase minute ventilation

• Sometimes it is impossible to sufficiently increase MV and maintain normoventilation

– Reduce insufflation pressure– Muscle relaxation

• May facilitate mechanical ventilation (?)

– If PCO2 remains too high• Determine if hypercapnia is acceptable

• Limit duration of surgery

• Desufflate intermittently

• Abolish laparoscopic procedure– Determined by PCO2 and cardiopulmonary status

CO2 – PP: Subcutaneous Emphysema (3)

• Postoperative attention points

– Subcutaneous CO2 readily resolves after desufflation

– Keep patient mechanically ventilated until hypercapnia is sufficiently corrected

• This avoids excessive work of breathing– Be aware of risk of pharyngeal emphysema

• Generally, patients can be extubated, but if in doubt check presence of air leak with deflated cuff

Anesthesia and Analgesia 1995; 80: 201 - 203

CO2-PP: Pneumothorax, Pneumomediastinum, Pneumopericar dium

• Increased PetCO2

• Pneumothorax: differential diagnosis

– Capnothorax (CO2 pneumothorax)• PetCO2 increase

• IPPV + PEEP � decrease of capnothorax

• Chest drain is generally not necessary

– Pneumothorax due to lung injury• PetCO2 decrease

• IPPV� risk of tension pneumothorax

• Chest drain is generally indicated

From: Wolf and Stoller, J. Urol. 152 (1994)

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CO2 - PP: Gas Embolism (1)

• Venous CO2 embolism– During insufflation, early after Veress needle insertion: massive CO2 embolism

• Direct intravenous insufflation• Insufflation in abdominal organs� Gas lock in v. cava and right atrium � fall in cardiac output, possibly circulatory arrest

– During laparoscopic surgery• Passage of CO2 into abdominal wall and peritoneal vessels• Open vessels on liver surface during gallbladder dissection� Generally, signs and symptoms of gas embolism develop slower

• Paradoxal embolism through patent foramen ovale or ASD– Acute right ventricular hypertension– Cerebral CO2 embolism

CO2 - PP: Gas Embolism (2)

• Lethal volume of CO2 embolism is 5 x greater than of air• Signs and symptoms

– “Mill-wheel” murmur (precordial stethoscope)– Decrease in PetCO2

• Sometimes preceded by a brief increase in PetCO2 due to pulmonary excretion of absorbed CO2

– Hypoxemia– Hypotension– ECG changes– Cardiovascular collapse

No physiologic changes •Transesophageal echocardiography•Precordial doppler

Modest physiologic changes •Decreased PetCO2

•Increased pulmonary artery pressure

Clinical symptoms •Hypoxemia•Hypotension•Increased central venous pressure•Decreased cardiac output

Cardiovascular collapse •ECG changes•Arrhythmias•Aspiration of foamy blood from central venous line

CO2 - PP: Gas Embolism (2)

• Lethal volume of CO2 embolism is 5 x greater than of air• Signs and symptoms

– “Mill-wheel” murmur (precordial stethoscope)– Decrease in PetCO2

• Sometimes preceded by a brief increase in PetCO2 due to pulmonary excretion of absorbed CO2

– Hypoxemia– Hypotension– ECG changes– Cardiovascular collapse

No physiologic changes

Modest physiologic changes •Decreased PetCO2

Clinical symptoms •Hypoxemia•Hypotension

Cardiovascular collapse •ECG changes•Arrhythmias

CO2 - PP: Gas Embolism (3)

• Treatment

– Immediately stop insufflation and release pneumoperitoneum

– Ventilation with 100 % oxygen

– Durant’s position to clear right ventricular outflow• Left lateral decubitus

• Steep Trendelenburg

– Aspiration of gas (if central venous catheter in situ)– Cardiopulmonary resuscitation

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CO2 – PP: Endobronchial Intubation

• Cephalad displacement of the diaphragm (and carina)

• Increase in airway pressure

• O2 saturation decrease

Lobato et al., Anesth Analg 1998; 86: 301 - 303

Peripheral Nerve Damage

Careful positioning

• Head-down position

– Avoid shoulder braces (risk of brachial plexus lesion)

– Vacuum / anti-slip mattress• Lithotomy position

– Common peroneal nerve lesion

– Long-lasting procedures: compartment syndrome

CO2 – PP: Contra-indications (1)

• Patients with or at risk for an increased ICP

– Cerebral trauma

– Intracranial space occupying lesions (tumor, aneurysm)

– Hydrocephalus

ICPBaseline PP

(15 mmHg)Epid

balloonEB + PP EB +

Retractor

Pressure(mmHg)

� � � � �

� � � � �

0

10

20

30

0

20

40

60

80

100Pressure(mmHg)

� MAP� PaCO2

Este-McDonald et al., Arch Surg 130 (1995)

CO2 – PP: Contra-indications (2)

• Significant hypovolemia, shock

� More pronounced hemodynamic effects of increased IAP

• Low cardiac output

• Renal and splanchnic hypoperfusion• Selected cardiopulmonary problems

– Very low cardiac output

– Severe heart failure– Cardiac right-left shunt

– Severe aortic valve insufficiency

– Severe pulmonary hypertension

– Some complex congenital cardiopathies• Closed angle glaucoma

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CO2 – PP: Relative Contra-indications

• Heart failure

• Patent foramen ovale

• Severe pulmonary disease

– Intra-operative ventilation problems– However: less severe postoperative pulmonary dysfunction compared to laparotomy

• Significantly impaired renal function?

– Avoid prolonged laparoscopic surgery with high IAP?– Hemodynamic optimalization to better tolerate increased IAP?

• Patients at risk for splanchnic ischemia?

– Avoid prolonged laparoscopic surgery with high IAP?

• Patient in whom an increased intraocular pressure (IOP) should be avoided

Anesthesia for Laparoscopy with CO 2 – PP (1)

• Preoperatively

– Standard

– Identify contra-indications

– Thrombosis prophylaxis• Premedication

– Standard

– Antacids? No.• No indication of increased risk of regurgitation

• Preservation of gastro-esophageal barrier pressure

Jones et al. Anest Analg 1989; 68: 63-5

Anesthesia for Laparoscopy with CO 2 – PP (2)

• Monitoring

– Standard intraoperative monitoring

• Non-invasive blood pressure, ECG, capnography, pulse oxymetry� Only indirect evidence of PP-induced hemodynamic changes

– Arterial line

• Severe pre-existing cardiac and pulmonary disease

– Hemodynamic response to PP + positioning– Arterial – end tidal PCO2 difference

• Surgical procedure

– Transesophageal echocardiography

• Severe cardiac co-morbidity, but indication for laparoscopy?

Anesthesia for Laparoscopy with CO 2 – PP (3)

• Neuraxial anesthesia (epidural, CSE, spinal): indications are limited

– Extensive block is necessary (T4 - L5) for surgical laparoscopy

– Short procedures, lower abdomen

• E.g. tubal ligation– Reduced insufflation pressure

– No extreme head-down positioning

– Hemodynamic effects of PP under epidural anesthesia: no data– Insufflation gas

• Nitrous oxide?– Less irritation of peritoneum and diaphragm– No electrocautery possible

• CO2

– Increased minute ventilation (increased work of breathing) to maintain PaCO2

� For selected, brief procedures without electrocautery only

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Anesthesia for Laparoscopy with CO 2 – PP (4)

• General anesthesia: technique of choice for laparoscopy

– Intubation and mechanical ventilation

• Technique of choice

• Adjust minute volume to maintain PetCO2 between 35 - 40 mmHg• Check position of endotracheal tube after induction of PP

– Risk of endobronchial intubation

– Check again with Trendelenburg positioning

• Laryngeal mask?– Traditional LM does not protect airway against aspiration of gastric contents

» Second generation LM

– Ventilation problems » ↓ thoracopulmonary compliance and airway pressure > 20 cmH2O

Anesthesia for Laparoscopy with CO 2 – PP (5)

• General anesthesia: technique of choice for laparoscopy

– Antiemetic

• Laparoscopy: increased risk of PONV (40 – 75% of patients)

– Nitrous oxide ? Controversial• Bowel distension?

– Not convincingly demonstrated

• Worsens cardiovascular effects of CO2 emboli

• Explosion hazard?– Bowel perforation and combustion of bowel gases

– Unlikely in routine clinical practice

• Increased incidence of PONV?

� No conclusive evidence against the use of N2O

Anesthesia for Laparoscopy with CO 2 – PP (6)

• Recovery and postoperative care

– Postoperative elimination of absorbed CO2

• Absorption in blood of residual CO2

• CO2 release from body stores�Increased work of breathing

�Caution in patients with severe cardiopulmonary disease

– Nausea and vomiting• Laparoscopy: increased risk for PONV

• Prevention is absolutely indicated

Anesthesia for Laparoscopy with CO 2 – PP (7)

• Postoperative analgesia

– Incisional pain, intra-abdominal (visceral) pain, shoulder pain

– After laparoscopy pain is generally less intense and of shorter duration than after laparotomy, but

• Pain is variable in duration, severity and character• Patients may experience severe pain after laparoscopic surgery

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Anesthesia for Laparoscopy with CO 2 – PP (8)

• Postoperative analgesia: multimodal approach

– Intraperitoneal local anesthetic

• Conflicting results

• More successful after pelvic laparoscopy? • Generally not effective for visceral pain

– Infiltration of skin with local anesthetic

– Evacuation of insufflation gas• Residual CO2 causes shoulder pain

• Gas drain

– NSAIDs

• Reduced need for opioid analgesia– Opioids may be necessary!