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Interesting case
Conceal Rupture Abdominal
Aortic Aneurysm
Patient Profile
• 60 years old thai male patient
• Chief complaint : มีอาการปวดท ้อง ร ้าวไปหลัง 1 วันก่อนมาโรงพยาบาล
• Present illness : 10 วันก่อนมาโรงพยาบาล มีอาการปวท ้อง ร ้าวไปหลัง ไปรักษารพพระ
นาราย์มหาราช Dx Conceal rupture AAA ยังไม่ได ้ผ่าตัด อาการปวดลดลง ได ้กลับบ ้าน
1 วันก่อนมารพ มีอาการปวดท ้องมาขึ้น + เหนื่อยอ่อนเพลีย repeat CTA : conceal
rupture AAA ร่วมกับ HCT 23 จึงส่งตัวรักษาต่อโรงพยาบาลพุทธ ชินราช
Diagnosis : Conceal Rupture infrarenal AAA
Operation : Open repain abdominal aortic aneurysm
Past History
Underlying disease
HT
losartan (100)1/2*1
Hypothyroid
lovothyroxin(100)1/2*1
IHD
ASA(81)1*1
Atorvsastatin(40)1*1
EF :69% ผล echo ปี 2560
ไม่เคย CAG
No Smoking
No alcohol drinking
No drug and food allergy
No family history of MH
No previous surgery
Functional Class 2
Physical Examination
• General Apprance : A man of his age Full consciousness , well co operation
• Vital sign : BT 36.8 C RR 20/min HR 96/ min BP 112/88 SpO2 100%
• BW : 69 kg HT : 160 CM BMI : 23.4 kg/m²
• HEENT : mild pale conjunctiva , aniteric sclerae
• CVS : Audible S1S2 no Murmur
• RS : Equal Breath sounds both lung no adventitious Sound
• Abdomen : pulsatile mass at abdomen with mild tender active bowel sound
• EXT : nodedma both leg
• Neuro E4V5M6, puipill 2 mm rtlbe, motor grade V all
Airway Examination
• Mouth poening : ≥2FB
• Denture : no
• Mallapati : 2
• Thyromental : ≥6 cm
• Hyomental : ≥2 FB
• Neck movement : no limitation of neck movement
Invsetigation
Invsetigation
Invsetigation
cxr
EKG
CTA
CTA
CTA
CTA
11
Problem List
• Conceal Ruprture infrarenal AAA
• Old Age
• HT
• IHD
• Anemia
1 E3333
ASA Classification
2 4
3
1
Preoperative evaluation
& Preparation
Choice of anesthesia
Intraoperative Care
Postoperative care
Abdominalaorticaneurysm
A 50% increase in diameter compared with normal, or greater than 3 cm in diameter
65% of all aneurysms of the aorta and 95% are below the renal arteries
Incidence 8% in elderly men
Risk factors : increasing age, smoking, family history of AAA and atherosclerosis disease
Fusiform type
Saccular type
Eccentric
Concentric
Pathogenesis
• Degenerative
Adventitial elastin degradation (elastolysis)
Associated with smoking
• Inflammatory
Chronic inflammation → destruction of connective tissue in the aortic wall
Takayasu arteritis, Giant cell arteritis, Polyarteritis nodosa
• Aneurysm associated with arterial dissection
• Traumatic
Almost → pseudoaneurysm due to perforation
• Developmental and congenital anomalies
Embryonic defect : Congenital AAA
Collagen disease : Marfan syndrome, Ehler danlos syndrome
• Infectious (Mycotic) : Bacterial, Fungi, Tuberculosis and Syphilis
• Drug abuse : Chronic amphetamine use
Abdominalaorticaneurysm
Risk factors
Nonmodifiable risk factors
Advanced age (>50 years)
Gender (male)
Family history
Modifiable risk factors
Smoking
Obesity
Hyperlipidemia
Hypertension
Atherosclerotic arteriopathy (e.g. CAD)
Abdominalaorticaneurysm
Clinical features
• Most AAAs are asymptomatic and often discovered incidentally
• Abdominal pain
• Pulsatile abdominal mass
• Large AAA → Mass effect on related structures
GI compression → vomiting
Ureteral compression → urinary symptoms
Iliocaval compression → venous complications
• Most AAAs become symptomatic secondary to growth or rupture
Abdominalaorticaneurysm
• Risk of rupture is directly related to the luminal diameter of aortic aneurysm
• Rupture of an AAA is most often lethal with a mortality rate of 75%
• Major management goal is to identify and treat AAAs before they rupture
Abdominalaorticaneurysm
Indications for AAA intervention
• Current evidence-based guidelines suggest repair when aneurysm diameter exceeds
5.0 cm. (women) and 5.5 cm. (men)
• Rapid aneurysm growth: greater 10 mm per year
• Symptomatic nonruptured AAA
Abdominalaorticaneurysm
• Open AAA repair is first described in 1951
It is still considered a high-risk surgical procedure
Mortality rates range from 1.5 – 5.8%
Clinical outcomes have improved as a result of advances in
anesthetic and surgical techniques
• Endovascular aneurysm repair (EVAR) was pioneered in 1986
A mainstay of treatment for AAA
More than 50% AAAs undergo EVAR in this era
Endovascular versus open AAA repair
Abdominalaorticaneurysm
• High-quality RCT comparing endovascular to open AAA repair
EVAR: Short-term survival benefit (perioperative period)
No significant difference in mid- to long-term mortality
Open AAA repair has proven long-term durability
EVAR carries a higher risk of repeat intervention
• The decision depends on multiple factors – aortic anatomy, urgency, patient
preference and surgical expertise
Endovascular versus open AAA repair
Abdominalaorticaneurysm
Endovascular versus open AAA repair
Preoperative evaluation
History taking
• Symptoms: onset, duration, severity
• High-risk comorbidities: CAD, COPD, peripheral vascular disease, renal dysfunction
• Functional status
• Current medications
• Previous anesthesia and surgery
• Drug allergy
• Social history: Smoking, alcohol drinking
Cardiovascular
Assessment
Preoperative evaluation
• Stratified and minimize perioperative mortality and morbidity risk
Cardiovascular assessment
Renal function assessment
Cerebrovascular assessment
Pulmonary function assessment
Preoperative renal dysfunction→ Most important predictor of
acute renal failure
Adequate hydration
Avoidance of...
Hypovolemia
Hypotension
Low urine output
Avoid nephrotoxic drugs
Preoperative evaluation
• Stratified and minimize perioperative mortality and morbidity risk
Cardiovascular assessment
Renal function assessment
Cerebrovascular assessment
Pulmonary function assessment
• History of stroke or TIA
• PE : Neurological examination and carotid bruit
• Duplex imaging of the carotid arteries or angiography
of the brachiocephalic and intracranial arteries
• Carotid endarterectomy
Severe stenosis of one or both common or internal
carotid artery
• Chronic HT → Shift cerebral autoregulation
Preoperative evaluation
• Stratified and minimize perioperative mortality and morbidity risk
Cardiovascular assessment
Renal function assessment
Cerebrovascular assessment
Pulmonary function assessment • To decrease the incidence of respiratory
complications
○ Smoking cessation
○ COPD
Bronchodilators
Antibiotics
Chest physiotherapy
Pulmonary Function Studies
Preoperative Preparation
• NPO
• Informed consent
• Premedication
• IV fluid
• Blood components
• Airway devices
• Anesthetic machine, anesthetic
circuit
• Anestheticdrugs
• Vasopressor,inotropicdrugs
• Invasivemonitoring
• LargeboreIV
• Warmerdevice
• PostoperativeICUandventilator
• Cardiologistconsultation
Choice of anesthesia
General anesthesia with cuffed endotracheal tube with controlled
ventilation
General anesthesia is the most commonly employed technique
Monitoring
Standard monitoring Special monitoring
●Standard I
●Standard II
○EKG
○Pulse oximetry
○NIBP
○Temperature
○ETCO2,
ETO2
○Airway pressure
○Intake/Output
○Blood sugar
●Invasive monitoring
○Invasive arterial blood pressure
○CVP
○PAC
○TEE
●ABG
2 4
3
1
Acute hemodynamic
changes with aortic cross-
clamping and unclamping
Attenuate ischemic
reperfusion injury
Provide intraoperative and
postoperative analgesia
Maintain organperfusion and
oxygenation
Anesthetic
consideration
Aortic cross clamping
Aortic cross-clamping
Aortic cross-clamping
Ischemic
(1) Decrease in organ perfusion to organ located distal to occlusion &
(2) Hypovolemic state (Hemorrhage)
Spinal cord : paraplegia and paraparesis
Kidney : Acute kidney injury
Abdominal viscera : Bowel ischemia
Lower extremities : Acute limb ischemia, trash foot
(3) Increase afterload to organ above cross-clamping
Heart : Myocardial injury
Brain : Hypertensive stroke
Aortic cross-clamping
Decrease afterload ●Sodium nitroprusside 0.5-1.0 mcg/kg/min or Clevidipine
●Inhalation anesthetics
●Amrinone
Decrease blood pressure ●Increase depth of anesthesia
○Volatile
○opioid
Maintain preload ●Nitroglycerine 0.5-10 mcg/kg/min
Renal protection ●Fluid administration n (keep urine output ≥0.5-1 ml/kg/hr)
●Promote urine with loop diuretic, mannitol (if adequate hydration)
●Drug to augment renal perfusion
Maintain intravascular volume (keep urine output ≥0.5-1 ml/kg/hr) :Central venous pressure, pulse pressure variation
or non-invasive cardiac output monitoring can be used to guide intravascular filling
Keep normothermia (keep ≥ 36 oC)
Aortic Unclamping
Aortic declamping
Declamping hypotension
Rapid decreased perfusion to organ above clamp
Heart → Myocardial ischemia
Brain → Ischemic stroke
Systemic hypotension
Reperfusion injury
After proximal anastomosis reconstruction
Reperfusion to visceral (celiac artery, SMA and renal arteries)
After distal anastomosis reconstruction (bi-iliac arteries)
Reperfusion to pelvis and lower extremity
Aortic Unclamping
• During emergence
• Prevent hemodynamic variations outside the patient’s normal range
NTG
Esmolol
Other beta-adrenergic blocking agents
• If appropriate, the trachea should be extubated at the end or surgery
• Prophylactic beta-blockade should be continued if tolerated
Unstable patients → short acting agent such as esmolol
stable patients → LONG acting agent such as metoprolol
Postoperative care
Postoperative management
• Continuous BP monitoring
• Regular assessment
ABG
Hct
Serum electrolytes
Coagulogram
lower limb arteries: clinical, doppler
• Thromboembolic prophylaxis
• Pain control
CASE
Intraoperative
Monitor : NIBP,EKG,SpO2
BP 130/104 HR 94 RR 22
Induction and intubation
Fentanyl 50 mcg
Etomidate 14 mg
proprofol 100 mg
Cisatraculium 10 mg
ETT no 8.0 cuffed mark 22 by C-MAC
Local A-line
IV Access
IV NO 18G RA LL
IV NO 20G RA LA
CVP : rt internal jugular v.
Monitor Temperature : oropharynx
Maintenance :
NO : O2 : Sevoflurane
Fentanyl
Cisatracurium
SUMMARY
Operation Time 11.20-15.25
Operation : Open repair abdominal aortic aneurysm
Blood loss : 3500 ml
Fluid : NSS 2700 ml
Acetar 1900 ml
Blood component
PRC 1438 ml
FFP 1020 ml
Urine output
before clamp 25 ml/ hr
During clamp 10 ml /hr
after de clamp 200 ml/hr
Remain intubation to ICUSX
ABG 11.22 12.54 13.57 15.10 17.46
pH 7.390 7.307 7.324 7.372 7.426
PaO2
105.3 105.8 137.3 127.5 106.1
PaCO2
38.9 37.1 42.5 44.4 36.5
HCO3
23.1 18.0 21.5 25.2 23.6
Hb/Hct 5.6/16.5 5.9/17.3 6.9/20.3 5.9/17.3 8.5/25.0
K 3.25 3.10 2.93 3.08 3.67
iCa 3.48 2.08 2.00 2 3.80
BE -1.9 -8.3 -4.5 0 -0.8
Thank you

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IC TT 01.pptx

  • 1. Interesting case Conceal Rupture Abdominal Aortic Aneurysm
  • 2. Patient Profile • 60 years old thai male patient • Chief complaint : มีอาการปวดท ้อง ร ้าวไปหลัง 1 วันก่อนมาโรงพยาบาล • Present illness : 10 วันก่อนมาโรงพยาบาล มีอาการปวท ้อง ร ้าวไปหลัง ไปรักษารพพระ นาราย์มหาราช Dx Conceal rupture AAA ยังไม่ได ้ผ่าตัด อาการปวดลดลง ได ้กลับบ ้าน 1 วันก่อนมารพ มีอาการปวดท ้องมาขึ้น + เหนื่อยอ่อนเพลีย repeat CTA : conceal rupture AAA ร่วมกับ HCT 23 จึงส่งตัวรักษาต่อโรงพยาบาลพุทธ ชินราช
  • 3. Diagnosis : Conceal Rupture infrarenal AAA Operation : Open repain abdominal aortic aneurysm
  • 4. Past History Underlying disease HT losartan (100)1/2*1 Hypothyroid lovothyroxin(100)1/2*1 IHD ASA(81)1*1 Atorvsastatin(40)1*1 EF :69% ผล echo ปี 2560 ไม่เคย CAG No Smoking No alcohol drinking No drug and food allergy No family history of MH No previous surgery Functional Class 2
  • 5. Physical Examination • General Apprance : A man of his age Full consciousness , well co operation • Vital sign : BT 36.8 C RR 20/min HR 96/ min BP 112/88 SpO2 100% • BW : 69 kg HT : 160 CM BMI : 23.4 kg/m² • HEENT : mild pale conjunctiva , aniteric sclerae • CVS : Audible S1S2 no Murmur • RS : Equal Breath sounds both lung no adventitious Sound • Abdomen : pulsatile mass at abdomen with mild tender active bowel sound • EXT : nodedma both leg • Neuro E4V5M6, puipill 2 mm rtlbe, motor grade V all
  • 6. Airway Examination • Mouth poening : ≥2FB • Denture : no • Mallapati : 2 • Thyromental : ≥6 cm • Hyomental : ≥2 FB • Neck movement : no limitation of neck movement
  • 10. cxr
  • 11. EKG
  • 12. CTA
  • 13. CTA
  • 14. CTA
  • 15. CTA
  • 16. 11 Problem List • Conceal Ruprture infrarenal AAA • Old Age • HT • IHD • Anemia
  • 18. 2 4 3 1 Preoperative evaluation & Preparation Choice of anesthesia Intraoperative Care Postoperative care
  • 19. Abdominalaorticaneurysm A 50% increase in diameter compared with normal, or greater than 3 cm in diameter 65% of all aneurysms of the aorta and 95% are below the renal arteries Incidence 8% in elderly men Risk factors : increasing age, smoking, family history of AAA and atherosclerosis disease Fusiform type Saccular type Eccentric Concentric
  • 20. Pathogenesis • Degenerative Adventitial elastin degradation (elastolysis) Associated with smoking • Inflammatory Chronic inflammation → destruction of connective tissue in the aortic wall Takayasu arteritis, Giant cell arteritis, Polyarteritis nodosa • Aneurysm associated with arterial dissection • Traumatic Almost → pseudoaneurysm due to perforation • Developmental and congenital anomalies Embryonic defect : Congenital AAA Collagen disease : Marfan syndrome, Ehler danlos syndrome • Infectious (Mycotic) : Bacterial, Fungi, Tuberculosis and Syphilis • Drug abuse : Chronic amphetamine use
  • 21. Abdominalaorticaneurysm Risk factors Nonmodifiable risk factors Advanced age (>50 years) Gender (male) Family history Modifiable risk factors Smoking Obesity Hyperlipidemia Hypertension Atherosclerotic arteriopathy (e.g. CAD)
  • 22. Abdominalaorticaneurysm Clinical features • Most AAAs are asymptomatic and often discovered incidentally • Abdominal pain • Pulsatile abdominal mass • Large AAA → Mass effect on related structures GI compression → vomiting Ureteral compression → urinary symptoms Iliocaval compression → venous complications • Most AAAs become symptomatic secondary to growth or rupture
  • 23. Abdominalaorticaneurysm • Risk of rupture is directly related to the luminal diameter of aortic aneurysm • Rupture of an AAA is most often lethal with a mortality rate of 75% • Major management goal is to identify and treat AAAs before they rupture
  • 24. Abdominalaorticaneurysm Indications for AAA intervention • Current evidence-based guidelines suggest repair when aneurysm diameter exceeds 5.0 cm. (women) and 5.5 cm. (men) • Rapid aneurysm growth: greater 10 mm per year • Symptomatic nonruptured AAA
  • 25. Abdominalaorticaneurysm • Open AAA repair is first described in 1951 It is still considered a high-risk surgical procedure Mortality rates range from 1.5 – 5.8% Clinical outcomes have improved as a result of advances in anesthetic and surgical techniques • Endovascular aneurysm repair (EVAR) was pioneered in 1986 A mainstay of treatment for AAA More than 50% AAAs undergo EVAR in this era Endovascular versus open AAA repair
  • 26. Abdominalaorticaneurysm • High-quality RCT comparing endovascular to open AAA repair EVAR: Short-term survival benefit (perioperative period) No significant difference in mid- to long-term mortality Open AAA repair has proven long-term durability EVAR carries a higher risk of repeat intervention • The decision depends on multiple factors – aortic anatomy, urgency, patient preference and surgical expertise Endovascular versus open AAA repair
  • 28. Preoperative evaluation History taking • Symptoms: onset, duration, severity • High-risk comorbidities: CAD, COPD, peripheral vascular disease, renal dysfunction • Functional status • Current medications • Previous anesthesia and surgery • Drug allergy • Social history: Smoking, alcohol drinking
  • 30. Preoperative evaluation • Stratified and minimize perioperative mortality and morbidity risk Cardiovascular assessment Renal function assessment Cerebrovascular assessment Pulmonary function assessment Preoperative renal dysfunction→ Most important predictor of acute renal failure Adequate hydration Avoidance of... Hypovolemia Hypotension Low urine output Avoid nephrotoxic drugs
  • 31. Preoperative evaluation • Stratified and minimize perioperative mortality and morbidity risk Cardiovascular assessment Renal function assessment Cerebrovascular assessment Pulmonary function assessment • History of stroke or TIA • PE : Neurological examination and carotid bruit • Duplex imaging of the carotid arteries or angiography of the brachiocephalic and intracranial arteries • Carotid endarterectomy Severe stenosis of one or both common or internal carotid artery • Chronic HT → Shift cerebral autoregulation
  • 32. Preoperative evaluation • Stratified and minimize perioperative mortality and morbidity risk Cardiovascular assessment Renal function assessment Cerebrovascular assessment Pulmonary function assessment • To decrease the incidence of respiratory complications ○ Smoking cessation ○ COPD Bronchodilators Antibiotics Chest physiotherapy Pulmonary Function Studies
  • 33. Preoperative Preparation • NPO • Informed consent • Premedication • IV fluid • Blood components • Airway devices • Anesthetic machine, anesthetic circuit • Anestheticdrugs • Vasopressor,inotropicdrugs • Invasivemonitoring • LargeboreIV • Warmerdevice • PostoperativeICUandventilator • Cardiologistconsultation
  • 34. Choice of anesthesia General anesthesia with cuffed endotracheal tube with controlled ventilation General anesthesia is the most commonly employed technique
  • 35. Monitoring Standard monitoring Special monitoring ●Standard I ●Standard II ○EKG ○Pulse oximetry ○NIBP ○Temperature ○ETCO2, ETO2 ○Airway pressure ○Intake/Output ○Blood sugar ●Invasive monitoring ○Invasive arterial blood pressure ○CVP ○PAC ○TEE ●ABG
  • 36. 2 4 3 1 Acute hemodynamic changes with aortic cross- clamping and unclamping Attenuate ischemic reperfusion injury Provide intraoperative and postoperative analgesia Maintain organperfusion and oxygenation Anesthetic consideration
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  • 39. Aortic cross-clamping Aortic cross-clamping Ischemic (1) Decrease in organ perfusion to organ located distal to occlusion & (2) Hypovolemic state (Hemorrhage) Spinal cord : paraplegia and paraparesis Kidney : Acute kidney injury Abdominal viscera : Bowel ischemia Lower extremities : Acute limb ischemia, trash foot (3) Increase afterload to organ above cross-clamping Heart : Myocardial injury Brain : Hypertensive stroke
  • 40. Aortic cross-clamping Decrease afterload ●Sodium nitroprusside 0.5-1.0 mcg/kg/min or Clevidipine ●Inhalation anesthetics ●Amrinone Decrease blood pressure ●Increase depth of anesthesia ○Volatile ○opioid Maintain preload ●Nitroglycerine 0.5-10 mcg/kg/min Renal protection ●Fluid administration n (keep urine output ≥0.5-1 ml/kg/hr) ●Promote urine with loop diuretic, mannitol (if adequate hydration) ●Drug to augment renal perfusion Maintain intravascular volume (keep urine output ≥0.5-1 ml/kg/hr) :Central venous pressure, pulse pressure variation or non-invasive cardiac output monitoring can be used to guide intravascular filling Keep normothermia (keep ≥ 36 oC)
  • 42. Aortic declamping Declamping hypotension Rapid decreased perfusion to organ above clamp Heart → Myocardial ischemia Brain → Ischemic stroke Systemic hypotension Reperfusion injury After proximal anastomosis reconstruction Reperfusion to visceral (celiac artery, SMA and renal arteries) After distal anastomosis reconstruction (bi-iliac arteries) Reperfusion to pelvis and lower extremity
  • 44. • During emergence • Prevent hemodynamic variations outside the patient’s normal range NTG Esmolol Other beta-adrenergic blocking agents • If appropriate, the trachea should be extubated at the end or surgery • Prophylactic beta-blockade should be continued if tolerated Unstable patients → short acting agent such as esmolol stable patients → LONG acting agent such as metoprolol
  • 45. Postoperative care Postoperative management • Continuous BP monitoring • Regular assessment ABG Hct Serum electrolytes Coagulogram lower limb arteries: clinical, doppler • Thromboembolic prophylaxis • Pain control
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  • 47. CASE
  • 48. Intraoperative Monitor : NIBP,EKG,SpO2 BP 130/104 HR 94 RR 22 Induction and intubation Fentanyl 50 mcg Etomidate 14 mg proprofol 100 mg Cisatraculium 10 mg ETT no 8.0 cuffed mark 22 by C-MAC Local A-line IV Access IV NO 18G RA LL IV NO 20G RA LA CVP : rt internal jugular v. Monitor Temperature : oropharynx Maintenance : NO : O2 : Sevoflurane Fentanyl Cisatracurium
  • 49. SUMMARY Operation Time 11.20-15.25 Operation : Open repair abdominal aortic aneurysm Blood loss : 3500 ml Fluid : NSS 2700 ml Acetar 1900 ml Blood component PRC 1438 ml FFP 1020 ml Urine output before clamp 25 ml/ hr During clamp 10 ml /hr after de clamp 200 ml/hr Remain intubation to ICUSX
  • 50. ABG 11.22 12.54 13.57 15.10 17.46 pH 7.390 7.307 7.324 7.372 7.426 PaO2 105.3 105.8 137.3 127.5 106.1 PaCO2 38.9 37.1 42.5 44.4 36.5 HCO3 23.1 18.0 21.5 25.2 23.6 Hb/Hct 5.6/16.5 5.9/17.3 6.9/20.3 5.9/17.3 8.5/25.0 K 3.25 3.10 2.93 3.08 3.67 iCa 3.48 2.08 2.00 2 3.80 BE -1.9 -8.3 -4.5 0 -0.8