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Dr. Dinesh Mannapperu
Registrar Anaesthesia
TH- Kandy
Splanchnic Circulation
24th June 2016
• Briefly describe the splanchnic circulation.
• What is abdominal compartment syndrome
• What are the pathophysiological effects of abdominal compartment
syndrome
• Out line the management of abdominal compartment syndrome.
• Splanchnic circulation in Anaesthesia and critical care.
Objectives
Briefly describe the splanchnic circulation. 30%
• Coeliac artery T12
1. Common Hepatic
2. Left gastric
3. Splenic
• Superior mesenteric artery L2
1. Inferior pancreatico duodenal
2. Intestinal arteries
3. Ileocolic
4. Right colic
5. Middle colic
• Inferior mesenteric L3
1. Left colic
2. Sigmoid branches
3. Superior rectal
SBF about 25-30% of COP
30ml/min/100g ( <10ml/min/100g-250ml/min/100g)
Highly adaptive and act as a reservoir of blood
Physiological regulation of SBF
Intrinsic
control
Humoral control
Extrinsic
control
Metabolic
H+, K+ , adenosine , CO2
, hypoxia
Myogenic
Mechano sensitive Na+
Channels,
Depolarization,
Ca2+ channels
Sympathetic NS
Noradrenaline mediated
- adrenergic
vasoconstriction
Parasympathetic NS
Vagal and pelvic nerves
M1 mediated NO release
Vasodialators
Bradykinin, gastrin,
secretin, cholecystokinin,
substance P, dopamine,
Vasoconstrictors
Vasopressin, Angiotensin
ii,
Neuropeptide Y,
Disorders of Splanchnic Blood flow
1. Ischemic reperfusion injury
2. Sepsis /gut origin hypothesis
3. Portal hypertention
What is abdominal compartment syndrome 5%
• Intra Abdominal Hypertention.
Normal IA pressure is 5-7mmHg, if it increases more than 12mmHg
• Intra Abdominal Compartment syndrome
When IA pressure exceeds 20mmHg .
• Grade 1 - 12–15 mm Hg;
• Grade 2 - 16–20 mm Hg;
• Grade 3 - 21–25 mm Hg;
• Grade 4 - >25mm Hg.
Definitions
What is abdominal compartment syndrome 5%
1. Diminished abdominal wall compliance
Acute respiratory failure, especially with elevated Intra thoracic
pressure
Abdominal surgery with subjectively tight primary closure
Major trauma/burns
Prone positioning, head of bed elevated >30°
High BMI, central obesity
Causes for IA compartment syndrome
2. Increased intra-luminal contents
Gastroparesis
Ileus
Colonic pseudo-obstruction
3. Increased abdominal contents
Haemoperitoneum/ pneumoperitoneum
Ascites/liver dysfunction
4. Capillary leak/fluid resuscitation
 Acidosis (pH <7.2)
 Hypotension
 Hypothermia (core temperature <33°C)
 Polytransfusion (>10 units of blood/24 h)
 Coagulopathy (platelets ,55 000 mm-3, prothrombin time >15 s,
partial thromboplastin time 2 times normal, or international
standardized ratio >1.5)
 Massive fluid resuscitation (>5 litre/24 h)
 Pancreatitis
 Oliguria
 Sepsis
 Major trauma/burns
 Damage control laparotomy
Abdominal Perfusion Pressure = MAP - IAP
Measurement of IA pressure
1. Direct methods
2. Indirect methods
• Intra-gastric
• Intra-uterine
• Rectal
• Intra-vesicular
What are the pathophysiological effects of
Abdominal Compartment Syndrome 15%
Cardiovascular System
• Increase IAP Direct pressure over abdominal vasculature
Compression of IVC Compression of Aorta
Reduce preload Increase afterload
Increase intra
thoracic
pressure
Reduce compliance and
contractility Reduce COP
Catastrophic intra abdominal ischaemia
• basal collapse/atelectasis,
• increasing V/Q mismatch
• decreased pulmonary and chest wall compliance
• increasing hypoxia and hypercarbia
• increased inspiratory pressures and PEEP in ventilated pts can
further compromise VR and COP
Respiratory system
•Treatment of intra-abdominal hypertension
has been associated with reduced ventilatory
days
Renal system
Reduced GFR
Reduced RBF
Reduced COPIncresed IAP
renal outflow
tract
FG = ( MAP – IAP ) -PTP
Normal PTP=15-18mmHg
FG = ( MAP - IAP ) - IAP
= MAP - 2IAP
If PTP = IAP, then
Hormonal effects from activation of the renin/angiotensin
system and increased ADH have a further adverse effect.
Central nervous system
Increased IAP Increased intra thoracic pressure
Reduced venous return
Increased ICP
hypercarbia
Cerebral
vasodilatation
• The decrease in gut perfusion
• increased venous obstruction leading to bowel wall oedema.
leading to bowel ischaemia
• loss of cellular integrity, and translocation of bacteria into the systemic
circulation
Gastrointestinal system
Hepatic blood flow within the hepatic artery, vein, and
portal system is also adversely affected, leading to
mitochondrial dysfunction and eventually liver
dysfunction and failure.
Out line the management of abdominal
compartment syndrome.
Non-surgical
management
surgical
management
Lowering intra abdominal pressure
Organ support
open abdomen
• supine positioning ?? Aspiration
• passing a nasogastric tube
• Enemas, flatus tubes, aperients, and pro-kinetic agents
• endoscopic or percutaneous decompression of the
gastrointestinal tract
• Avoid Coughing, straining, and ventilator dyssynchrony
Lowering intra abdominal pressure
 optimize cardiac output
 target’ abdominal perfusion pressure of 60 mm Hg
 Initial fluid resuscitation should be aimed at restoring normovolaemia.
 inotrope or vasopressor
 Renal replacement therapy may be necessary
 Lung protective strategies
Organ support
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Category 1 Category 2 Category 3 Category 4
Series 1 Series 2 Series 3
Title and Content Layout with Chart
Group 1 Group 2
Class 1 82 95
Class 2 76 88
Class 3 84 90
• First bullet point here
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• Third bullet point here
Two Content Layout with Table
• Task description
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Step 1 Title
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• Task description
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Step 3 Title
Title and Content Layout with SmartArt

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Splanchnic circulation

  • 1. Dr. Dinesh Mannapperu Registrar Anaesthesia TH- Kandy Splanchnic Circulation 24th June 2016
  • 2. • Briefly describe the splanchnic circulation. • What is abdominal compartment syndrome • What are the pathophysiological effects of abdominal compartment syndrome • Out line the management of abdominal compartment syndrome. • Splanchnic circulation in Anaesthesia and critical care. Objectives
  • 3.
  • 4.
  • 5. Briefly describe the splanchnic circulation. 30%
  • 6. • Coeliac artery T12 1. Common Hepatic 2. Left gastric 3. Splenic
  • 7. • Superior mesenteric artery L2 1. Inferior pancreatico duodenal 2. Intestinal arteries 3. Ileocolic 4. Right colic 5. Middle colic
  • 8. • Inferior mesenteric L3 1. Left colic 2. Sigmoid branches 3. Superior rectal SBF about 25-30% of COP 30ml/min/100g ( <10ml/min/100g-250ml/min/100g) Highly adaptive and act as a reservoir of blood
  • 9. Physiological regulation of SBF Intrinsic control Humoral control Extrinsic control Metabolic H+, K+ , adenosine , CO2 , hypoxia Myogenic Mechano sensitive Na+ Channels, Depolarization, Ca2+ channels Sympathetic NS Noradrenaline mediated - adrenergic vasoconstriction Parasympathetic NS Vagal and pelvic nerves M1 mediated NO release Vasodialators Bradykinin, gastrin, secretin, cholecystokinin, substance P, dopamine, Vasoconstrictors Vasopressin, Angiotensin ii, Neuropeptide Y,
  • 10. Disorders of Splanchnic Blood flow 1. Ischemic reperfusion injury 2. Sepsis /gut origin hypothesis 3. Portal hypertention What is abdominal compartment syndrome 5%
  • 11. • Intra Abdominal Hypertention. Normal IA pressure is 5-7mmHg, if it increases more than 12mmHg • Intra Abdominal Compartment syndrome When IA pressure exceeds 20mmHg . • Grade 1 - 12–15 mm Hg; • Grade 2 - 16–20 mm Hg; • Grade 3 - 21–25 mm Hg; • Grade 4 - >25mm Hg. Definitions What is abdominal compartment syndrome 5%
  • 12. 1. Diminished abdominal wall compliance Acute respiratory failure, especially with elevated Intra thoracic pressure Abdominal surgery with subjectively tight primary closure Major trauma/burns Prone positioning, head of bed elevated >30° High BMI, central obesity Causes for IA compartment syndrome
  • 13. 2. Increased intra-luminal contents Gastroparesis Ileus Colonic pseudo-obstruction 3. Increased abdominal contents Haemoperitoneum/ pneumoperitoneum Ascites/liver dysfunction
  • 14. 4. Capillary leak/fluid resuscitation  Acidosis (pH <7.2)  Hypotension  Hypothermia (core temperature <33°C)  Polytransfusion (>10 units of blood/24 h)  Coagulopathy (platelets ,55 000 mm-3, prothrombin time >15 s, partial thromboplastin time 2 times normal, or international standardized ratio >1.5)
  • 15.  Massive fluid resuscitation (>5 litre/24 h)  Pancreatitis  Oliguria  Sepsis  Major trauma/burns  Damage control laparotomy
  • 16. Abdominal Perfusion Pressure = MAP - IAP Measurement of IA pressure
  • 17. 1. Direct methods 2. Indirect methods • Intra-gastric • Intra-uterine • Rectal • Intra-vesicular
  • 18.
  • 19. What are the pathophysiological effects of Abdominal Compartment Syndrome 15%
  • 20. Cardiovascular System • Increase IAP Direct pressure over abdominal vasculature Compression of IVC Compression of Aorta Reduce preload Increase afterload Increase intra thoracic pressure Reduce compliance and contractility Reduce COP Catastrophic intra abdominal ischaemia
  • 21. • basal collapse/atelectasis, • increasing V/Q mismatch • decreased pulmonary and chest wall compliance • increasing hypoxia and hypercarbia • increased inspiratory pressures and PEEP in ventilated pts can further compromise VR and COP Respiratory system
  • 22. •Treatment of intra-abdominal hypertension has been associated with reduced ventilatory days
  • 23. Renal system Reduced GFR Reduced RBF Reduced COPIncresed IAP renal outflow tract
  • 24. FG = ( MAP – IAP ) -PTP Normal PTP=15-18mmHg
  • 25. FG = ( MAP - IAP ) - IAP = MAP - 2IAP If PTP = IAP, then
  • 26. Hormonal effects from activation of the renin/angiotensin system and increased ADH have a further adverse effect.
  • 27. Central nervous system Increased IAP Increased intra thoracic pressure Reduced venous return Increased ICP hypercarbia Cerebral vasodilatation
  • 28. • The decrease in gut perfusion • increased venous obstruction leading to bowel wall oedema. leading to bowel ischaemia • loss of cellular integrity, and translocation of bacteria into the systemic circulation Gastrointestinal system
  • 29. Hepatic blood flow within the hepatic artery, vein, and portal system is also adversely affected, leading to mitochondrial dysfunction and eventually liver dysfunction and failure.
  • 30. Out line the management of abdominal compartment syndrome. Non-surgical management surgical management Lowering intra abdominal pressure Organ support open abdomen
  • 31. • supine positioning ?? Aspiration • passing a nasogastric tube • Enemas, flatus tubes, aperients, and pro-kinetic agents • endoscopic or percutaneous decompression of the gastrointestinal tract • Avoid Coughing, straining, and ventilator dyssynchrony Lowering intra abdominal pressure
  • 32.  optimize cardiac output  target’ abdominal perfusion pressure of 60 mm Hg  Initial fluid resuscitation should be aimed at restoring normovolaemia.  inotrope or vasopressor  Renal replacement therapy may be necessary  Lung protective strategies Organ support
  • 33. 0 1 2 3 4 5 6 Category 1 Category 2 Category 3 Category 4 Series 1 Series 2 Series 3 Title and Content Layout with Chart
  • 34. Group 1 Group 2 Class 1 82 95 Class 2 76 88 Class 3 84 90 • First bullet point here • Second bullet point here • Third bullet point here Two Content Layout with Table
  • 35. • Task description • Task description Step 1 Title • Task description • Task description Step 2 Title • Task description • Task description Step 3 Title Title and Content Layout with SmartArt

Editor's Notes

  1. What is splanchnic circulation- the term SC describes blood flow to abdominal GI organs.
  2. <10ml/min/100g in low COP states 250ml/min/100g after a meal
  3. Causes for non occlusive ischemia Low COP ( septic shock, hypovolemic shock, cardiogenic shock) Abdominaal compartment Xd
  4. When pressure inside a fixed myofascial compartment is increased to a certain level sufficient to compromise perfusion, it is called compartment Xd.
  5. In direct method we introduce needle/line connected to pressure transducer into peritonium
  6. The pressure is transmitted to the glomeruli aswell
  7. The FG is the pressure difference between the abdominal perfusion pressure and the proximal tubular pressure (PTP)
  8. Healing of bowel anastamosis and abdominal wounds is impaired leading to anastomotic and wound breakdown
  9. failure of clotting factor and protein synthesis, increased susceptibility to infection, and encephalopathy. Lactic acid clearance is compromised, making it less useful as a marker of resuscitation and drug metabolism may also be affected, so careful consideration to drug pharmacokinetics and dynamics is needed.
  10. for this reason, adequate sedation is essential and a period of muscular paralysis may be beneficial
  11. There is no clear evidence as to which inotrope or vasopressor should be started as first line, but therapy should be tailored to the individual patient. RRT may be necessary in all patients with clinical and biochemical signs of renal dysfunction.