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Stress Ulcer(2009)

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stress ulcer

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Stress Ulcer(2009)

  1. 1. Stress Ulcer Tianjin medical university general hospital Songtao shou
  2. 2. sex :male age: 75y chief complaints : cough,gasp and spitting for 10 days,fever for 3 days. lethargy for 1 day . past history : COPD for 10 years. After admission to ICU,we found his stools were dark stools. ( no history of peptic ulcer.) Symptoms :cough, expectoration, gasp and fever,without abdominal pain . laboratory examination : ABG:pH 7.40,PaO 2 50mmHg ,PaCO 2 80mmHg Chest x-ray : Diagnosis : COPD , respiratory failure, pneumonia
  3. 3. lung markings
  4. 4. What should we do next?
  5. 5. laboratory examination 1. BRT:WBC 15×10 9 /L,N 90%,Hb140g/L,PLT 300×10 9 /L . 2.ABG:pH 7.40,PaO 2 50mmHg ,PaCO 2 80mmHg 3.stool :OB(++++), WBC(-),RBC(3/hp) the occult blood is positive after admission for 24 hours.
  6. 6. Diagnosis ? <ul><li>1.Respairatory failure </li></ul><ul><li>2.Bleeding of gastrointestinal </li></ul><ul><li>Peptic ulcer </li></ul><ul><li>Acute bacillary dysentery </li></ul><ul><li>Stress ulcer syndrome </li></ul>
  7. 7. Therapy? 1 . positively correct the primary disease. 2. Antiacides(Omeprazole) 3. Cytoprotection( Sucralfate) 4. H 2 recepter antagonist(cimetidine) 5. enteral feeding
  8. 8. contents <ul><li>Definition of stress ulcer syndrome </li></ul><ul><li>Etiology of stress ulcer syndrome </li></ul><ul><li>Characters of stress ulcer syndrome </li></ul><ul><li>Characters of peptic ulcer </li></ul><ul><li>Pathophysiology of stress ulcer </li></ul><ul><li>Diagnosis of stress ulcer syndrome </li></ul><ul><li>Treatment of stress ulcer </li></ul><ul><li>Prophylaxis of stress ulcer </li></ul><ul><li>insight </li></ul>
  9. 9. Stress? <ul><li>To subject to physical or mental pressure, tension, or strain. </li></ul><ul><li>In medicine,stress refers to physical or psychological trauma. </li></ul>
  10. 10. fight or flight
  11. 11. LC-sympathetic nerve-adrenal medullar Stress neuroendocrine Cell fluid H-P-A system Other hormones AP HSP Cytokine enzyme
  12. 12. <ul><li>diseases stress </li></ul>neuroendocrine Cell,body fluid hypermetabolism Cell , tissue , organ and system dysfunction
  13. 13. Change from gene to whole body Clinical expression of stress reaction
  14. 14. LC cerebrum brainstem Spinal cord adrenal kidney LC-Sympathetic-adrenal gland medullar
  15. 15. LC
  16. 16. Main effects <ul><li>CNS —— </li></ul>Brain Adr-N stressor PVN CRH excite 、 alert ; nervous 、 anxious Active HPA axis ② ①
  17. 17. 1 catabolize glycogen and fat , 2 HR  ,BP  , 3 redistribution of blood to ensure the supply of main organs. 4 dilate bronchi,oxygen supply <ul><li>Periphery effects: CA  </li></ul>defense
  18. 18. <ul><li>1.organ ischemia </li></ul><ul><li>2.hypertension </li></ul><ul><li>3.thrombosis </li></ul><ul><li>4.oxygen expenditure </li></ul>Adverse effects
  19. 19. stressor CRH↑ ACTH↑ GC↑ Cerebral cortex and limbic system 、 amygdaloid body 、 hippocamp Hypothalamus-pituitary-adrenal
  20. 20. Main effects <ul><li>(1)CNS </li></ul>stressor PVN CRH ↑ ACTH↑ control behaviour and feeling—— eustress:euphoria distress:anxious 、 depression hypoxia Amygdaloid body endorphin ↑ LC-NE axis
  21. 21. (2)Periphery effects GC ↑ >25~37mg/d <ul><li>1.Blood glucose ↑ </li></ul><ul><li>2.Sustain reactivity of circular system to catecholamine. </li></ul><ul><li>3.anti-inflammation,anti-sensitivity 、 stable lysosome membrane </li></ul>
  22. 22. Adverse effects of GC↑ <ul><li>1.inhibit immunity </li></ul><ul><li>2.inhibit develope </li></ul><ul><li>3.behavior abnormal </li></ul><ul><li>4.inhibit sex axis and thyroid axis </li></ul><ul><li>5.change metabolism </li></ul>
  23. 23. Other hormones <ul><li>1 glucagon↑ , insulin↓ </li></ul><ul><li>2 ADH↑ </li></ul><ul><li>3  -endorphine↑ </li></ul><ul><li>4 sex hormone and thyroxine↓ </li></ul>Other hormones
  24. 24. Reaction of cell and body fluid Cell AP HSP Some enzymes Some cytokines stressors                          
  25. 25. stressors Sympathetic nerve-adrenal medullar  CA  H-P-A active  GC  ALD 、 ADH 、 Endopeptide,ect  Insulin  Neuroendocrine change AP  HSP  Metabolic change summary
  26. 26. Several concepts <ul><li>1. stress disease </li></ul><ul><li>The disease is caused all by stress.eg:stress ulcer </li></ul><ul><li>2. stress related disease </li></ul><ul><li>the disease is related to stress.eg:CAD 、 PH or asthma </li></ul>
  27. 27. Stress ulcer
  28. 28. Ulcer? <ul><li>A lesion of the mucous membrane that is accompanied by edema and necrosis of surrounding tissue, usually resulting from inflammation. </li></ul><ul><li>It achieves to the muscularis mucosa. </li></ul>
  29. 29. What is stress ulceration? <ul><li>Stress ulceration is a gastrointestinal mucosal injury related to critical illness. </li></ul><ul><li>The ulceration may vary from diffuse superficial injuries to deep hemorrhaging ulcerations. </li></ul>
  30. 30. Why is it important? <ul><li>There is a relationship between severity of disease and incidence of ulceration </li></ul><ul><li>A GI bleed may be a marker of the patient’s condition </li></ul>
  31. 31. Stress ulcer syndrome(SUS) <ul><li>It is the acute changes confined to the gastric mucosa under the condition of physiologic or psychological stress.the mucosal lesion and associated clinical bleeding or perforation have been termed SUS. </li></ul>
  32. 32. sus <ul><li>It was introduced by Hans Selye in 1936 to describe the association between psychosomatic illness and peptic ulcer. </li></ul><ul><li>The incidence of stress ulcer ranges from 20% to 100% in ICU (Intensive care unit) patients. </li></ul>
  33. 33. What causes it? <ul><li>Ulceration is caused by ischemic injury to the gastric mucosa, loss of cytoprotectants and assault by gastric acid. </li></ul><ul><li>The mucosa is injured and cannot repair itself sufficiently well to ward off aggressive factors present in the gut lumen (these aggressors include gastric acid, bile and digestive enzymes. ) </li></ul>
  34. 34. Stress Ulceration Risk Factors <ul><li>The major risk factors are respiratory failure, coagulopathy, sepsis, hypotension and hepatic and renal failure. </li></ul><ul><li>there is a good relationship between severity of illness (as determined by, for example, APACHE II scores) and incidence of ulceration. </li></ul><ul><li>Moreover, the longer a patient in ICU, the more likely they are to have a GI bleed . Patients who are likely to have a number of these risk factors – burns patients for example (ventilated, hypotensive, coagulopathic), are more likely to have ulceration and bleeding. </li></ul>
  35. 35. Pathogenesis of stress ulcer stress ulcer syndrome appears to be mucosa ischemia resulting form splanchnic hypofusion in the setting of physiologic stress and an acid
  36. 36. ( 1 ) mucosa ischemia ( 2 ) H + diffuse to intramucosa ( 3 ) others : acidosis CA  Mucosa barrier  H + diffuse to intramucosa Blood flow  H + pump out  ulcer GC  stressor Mucosa ischemia
  37. 37. Gastric mucosal circulation <ul><li>Disproportionate vasoconstrictor response to stress </li></ul><ul><ul><li>Neural nor-adrenaline and circulating adrenaline have similar effects on vasoconstriction in gastric mucosal and systemic vascular beds </li></ul></ul><ul><ul><li>Renin-angiotensin system and to a lesser degree vasopressin are responsible for the disproportionate response. </li></ul></ul>
  38. 38. The mucosa is compromised by ischemia and attacked (mostly) by acid. It is injured, and, due to the presence of acid, cannot repair itself (hostile environment). The use of external agents to neutralize acid resolves this problem.
  39. 39. Diagnosis of sus <ul><li>Symptom most patients have no symptoms. Abdominal pain and perforation are rare. </li></ul><ul><li>Body signs </li></ul><ul><li>Lab test Positive occult blood in both vomitus and melena,these lesions have been found with endosocopy as early as 5h after ICU admission and most will be evident within 72h. </li></ul><ul><li>Endoscopy:Commonly mucosal erosions are found in the fundus or acid secreting parts of the stomach . </li></ul>
  40. 40. Important sources of OB error <ul><li>False –positive </li></ul><ul><li>Cimetidine </li></ul><ul><li>pH=2~4 </li></ul><ul><li>Red meat </li></ul><ul><li>Horseradish </li></ul><ul><li>Raw turnips </li></ul><ul><li>Apple,orange,banana </li></ul><ul><li>False –negative </li></ul><ul><li>Antacids </li></ul><ul><li>pH<2 </li></ul><ul><li>Vitamine C </li></ul>
  41. 41. <ul><li>characters </li></ul><ul><li> acute </li></ul><ul><li> multi , superficial </li></ul><ul><li> easy to heal ; bleeding and perforation are seldom </li></ul>
  42. 42. Differences between PU and SU Endoscopic barium meal and endoscope diagnose Abdominal pain, Bleeding and Perforation are unusual Abdominal pain,perforation and bleeding Signs and symptoms Multiple Single or two Ulceration cardia ,fundus and body antrum Location acute chronic Attack SU PU
  43. 43. The mucosa plica in the gastric body is smooth.
  44. 44. Before making gastroscope,we have to fulfill the stomach with enough air,so under gastroscope the mucosa is very smooth.pylorus is round and always in contraction.
  45. 45. Mucus lake
  46. 46. thrombosis Peptic ulcer + complication (Bleeding)
  47. 47. Minal clot
  48. 48. petechia
  49. 49. Treatment Strategy <ul><li>Patients who do not have one of the six major risk factors do not require treatment. </li></ul><ul><li>Patients in shock, sepsis, respiratory, hepatic or renal failure, or who have a coagulopathy, who are admitted to intensive care, should all be given stress ulcer prophylaxis. </li></ul>
  50. 50. The goal of therapy Stress ulcers are not deep craters like those seen in peptic ulcer disease,but are superficial erosions confined to the surface of the mucosa.Therefore, the goal of therapy is not so much to prevent their appearance but to limit the incidence of troublesome bleeding.
  51. 51. <ul><li>Da huang </li></ul>
  52. 52. Principle of Treatment <ul><li>Cytoprotection(Sucralfate) </li></ul><ul><li>H 2 recepter antagonist(cimetidine) </li></ul><ul><li>Antiacides(losec) </li></ul><ul><li>Surgery therapy </li></ul><ul><li>Enteral feeding </li></ul>
  53. 53. <ul><li>Ranitidine and sucralfate are the most effective agents. Ranitidine is associated with a lower incidence of clinically significant bleeding, sucralfate with a lower incidence of pneumonia. </li></ul>
  54. 54. Principle of enteral feeding 1. To neutralize gastric pH(to dilute the relatively acid enviroment) 2. To provide the cells of the gastric mucosa with a nutrient.the cells may use luminal nutrients as a source of energy to produce the protective surface lining. 3. It solves the problems of nutrition and stress ulcer prophylaxis.
  55. 55. Prophylaxis of stress ulcer <ul><li>Enteral feedings </li></ul><ul><li>Control of the gastric PH </li></ul><ul><li>Cytoprotection </li></ul><ul><li>Hemodynamatic management </li></ul><ul><li>Oxygen supplement </li></ul>
  56. 56. Prophylaxis <ul><li>prophylaxis for SUS should be confined to carefully selected at-risk patients </li></ul><ul><li>Stress ulcers are often present within hours of admission to an intensive care unit.So,to a certain extent ,it is more important to prophylaxis stress ulcers than to treat them. </li></ul>
  57. 57. Importants <ul><li>Etiology and risk factors of sus </li></ul><ul><li>Characters of sus </li></ul><ul><li>Prophylaxis of sus </li></ul>
  58. 58. SUS are often viewed as a primary illness instead of a signal for mucosal ischemia . The misconception has created some confusion about the appropriate therapy for stress ulcers and specifically about the role of gastric acid suppression therapy.through the chapter ,we know stress ulcers are a manifestation of mucosa ischemia and NOT a manifestation of gastric hyperacidity.
  59. 59. insight <ul><li>Ulcer achieves to the muscularis mucosa </li></ul><ul><li>Stress ulcers are confined the gastric mucosa </li></ul><ul><li>So ,stress ulcers are not the real ulcers </li></ul>
  60. 61. THANK YOU