Shock seminar 2016 anesthesia.........pptx

Shock seminar 2016 anesthesia

1. Shock

2. Definition of shock Pathophysiology of shock Severity of shock Classification of shock Investigation of shock Management of shock Prevention of shock Outline

3. Shock is the most common cause of death of surgical patients. Shock is a state of tissue hypoxia due to either reduced oxygen supply, increased oxygen consumption, inadequate oxygen utilization or a combination of these factors. Definition

4. Physiologic responses to shock are based upon a series of afferent (sensing) signals and efferent responses that include neuroendocrine, metabolic and inflammatory signaling. Cellular : as perfusion to the tissues is reduced, cells are deprived of oxygen and must switch from aerobic to anaerobic metabolism. The product is not carbon dioxide but lactic acid. when enough tissue is under perfused, lactic acid accumulation in the blood produces systemic metabolic acidosis. Pathophysiology

5. As glucose within cells is exhausted, anaerobic respiration ceases and there is failure of sodium/potassium pumps in the cell membrane and intracellular organelles. Intracellular lysosomes release autodigestive enzymes and cell lysis ensues. Intracellular contents like potassium are released into the blood stream.

6. Systemic: there will be several organ specific responses trying to restore the normal perfusion like increased heart and respiratory rate, increased absorption of water and salt and activation of the RAAS system which are regulated baroreceptors , stretch receptors, cerebral ischemic responses and many other factors .

7. Shock can be classified: Compensated shock (Non progressive) As shock progresses the body’s cardiovascular and endocrine compensatory responses reduce flow to non essential organs like muscle, skin and GIT to preserve for the vital organs. The patient will be tachycardic and will have cool peripheries. Severity of shock

8. Decompensation shock(Progressive) This occurs when the compensatory mechanism fails. So there is progressive renal, respiratory and cardiovascular decompensation . Mild shock: mild reduction in urine output, mild anxiety, blood pressure is maintained. Moderate shock: urine output declines, low BP, confusion and drowsiness.

9. Severe shock(Irreversible phase): In severe shock there is profound tachycardia and hypotension. Urine output falls to zero and patients are unconscious with labored respiration.

10. Based on the initiating mechanism: HYPOVOLAEMIC SHOCK Due to reduced circulating volume It can be hemorrhagic or non hemorrhagic The amount of circulating blood in your body may drop due to: vomiting, diarrhea, diuresis, burn and dehydration. hemorrhagic causes are secondary to trauma or injury. Classification of shock

11. A type of hypovolaemic shock which is caused by excessive blood lose that can be internal or external During this shock there is a neuroendocrine response. These response is vital to maintain the perfusion of brain and heart even at the expense of other organs. There will be peripheral vasoconstriction and inhibition of fluid excretion. Hemorrhagic shock

12. Some of the neuroendocrine responses are activation of sympathetic stimulation leading to the release of epinephrine and norepinephrine, activation of RAAS, increased antidiuretic release. In severe blood loss caused by fatal injuries there is a stage called necrobiosis that occurs prior to death characterized by reduced oxygen consumption and body temperature.

13. According to American college of Surgeon’s Advanced Trauma Life Support program, Based on the expected amount of blood lose in 70 kg patient: Class 1: blood loss is up to 15% of the total blood volume Class 2: 15-30% loss of the total blood volume Class 3: 30-40% loss of the total blood volume Class 4: >40% loss of their total blood volume Classes of hemorrhagic shock

14. 2. Cardiogenic shock life-threatening condition in which the heart fails to pump enough blood to meet the body’s needs because of myocardial damage and other factors It is generally characterized by systolic and dystolic dysfunction or impaired cardiac output. Causes of cardiogenic shock can be Myocardial infarction/heart attack due to CHD Slow heart rhythm Cardiomyopathy Cardiac injury Systemic or pulmonary hypertension

15. Reduced cardiac output due to inability of the heart to pump adequate amount of blood in the presence of normal blood volume. PH pulmonary hypertension can strain the right ventricle of the heart, leading to right ventricular failure. Cardiomyopathy stiffness of heart muscle, cause for decrease contractility and cardiac output

16. Clinical presentation Rapid breathing. Severe shortness of breath. Sudden, rapid heartbeat (tachycardia) Loss of consciousness. Weak pulse. Low blood pressure (hypotension) Sweating. Pale skin.

17. 3.Obstructive shock It occurs when blood doesn’t get to where it needs to go. Preload decrease because of mechanical obstruction. Pulmonary embolism one condition that interferes with blood flow. Conditions that build up air or fluid in the chest cavity can also cause it. These may include T ension Pneumothorax Hemothorax Cardiac tamponade

18. Cardiac tamponade cause of unable to fully stretch the myocardium a nd also decrease venous return Tension pneumothorax compress the vena cava

19. Clinical presentation Unusually fast breathing. Hypotension (low blood pressure). Tachycardia (fast heart rate). Altered consciousness. Very little pee output. Cool, clammy skin. Chest pain Dilated neck vain

20. 4.Distributive shock Is explained by conditions that cause blood vessels lose their tone and increase their permeability. Further divided into Anaphylactic shock Neurogenic shock Septic shock

21. Anaphylactic shock Anaphylaxis is severe immune reaction of the body to potentially harmless bodies generally called allergen. Allergen can be food, medications, insect venom and any other foreign body. When allergen gets in our body naive B cells recognize it and present it to T helper cells through and T helper cell activates them through IL4.

22. B cells upon stimulation of T helper cells differentiate to plasma cells that are capable of producing antibody and they produce the IgE antibody. IgE will go to mast cells and mast cell recognizes and on the second exposure it degranulates releasing histamine, prostaglandin, heparin and many other mediators. These mediators cause vasodilation, bronchospasm and increased vascular permeability.

23. Clinical presentation skin reactions such as hives, flushed skin, or paleness Hypotension Bronchospasm Tachycardia Confusion dizziness

24. Neurogenic shock Characterized by massive vasodilation leading to blood pooling secondary to spinal cord injury. Causes can be spinal cord trauma, spinal cord neoplasm, spinal anaesthetics and traumatic brain injury. In simple terms, the trauma causes a sudden loss of background SNS stimulation to the blood vessels. This causes them to relax (vasodilation) resulting in a sudden decrease in blood pressure (secondary to a decrease in peripheral vascular resistance).

25. Clinical presentation Bradycardia Cyanosis Hypotension Lack of full consciousness

26. Septic shock R esults from arterial vasodilation and venous blood pooling that stems from the systemic immune response to microbial infection. The decreased vascular tone is accompanied by widespread endothelial cell activation, often triggering a hypercoagulability state manifesting as disseminated intravascular coagulation . In addition, septic shock is associated with perturbations of metabolism that directly suppress cell and tissue function. The net effect of these abnormalities is hypo perfusion and dysfunction of multiple organs .

27. Clinical presentation Hypotension Confusion Pale skin Tachycardia Tachypnea

28. Sepsis Normally immune reactions to pathogens should be localized. Sepsis is a life-threatening reaction to an infection. It happens when your immune system overreacts to an infection and starts to damage your body's own tissues and organs. You cannot catch sepsis from another person. Sepsis is sometimes called septicemia or blood poisoning.

29. Sepsis is a serious condition in which the body responds improperly to an infection. The infection-fighting processes turn on the body, causing the organs to work poorly. Sepsis may progress to septic shock. This is a dramatic drop in blood pressure that can damage the lungs, kidneys, liver and other organs. When the damage is severe, it can lead to death.

30. Risk factors Some factors that increase the risk infection will lead to sepsis include: People over age 65. Infancy. People with lower immune response, such as those being treated for cancer or people with HIV. People with chronic diseases, such as diabetes, kidney disease or COPD. Admission to intensive care unit or longer hospital stays. Devices that go in the body, such as catheters in the vein, called intravenous, or breathing tubes. Treatment with antibiotics in the last 90 days. A condition that requires treatment with corticosteroids, which can lower immune response.

31. The infections that cause sepsis can be bacterial which are encountered in most of the cases, viral infections like COVID-19 or fungal infections. These infections are most often associated with sepsis: Lung infections (pneumonia) Urinary tract infections Skin infections Infections in the intestines or gut

32. These bacterial agents most frequently develop into sepsis are Staphylococcus aureus (staph) Escherichia coli (E. coli) Some types of Streptococcus

33. Severe sepsis occurs when one or more of your body’s organs is damaged from this inflammatory response. Any organ can be affected, the heart, brain, kidneys, lungs, and liver. The symptoms experienced are based on which organ or organs that are affected.

34. Sepsis-related organ dysfunction Respiratory failure Liver failure Kidney failure Heart failure Gut permeability DIC (disseminated intravascular coagulation) Altered mental status Brain death

35. SIRS Systemic inflammatory response syndrome Systemic inflammatory response syndrome (SIRS) is an inflammatory state affecting the whole body. It is the body's response to an insult. Although the definition of SIRS refers to it as an "inflammatory" response, it actually has pro- and anti-inflammatory components. Feared complications are acute renal failure, shock and multiple organ dysfunction syndrome which is also end result of septic shock.

36. The causes of SIRS are broadly classified as infectious or noninfectious. Causes of SIRS include bacterial infections Severe malaria Trauma Burns Pancreatitis Ischemia Hemorrhage Other causes includ e Complications of surgery Adrenal insufficiency Pulmonary embolism Complicated aortic aneurysm Cardiac tamponade Anaphylaxis Drug overdose

37. Sepsis is an infection which has evoked a systemic inflammatory response while SIRS is the inflammatory response given by the body for the infectious or non infectious insult. Sepsis= SIRS + Infection

38. Prophylaxis in sepsis patients Generally to prevent formation DVT (deep venous thrombosis) and VTE ( venous thromboembolism) anticoagulant prophylaxis is given usually heparin (LMWH). But the amount of anticoagulant given should be i n low doses to prevent bleeding and thrombocytopenia. The other is GI prophylaxis to prevent stress ulcer which are multiple and superficial erosions that mainly appear at the fundus and body of the stomach and they result in GI bleeding.

39. We may use several medications like proton pump inhibitors and histamine receptor blockers. Nutritional support is also one thing to be considered The enteral route is preferable but if it is impossible or not tolerated nutrition can be given parentally. Associated with sepsis there is severe catabolism resulting in waste of lean body mass, immune dysfunction and compromised wound healing to prevent these complications nutritional prophylactic therapy is the cornerstone. Generally proteins and calories are given. Omega-3 polyunsaturated fatty acids to modulate metabolic processes can be safely used.

40. Investigations of shock Blood tests To evaluate extent of blood lose Infections in blood To detect allergens Imaging To look at organ injuries Bone fractures associated to trauma Chest x ray, ultrasound , MRI and CT can be used.

41. ECG to detect abnormalities of heart. Chest x ray to look at size and shape of the heart and whether there is fluid in the lungs. Trauma ultrasound: FAST (focused assessment with sonography for trauma. Urine tests Hemodynamic tests Serum lactate

42. Management of shock First aid Lay the patient down Begin CPR Treat obvious injury Make patient warm and comfortable. Take patient to the hospital. Generally first aiders expected to support critically ill patients of their ABC. airway, breathing and circulation.

43. At the hospital General management strategies are ensuring patent airway and maximizing oxygen delivery. Cornerstone therapy for shock is volume expansion achieved by providing isotonic crystalloids like normal saline for initial resuscitation of shock. If patient doesn’t respond to 2-3 litres of crystalloids blood should be instituted Major complications of fluid resuscitation are hypothermia and coagulopathy.

44. Drug therapy also applied to correct tissue perfusion. Vasopressor drugs like epinephrine to correct systemic vasodilation in case of septic, anaphylactic and neurogenic shock. But reserved for patients unresponsive to other treatments. Vasodilator drugs like nitroglycerin for cardiogenic shock and nitroprusside for non cardiogenic shock are used to increase tissue perfusion.

45. Nutritional therapy is also essential as it decreases morbidity secondary to shock so should be started in the first 24 hours. The enteric way is best but if it fails use parenteral one. Cardiogenic shock Restore blood flow to the myocardium by restoring the balance between O2 supply and demand Thrombolytic therapy Angioplasty with stenting Emergency revascularization Valve replacement

46. Hypovolemic shock Management focuses on stopping the loss of fluid and restoring the circulating volume Fluid replacement is calculated using a 3:1 rule (3 ml of isotonic crystalloid for every 1 ml of estimated blood loss) Septic shock Fluid replacement (e.g., 6 to 10 L of isotonic crystalloids and 2 to 4 L of colloids) to restore perfusion Vasopressor drug therapy; vasopressin for patients refractory to vasopressor therapy

47. Antibiotics after obtaining cultures (e.g., blood, wound exudate, urine, stool, sputum) Drotrecogin alfa ( Xigris ) Major side effect: Bleeding Glucose levels <150 mg/dl Stress ulcer prophylaxis with histamine (H2)-receptor blockers Deep vein thrombosis prophylaxis with low-dose unfractionated heparin or low-molecular-weight heparin

48. Neurogenic shock In spinal cord injury: Spinal stability Treatment of the hypotension and bradycardia with vasopressors and atropine Fluids used cautiously as hypotension is generally not related to fluid loss Monitor for hypothermia

49. Anaphylactic shock Epinephrine, diphenhydramine Maintaining a patent airway Nebulized bronchodilators Endotracheal intubation or cricothyroidotomy may be necessary . While managing all these things it is important not to forget monitoring.

50. Prevention If you’ve been diagnosed with severe allergies, avoid your triggers, carry an epinephrine auto-injector, and use it at the first sign of an anaphylactic reaction. To lower your risk of blood loss from injuries, wear protective gear when taking part in contact sports, riding your bike, and using dangerous equipment. Wear a seatbelt when traveling in motor vehicles. To lower your chances of heart damage, eat a well-balanced diet, exercise regularly, and avoid smoking and secondhand smoke.

51. p reventing infections with good and consistent hygiene and avoiding people with infections. Other infections can be prevented through the use of vaccinations.

52. References Bailey 27 th edition Sabiston text book of surgery 21th edition Schwartz’s principles of surgery 11 th edition ATLS 10 th edition update The Internet