SHOCK shock, types of shock and management.

shock, types of shock and management.

1. SHOCK Dr shitu hauwa

2. Shock A state of cellular and tissue hypoxia with either reduced oxygen delivery or poor oxygen utilisation or increased oxygen consumption with circulatory failure (collapse) and poor perfusion. cells switch from aerobic to anaerobic metabolism If perfusion is not restored in time, cell death ensues. Shock is meant by 'inadequate perfusion' to maintain normal organ function. Dr Shitu.Hauwa.

3. Pathophysiology Cellular: In reduced tissue perfusion, cells must switch from aerobic to anaerobic metabolism. The product of anaerobic respiration is lactic acid. Accumulation of LA produces a systemic metabolic acidosis . As glucose within cells is exhausted, anaerobic respiration ceases, there is failure of Na+/k+ pumps in the cell and organelles. Intracellular lysosomes release autodigestive enzymes and lysis ensues. Intracellular contents, including k+ are released into the blood stream. Dr Shitu.Hauwa.

4. Microvascular: As tissue ischaemia progresses, changes in the local milieu result in activation of the immune and coagulation systems . Hypoxia and acidosis activate complement and prime neutrophils, resulting in the generation of oxygen free radicals and cytokine release . These leads to injury of the capillary endothelial cells . Damaged endothelium loses its integrity and becomes ‘leaky’. fluid leak out and tissue oedema ensues, exacerbating cellular hypoxia . Dr Shitu.Hauwa.

5. Systemic Cardiovascular: As preload and afterload decrease, there is a compensatory baroreceptor response resulting in increased sympathetic activity and release of catecholamines into circulation. This results in tachycardia and systemic vasoconstriction (except in sepsis). Respiratory: The metabolic acidosis and increased sympathetic response result in an increased RR and minute ventilation to increase the excretion of CO2 (and so produce a compensatory respiratory alkalosis ). Dr Shitu.Hauwa.

6. Renal : Decreased perfusion pressure in the kidney leads to reduced GFR and a decreased urine output.The RAAS axis is stimulated, resulting in further vasoconstriction and increased sodium and water reabsorption by the kidney Endocrine : As well as activation of the adrenal and RAAS, vasopressin is released,results in vasoconstriction, Cortisol is also released contributing to the Na/water resorption and sensitizing the cells to catecholamines . Dr Shitu.Hauwa.

7. Dr Shitu.Hauwa.

8. Ischemia–reperfusion syndrome During systemic hypoperfusion , cellular/organ damage progresses due to effects of tissue hypoxia and local inflammation. Further injury occurs once normal circulation is restored to these tissues . The acid and K+ built up can lead to direct myocardial depression, vasodilatation and further hypotension . The elements activated by the hypoxia ( complement, neutrophils, microvascular thrombi ) are flushed back Into the circulation causing further injury, ALI, AKI, MODS and death. “Reperfusion injury can currently only be attenuated by reducing extent and duration of tissue hypoperfusion .” Dr Shitu.Hauwa.

9. CLASSICFICATION HYPOVOLEMIC SHOCK CARDIOGENIC SHOCK DISTRIBUTIVE SHOCK OBSTRUCTIVE SHOCK ENDOCRINE SHOCK Dr Shitu.Hauwa.

10. HYPOVOLEMIC SHOCK Loss of blood – hemorrhagic shock. Loss of plasma – as in burns shock Loss of fluid – dehydration as in gastroenteritis or ‘third-spacing’ Dr Shitu.Hauwa.

11. Hypovolemia is the most common form of shock. It is due to a reduced circulating volume. Hypovolemia may be due to hemorrhagic or non- haemorrhagic causes. The primary problem is a decrease in preload which causes a decrease in stroke volume. Clinical features depend on the degree of hypovolemia. Dr Shitu.Hauwa.

12. Dr Shitu.Hauwa.

13. Treatment Replace the lost blood volume. Primary goal = restore tissue perfusion & oxygenation ASAP. Crystalloids: If crystalloids are used to replace blood loss, 2–3 times the volume lost needs to be given R/L =crystalloid of choice.  Saline = Large volumes infusion can cause hyper chloraemic metabolic acidosis. 5% dextrose is not used to expand the intravascular volume as it is hypotonic once the dextrose is metabolised . If large volume of blood is lost, transfuse blood products. Dr Shitu.Hauwa.

14. Hemorrhage I. Depending on Nature of the Vessel Involved A. Arterial haemorrhage : Bright red in colour , jets out. Pulsation of the artery can be seen. It can be easily controlled, as it is visible. B. Venous haemorrhage C. Capillary haemorrhage Dr Shitu.Hauwa.

15. II. Depending on the Timing of Haemorrhage A . Primary hemorrhage: Occurs at the time of surgery B. Reactionary haemorrhage : Occurs after 6–12 hours of surgery. Hypertension in the postop period, violent sneezing, coughing or retching, are the usual causes, e.g . superior thyroid artery can bleed after thyroidectomy, if the ligature slips. Hence, it is better to ligate it twice. C. Secondary haemorrhage : Occurs after 5–7 days of surgery. It is due to infection. Dr Shitu.Hauwa.

16. V. Depending on the Nature of Bleeding A. External haemorrhage /revealed haemorrhage , e.g. epistaxis, haematemesis . B. Internal haemorrhage /concealed haemorrhage , e.g. splenic rupture, ruptured ectopic gestation, liver laceration following injury Dr Shitu.Hauwa.

17. III. Depending on the Duration of Hemorrhage A. Acute hemorrhage: Occurs suddenly, e.g. esophageal variceal bleeding due to portal hypertension. B. Chronic hemorrhage: Occurs over a period of time, e.g. hemorrhoids/piles or chronic duodenal ulcer, tuberculous ulcer of the ileum, diverticular disease of the colon Dr Shitu.Hauwa.

18. PATHOPHYSIOLOGY OF HAEMORRHAGIC SHOCK A loss of more than 30–40% blood volume results in a fall in blood pressure and gross hypoperfusion of the tissues/vital organs leading to haemorrhagic shock. The evolution of haemorrhagic shock can be classified into four stages Dr Shitu.Hauwa.

19. Class I - M ild hemorrhage. • Blood loss less than 750 ml ( <15% of blood volume) • When there is blood loss, peripheral vasoconstriction compensates by shifting some blood into the central circulation. With withdrawal of fluid from the interstitial spaces. • Hence mild tachycardia and thirst, may be the only symptom or sign suggesting hypovolemia, Vitals, urine output and Mentation are all normal in Class I. Dr Shitu.Hauwa.

20. Class II • Loss of 800–1500 ml ( 15–30% of blood volume) • Peripheral vasoconstriction may not be sufficient. Hence, adrenaline and noradrenaline (catecholamine's) are released to cause powerful vasoconstriction • ADH causes retention of water and salt, thirst increases. • Clinically, HR of 100–120 b/m and elevated DBP , The SBP may remain normal. Urine output is ≤ 0.5 ml/kg/h , cap refill > 2 seconds. Extremities pale and patient is confused and thirsty . Dr Shitu.Hauwa.

21. Class III • Loss of 1500–2000 ml ( 30–40% of blood volume) produces Class III shock. All the signs and symptoms of Class II hemorrhage get worse. • SBP n DBP ↓ fall and the HR increases to > 120 b/m. • Pulse is thready. • Resp rate ↑ to > 20/m. • Urine output drops to 10 to 20 ml/hr. • The patient appears pale and is aggressive, drowsy or confused. Dr Shitu.Hauwa.

22. Class IV • A blood loss of more than 2000 ml (>40% of blood volume) The peripheries are cold and ashen, BPs are very low or unrecordable . • If persistent, can damage other organs, e.g. – Mucosal ulcerations, upper GI bleeding, bacteraemia – Liver: Reduced clearance of toxins – Kidney: Acute renal failure – Heart: Myocardial ischaemia , depression – Lungs: Acute lung Injury MOD associated with a high mortality rate. Dr Shitu.Hauwa.

23. MANAGEMENT OF HAEMORRHAGIC SHOCK I. Treatment—General Measures Hospitalisation Immediate resuscitation, and control of haemorrhage • O-M-IV: Firstly, provide Oxygen, attach a Monitor to record vitals and obtain two large bore IV Access. Blood sample For investigations, blood grouping and cross matching should be sent at this stage. Dr Shitu.Hauwa.

24. Two large peripheral lines (18 or 16 G) are preferred for initial resuscitation and intravenous fluids, preferably at 40–42°C (crystalloids—saline, Ringer lactate or plasmalyte ) infused very quickly to restore volume. NO IV access???, intraosseous needle can be inserted It may be necessary to activate massive transfusion protocol (when available at the hospital) In an actively bleeding patient who is also in hypovolaemic shock, the ratio of packed cells: fresh frozen plasma : platelets would be 1:1:1. Dr Shitu.Hauwa.

25. In cases of unachieved hemostasis, volume infusion should be controlled to maintain systolic BP at 80–90 mmHg till the bleeding can be stopped. This is called ‘hypotensive fluid resuscitation’ or ‘permissive hypotension’. fibrinolytic like tranexamic acid 1g stat and 8hrly is advised to reduce bleeding . Once bleeding is controlled, infuse volume to allow BP to reach normal levels ( first phase of resuscitation ). Recent data in trauma patients suggest that (SBP) of < 110 mmHg is a clinically relevant definition of hypotension and Hypoperfusion . Dr Shitu.Hauwa.

26. The second phase of resuscitation involves Continuation of fluid therapy to ensure base deficit is eliminated, and microcirculation is normal, this should happen within 12–24 hours. • It is VERY important to maintain the patient warmth. Hypothermia impairs coagulation,increases bleeding, depresses respiration, circulation as well as increases chances of infection. • Use of inotropes and vasoconstrictors is not indicated as they may harm tissue perfusion. Dr Shitu.Hauwa.

27. II. Treatment—Specific Measures Control Haemorrhage 1. Pressure and packing • Method of choice to stop bleeding when the bleeding site is accessible. 2. Position and rest. 3. Tourniquets • Reduction of fractures • When a bloodless field is desired during surgery Contraindications: Patient with peripheral vascular disease. Dr Shitu.Hauwa.

28. Cardiogenic Shock Cardiogenic shock is defined clinically as circulatory pump failure leading to diminished forward flow and subsequent tissue hypoxia , in the setting of adequate intravascular volume . Hemodynamic criteria include; Sustained hypotension (SBP <90 mmHg for at least 30 minutes), Reduced cardiac index(<2.2 L/min per square meter) Elevated pulmonary artery wedge pressure (>15 mmHg). Mortality rates of 50% to 80%. commonly seen in MI Dr Shitu.Hauwa.

29. FEATURES Decrease in heart contractility → decrease in stroke volume → Left ventricular pressures rise as forward CO reduces. The sympathetic nervous system is activated and consequently, SVR increases. • Tachycardia, low BP and ↓ urine output. • The JVP may be raised, with S3 or S4 gallop. • The lungs, bilateral extensive crepitation due to pulmonary edema. • Cold peripheries, patient may be confused or moribund Dr Shitu.Hauwa.

30. Diagnosis is established by: ECG, echocardiography. Arterial blood gas analysis. cardiac enzymes. PCWP (Pulmonary artery wedge pressure >15 mmHg) Electrolyte estimation ( hypokalemia,hypomagnesaemia are common) Dr Shitu.Hauwa.

31. TREATMENT Oxygenation with intubation , cardioversion, pacing, antiarrhythmic drugs, correction of electrolytes, avoiding fluid overload, prevention of pulmonary oedema as immediate measures. Dobutamine (B1 receptor agonist) is used to raise CO provided there is adequate preload and intravascular volume Anticoagulants and aspirin are given. Intra-aortic balloon pump (IABP) Percutaneous transluminal coronary angioplasty (PTCA) and coronary artery bypass graft (CABG) are the final choices. Dr Shitu.Hauwa.

32. Cardiac Compression Shock It is probably due to pericardial tamponade of any cause or kinking of great vessels, massive PE, tension pneumothorax , air embolism causes obstructive shock with reduced preload to heart. Acute massive PE from a thrombus or an air embolism (50 ml of air), obstructing more than 50% pulmonary vasculature leads to severe shock and sudden death. Tachycardia, hypotension, pulmonary oedema , raised JVP, gallop rhythm are the features Dr Shitu.Hauwa.

33. DISTRIBUTIVE SHOCK In distributive shock, the afterload is excessively reduced affecting circulation. Inadequate organ perfusion is accompanied by vascular dilatation with hypotension , low systemic vascular resistance , inadequate afterload and a resulting abnormally high cardiac output . Distributive shock can occur in the following situations: • Septic shock • Anaphylactic shock • Neurogenic shock • Acute adrenal insufficieny Dr Shitu.Hauwa.

34. Septic Shock Pathophysiology • Sepsis is the response of host to bacteraemia / endotoxaemia . •Produced by gram-/+ bacteria,viruses,fungi or protozoal infections. •can result in persistent hypotension despite adequate fluid resuscitation= septic shock. • Local inflammation and endotoxins, activate neutrophils, monocytes and tissue macrophages. This results in a cascade of proinflammatory and anti-inflammatory cytokines and other mediators, such as IL-1, IL-8, IL-10, TNFa , PgE , endogenous corticosteroids and catecholamines . Dr Shitu.Hauwa.

35. Dr Shitu.Hauwa.

36. Features • Persistent hypotension. • Generalized tissue hypoperfusion • Early phase, Dry mucous membranes, cool and clammy skin • After fluid resuscitation,clinical picture is consistent with hyperdynamic shock. This includes tachycardia, bounding pulses with a widened pulse pressure, a hyperdynamic precordium on palpation and warm extremities. Dr Shitu.Hauwa.

37. • Signs of possible infection will depend on the source of sepsis. These may include fever, localized erythema or tenderness, consolidation on chest examination, abdominal tenderness, guarding, rigidity and meningismus . • Signs of end-organ hypoperfusion include tachypnoea , cyanosis, mottling of the skin, digital ischaemia , oliguria and altered mental status. Dr Shitu.Hauwa.

38. Stages of septic shock Hyperdynamic (warm) shock: This stage is reversible stage. Patient is still having inflam matory response = fever, tachycardia, and tachypnea. Pyrogenic response is still intact. Patient should be treated, Based on blood/urine culture, Treat the underlying cause like draining the pus, laparotomy for peritonitis etc. Ventilatory support with ICU monitoring may prevent the patient going for the next cold stage of sepsis. Dr Shitu.Hauwa.

39. Hypodynamic hypovolaemic septic shock (cold septic shock) Here pyrogenic response is lost. Patient is in decompensated shock. It is an irreversible stage along with MODS ( multiorgan dysfunction syndrome) with anuria, respiratory failure ( cyanosis ), jaundice ( liver failure ), cardiac depression , pulmonary oedema , hypoxia, drowsiness, eventually coma and death occurs (Irreversible stage). Dr Shitu.Hauwa.

40. Treatment Removal of the septic focus e.g. resection of gangrenous bowels, appendicectomy . Early empirical antibiotic therapy oxygenation Intravenous fluids. If anaemic , blood transfusions to raise the patient’s haemoglobin levels at 8–10 g%. Vasoactive agents, such as norepinephrine to produce vasoconstriction and raise the systemic vascular resistance. Dopamine, Dobutamine or adrenaline may need to be added. Dr Shitu.Hauwa.

41. Anaphylactic Shock Features Occurs on exposure to an allergen a patient is sensitive to. It may be pollen, foodstuffs, preservatives or medication. The reaction may be in the form of mild rashes with or without bronchospasm or it may be a full blown anaphylactic shock with rashes, generalised oedema including laryngeal oedema , bronchospasm and hypotension, if not treated in time, cardiac arrest. Dr Shitu.Hauwa.

42. Treatment I. Primary • Oxygen, if necessary, endotracheal intubation and ventilation. • Adrenaline, 0.5–1 mg IM or 50–100 µg intravenous to maintain BP. • Intravenous fluids—isotonic saline or Ringer lactate • Leg end elevation of bed. II. Secondary • Chlorpheniramine maleate • Hydrocortisone 100 mg intravenously Blood sample to analyse for raised serum tryptase levels. Dr Shitu.Hauwa.

43. Neurogenic Shock Causes: High spinal cord injury, vasovagal shock Features: Hypotension without tachycardia, more often bradycardia , that can deteriorate to produce shock and cardiac arrest. Treatment: Intravenous fluids, Blood pressure control, oxygen delivery, maintenance of haemodynamics , IV methylprednisolone therapy Inotropes and vagolytics as necessary. Dr Shitu.Hauwa.

44. OBSTRUCTIVE SHOCK It can be due to cardiac tamponade or due to tension pneumothorax. A. Cardiac Tamponade. •There is impedance to either inflow or outflow of blood. • The pericardium is filled with blood and hampers venous filling as well as outflow. • The filling pressures of the left/right-sided chambers equalise . • The CVP is high and the blood pressure is low. • The patients also have pulsus paradoxus where there is at least 10% decrease in systolic blood pressure with inspiration. Dr Shitu.Hauwa.

45. Treatment To maintain preload with fluids or blood as indicated. Relief of obstruction, drain the pericardial cavity as early as possible. B. Tension Pneumothorax Causes • Injury to the lung due to trauma • Ventilator-induced barotrauma • Rupture of emphysematous bulla in a patient with chronic obstructive pulmonary disease. Dr Shitu.Hauwa.

46. Features • Profound cyanosis • Distended neck veins • Tachypnoea,Tachycardia , Dyspnoea , Hypotension and cardiac arrest Treatment • A wide (large) bore needle/cannula (needle thoracostomy) must be inserted into the pleural cavity to drain the air. Traditionally, it was advised that the needle be inserted in the midclavicular line in the 2nd intercostal space on the affected side. THIS recommendation remains the same for children. Dr Shitu.Hauwa.

47. Endocrine shock Endocrine shock may present as a combination of hypovolaemic , cardiogenic or distributive shock. Causes of endocrine shock include hypo/hyperthyroidism and adrenal insufficiency. Hypothyroidism causes a shock state similar to neurogenic shock due to disordered vascular and cardiac responsiveness to circulating catecholamines . Thyrotoxicosis may cause a high-output Cardiac failure. Adrenal insufficiency leads to shock due to hypovolaemia and a poor response to circulating and exogenous catecholamines . Dr Shitu.Hauwa.

48. ACUTE ADRENAL INSUFFICIENCY Adrenal crisis occurs if the adrenal gland is deteriorating as in: • Primary adrenal insufficiency (Addison’s disease) • Secondary adrenal insufficiency (pituitary gland injury, compression) • Inadequately treated adrenal insufficiency. Features • Low BP, dehydration, tachycardia,tachypnea,confusion or coma. • Headache, profound weakness, fatigue,lethargy,joint pain. •Nausea, vomiting, abdominal pain, high fever and chills. Dr Shitu.Hauwa.

49. Treatment • Care of airway, breathing and circulation • Intravenous fluids • Hydrocortisone IV 100 mg every 6h to provide mineralocorticoid activity • Treat the precipitating factor • Antibiotics as necessary Dr Shitu.Hauwa.

50. REFERENCE Schwartz’s Principles of Surgery Tenth Edition Bailey & Love’s SHORT PRACTICE of SURGERY 26 th EDITION SABISTON TEXTBOOK of SURGERY The BIOLOGICAL BASIS of MODERN SURGICAL PRACTICE 21 ST EDITION Manipal Manual of Surgery Fifth Edition SRBs manual of surgery 6 th EDITION Dr Shitu.Hauwa.