Shock : Types and Management

Property of Prof Dr. Nawel Hussein, Professor of Oncosurgery, Department of General Surgery, Faculty of Medicine, University of Zagazig, Egypt

1. بسم الله الرحمن الرحيم

2. THE shock PROF. DR. NAWEL HUSSEIN أ.د./ ناول حسين M.B.,B.Ch, M.S., FRCS (Ed. UK), MD PROFESSOR OF ONCOSURGERY

3. SHOCK Definition: It is a state of acute circulatory failure in which the cardiac output unable to maintain tissue perfusion for nutrition, oxygenation and waste disposal. Shock is common and the most important cause of death among surgical patients. In some cases a patient may have a combination of more than one types of shock, as in trauma and burn, hypovolaemic and neurogenic shock occurs at the same time.

4. SHOCK Types of shock: Neurogenic shock: this is due to peripheral vasodilatation and peripheral pooling of the blood. Hypovolaemic shock : due to decrease of blood volume. Cardiogenic shock : due to failure of the heart. Septic shock: when infection is sever, it releases chemical mediators which affects the microcirculation resulting in failure of peripheral resistance and ending in failure of the heart. Anaphylactic shock: due to antigen antibody reaction that leads to failure of peripheral resistance. Endocrinal shock: due to hypo- and hyperthyroidism and in adrenal insufficiency.

5. 1 - Neurogenic shock Definition: This is due to peripheral vasodilatation and peripheral pooling of the blood in the skeletal muscles and inadequate venous return, this type is also referred to as fainting , collapse or Vasovagal attack . Causes: Painful stimulation as catheterization or severe trauma to the testis or to the abdomen Reaction to fear or fight or hearing bad news . Following spinal anesthesia or fracture spin (spinal shock) Clinical pictures: Increasing pallor of the face, cold extremities. Fall of the blood pressure together with bradycardia. Nausea and vomiting. Deep sighing respiration Fainting attack, the mere act of falling to the ground, assists venous return and helps recovery.

6. 1 - Neurogenic shock Treatment: Put the patient in the shock position i.e. patient lie flat in the bed with elevation of the lower limbs to increase venous return and cardiac output Atropine in vasovagal shock to improve bradycardia which occurs due to increase of the vagal tone Vasoconstrictors as ephedrine in spinal shock to elevate blood pressure by increasing peripheral resistance. I.V fluids if the shock persists for more than 20 minutes.

7. 2 - Hypovolaemic shock Causes: Blood loss: as in haemorrhage due to trauma, operation, GIT bleeding or blood diseases. Plasma loss: as in burn Water and electrolyte loss: as in vomiting, diarrhea high output intestinal fistula. Third spacing loss: the fluid is lost into the GIT lumen and interstitial spaces as for example in intestinal obstruction and pancreatitis.

8. 2 - Hypovolaemic shock Clinical pictures: Mild shock: (up to 20% blood volume loss) non vital organs are affected as (skin, muscles and bone) Pallor, cold skin Mild tachycardia and may postural hypotension. Moderate shock: (up to 40% blood volume loss) where the kidneys, liver, intestine are also affected, so, plus to the above manifestations, there are: Tachycardia increased and hypotension. Oliguria or anuria (urine output of less 0.5 cc/kg/hours indicates marked hypovolaemia.) Severe shock: (more than 40% blood volume loss) brain and heart are also affected. so, plus to the above manifestations there are : Restlessness, agitation (sense of impending death) coma and may death Arrhythmia and may cardiac arrest. Thirst is an annoying feature. Rapid and shallow respiration

9. 2 - Hypovolaemic shock Irreversible shock: Progressive renal, respiratory, cardiac and CNS decompensations. Acidosis: due to accumulation of acidic metabolites Hypothermia Consumption coagulopathy due to DIC Electrolyte disturbance as hyperkalaemia Multiple organ failure syndrome

10. 2 - Hypovolaemic shock Patho-physiology Cardiovascular and endocrine compensatory responses: Aims to restores the intravascular volume, maintain blood pressure and tissue perfusion and reduce flow to non-vital organs to preserve flow to vital organs as (brain, heart and kidney) by: stimulation of baroreceptors in carotid sinus and aortic arch to increase heart rate and peripheral vasoconstriction then blood pressure elevated Increase secretion of ADH, which leads to vasoconstriction & oliguria, so, blood pressure elevated Renal ischaemia  rennin secretion  angiotensin I &II -  vasoconstriction and aldosterone secretion (salt & water retention)  so, blood pressure elevated. Stimulation of adrenal medulla  secretion of adrenaline and nor-adrenaline  increase heart rate and vasoconstriction  so, blood pressure elevated. If the patient is rapidly treated by adequate volume replacement, vital signs will return to normal and be saved. However with persistent hypovolaemia or lack of prompt treatment the intense sympatho-adrenal response will lead to irreversible shock and inevitable death.

11. Early compensated stage (adaptive phase or neuroendocrine response) : Neural reflexes : Stimulation of baroreceptors in wall of atria, carotid sinus & in aortic arch → ↑ sympathetic activity → S elective VC of blood vessels of skin, muscles, kidneys & splanchnic organs → Shift of blood to heart & brain. Vasoconstriction of veins (veins carry about 2/3 of blood volume) will shift the blood to arterial side of circulation. ↑ HR & contractility of heart. Stimulation of chemoreceptors in aortic arch & carotid bodies (sensitive to minor changes in PH, O2 tension & CO2 level) …. result in splanchnic VC (splanchnic blood flow represents 20% of blood volume) & coronary blood vessel dilatation.

12. 2 - Hypovolaemic shock Microcirculatory changes : In compensated shock : Under the effect of catecholamines the pre-capillary sphincters constrict  decrease of capillary pressure  refilling from the interstitial fluids to increase the intra vascular fluids (one liter / hour in healthy person  increase blood pressure. In de-compensated shock: Opening of A-V shunts leads to more capillary ischemia and more cellular distress  release of histamine and other chemical mediators  contraction of post-capillary sphincter  more slowing of the capillary flow & more ischemia. Paralysis of pre-capillary sphincter due to acidosis and hypoxia, while post-capillary sphincter still contracted (as it is accustomed to high acidic media) together with capillary damage from severe ischemia leads to 1- leakage of large protein molecules from the vessels into the interstitial space dragging with them huge amounts of fluid, this third space loss of fluid further reduces the blood volume. 2- Sludging of RBCs in the capillaries with formation of micro thrombi, if extensive, it is called disseminated intravascular coagulation (DIC). This depletes coagulation factors and induces bleeding tendency in the rest of the body (consumption coagulopathy). Paralysis of post-capillary sphincter leads to passage of these micro thrombi to the circulation The viscous circle of hypovolaemia  tissue hypoxia  capillary damage  more fluid loss in the tissues  more hypovolaemia is called (death cycle of MacDowell).

13. 2 - Hypovolaemic shock Cellular changes: Hypoxia  anaerobic glycolysis  lactic acid production (metabolic acidosis) and small amount of energy. Body tries to correct acidosis by hyperventilation. With more hypoxia  cellular functions deteriorates, specially Na/K pump which results in increase intracellular Na and water and increase extracellular potassium ( hyperkalaemia)

14. 2 - Hypovolaemic shock Multiple organ failure(MOF): MOF is defined as two or more failed organ systems Lung failure --  acute respiratory distress syndrome (ARDS) Kidney failure  acute renal insufficiency Liver failure -  acute liver insufficiency Clotting  coagulopathy Heart failure There is no specific treatment for MOF, management is by supporting organ systems with ventilation, cardiovascular support and dialysis until there is recovery of organ function MOF currently carries a mortality rate of 60%, thus prevention is vital by early aggressive identification and treatment of shock.

15. Adaptive mechanisms are very poor in children & elderly because: Pediatric patients: Have smaller total blood volumes & therefore, they are at risk to lose a proportionately greater percentage of blood. Children < 2 years, their kidneys are immature →  power to concentrate solute. Large body surface with rapid heat loss → early hypothermia, → Coagulopathy. Elderly people: Altered physiology Atherosclerosis &  elastin → Poor arterial contraction & retraction.  Ability to respond to hypotension by tachycardia. Preexisting medical conditions with medications that may affect the compensatory response to shock. Many older patients have significantly decreased creatinine clearance in the presence of near-normal serum creatinine.

16. 2 - Hypovolaemic shock Measurements needed in shock: Urine output : urine output of less 0.5 cc/kg/hour indicates marked hypovolaemia. Central venous pressure (CVP ): Normal 5-15 cm water Increased in: cardiogenic shock, Rt side heart failure, fluid overload Decreased in hypovolaemic shock Swan Ganz catheter : can measure COP and pulmonary artery wedged pressure  good indicator of left ventricular function. Arterial blood gases and blood PH . Serum electrolytes & haematocrit value .

17. 2 - Hypovolaemic shock Treatment of hypovolaemic shock : Immediate resuscitation for shocked patient is to insure a patent airway and adequate oxygenation and ventilation, then attention is directed to cardiovascular resuscitation. Fluid therapy: The mainstays of initial treatment of shock are the infusion of fluids Insert two large pore cannula , blood is drawn for typing and cross matching. 1000-2000 ml of lactated ringer's solution over 45 minutes. Patients can be divided into Responders in whom Bl.P and pulse improved with good urine output  as in only fluid loss (intestinal obstruction) or in mild non active bleeding

18. Transient responder  improvement then return to previous state over 20 min, these patients either have moderate on-going fluid losses. Non-responders are severely volume depleted and are likely to have major on-going fluid losses usually through uncontrolled haemorrhage. Blood: the most effective, specially with blood loss. In patients who are actively bleeding (major trauma, ruptured aortic aneurysm, GIT haemorrhage) elevation of Bl.P without controlling site of Hge., merely increase bleeding from these sites. Thus operative Hge. control should not be delayed and resuscitation should be done in parallel with surgery . Colloid solution: in the absence of whole blood, many substances have been proposed as human plasma, albumin solution, dextran and haemagel. Hypovolaemic shock from causes other than bleeding e.g., plasma loss in major burn, or crystalloid loss in intestinal obstruction does not usually need blood and infusion is by plasma or crystalloids respectively.

19. 2 - Hypovolaemic shock Pulmonary support : Mask oxygen for all shocked patient at high concentration Evidence of respiratory failure is an indication for endo-tracheal intubation and mechanical ventilation. Position : elevation of lower limb with maintaining the trunk in supine position Heating of the patient with blankets to avoid sense of coolness.

20. 2 - Hypovolaemic shock Medications: in the form of: Corticosteroids : may be beneficial in these cases. Sedation (morphine): relives pain& anxiety and reduces tissue requirements for oxygen. It is contraindicated in abdominal and head injuries and with respiratory depression. It must be give I.V to avoid toxicity. Antibiotics: third generation cephalosporines to avoid septic complications. Inotropic drugs (dopamine ): are used when the condition fails to improve despite adequate volume replacement and oxygenation. It is used to improve myocardial contractility and increase renal blood flow and urine output as well. Vasodilators (alpha adrenergic blockers ) may given to improve the tissue perfusion but after full correction of hypovolaemia. Sodium bicarbonate may be given for correction of acidosis After correction of shock, if urine output does not improved, mannitol 250 ml of 20% is given to clear the kidneys of any precipitated materials during shock and oliguria .

21. 3 - Septic shock This is the most lethal shock, and considered as one of the major killers in surgical practice. If not well treated mortality ranged from 25%-90%. Causes: The commonest organism is gram–ve bacteria & its endotoxins ( part of cell wall of dead bacteria), The common sources are peritonitis due to rupture viscus, cholangitis, GIT infection & severely infected diabetic foot. Predisposing factors includes, extremities of age, DM, malignancy ,chemotherapy, corticosteroid therapy &AIDS

22. 3 - Septic shock Pathophysiology: Bacterial endotoxin stimulates macrophages and Kupffer cells of the liver to release cytokines (as : tumour necrosis factor "TNF", platelet activation factor, prostaglandins & nitric acid) in large amount  harmful effect on microcirculation with capillary endothelium damage. These cytokines lead to peripheral vasodilatation and opening of A-V shunt, which lead to capillary bypass and tissue hypoxia. capillary endothelium damage under the effect of cytokines, lead to leakage of protein-rich fluid from the circulation to the interstitial space causing oedema. The excess production of lactic acid due to hypoxia leads to metabolic acidosis. In late sepsis multiple organ failure (MOF) proceeds faster than hypovolaemic shock, due to direct effect of cytokines on the organs.

23. 3 - Septic shock Clinical pictures: The patient passes through two stages, the diagnosis of the patient in the early stage and prompt management can save the patient. Hyperdynamic (warm) stage : diagnosis is difficult and a high index of suspicion is required to detect cases at this early stage. Fever (> 38oc) with warm dry skin. Tachycardia , hypotension & tachypnoea . Oliguria. The cardiac out-put is normal or elevated and If not treated, patient will pass to the next stage.

24. 3 - Septic shock Clinical pictures: Hypodynamic (cold) stage: Sever tachycardia , hypotension & tachypnoea Cold clammy skin Restlessness and confusion Marked oliguria. Complicated by: Acute erosive gastritis. Systemic inflammatory response syndrome(SIRS) Adult respiratory distress syndrome (ARDS) Multiple organ failure (MOF) DIC and death.

25. 3 - Septic shock Diagnosis: is helped by CBC  polymorphonuclear leucocytosis with abundant immature forms High lactate level in blood Search for the source of infection Repeated blood culture at peak of fever

26. 3 - Septic shock Treatment: Treatment must be started as early as possible and should be carried in ICU, by two arms hand by hand, 1-control infection 2- support of body systems with good monitoring . 1 - Control of infection : Eradication of infection: drainage of peritonitis or big abscess, resection of gangrenous bowel or amputation of diabetic severely infected limb. Antibiotics: aggressive multiple antibiotics as combination of (cephalosporin, garamycin and metronidazole), till results of culture and sensitivity is available. Control of predisposing conditions as DM Corticosteroids may have a role

27. 3 - Septic shock 2- Support of different systems: The main priority is to maintain cardiovascular system with reasonable blood pressure by: Fluid replacement: huge amount of ringer lactate may be needed to replace fluid deficits till CVP reach 12- 15 mm.Hg. Medications (inotropes and vasopressors) if the patient remains hypotensive despite adequate fluid replacement as shown by CVP dopamine drip is given to raise the blood pressure. If there is still no response careful noradrenaline administration may be used. Oxygen administration is essential by mask in mild hypoxia and by intubation and mechanical ventilation in severe hypoxia. Observing urine output, and if not improved by fluids, dopamine will be added, if no improvement haemodialysis may be needed in acute renal failure.

28. 4 - Cardiogenic shock Causes: The deficiency of tissue perfusion here is not due to loose of blood volume but due to failure of the heart to pump and low cardiac output as in Massive acute myocardial infarction (commonest cause). Severe arrhythmia. massive pulmonary embolism Cardiac tamponade. myocarditis High spinal anaesthesia, can cause paralysis of the sympathetic supply of the heart.

29. 4 - Cardiogenic shock Clinical pictures: Pictures of the cause Cold sweaty skin Manifestations of acute heart failure Dyspnea, cyanosis and pulmonary oedema. Congested neck veins and high CVP. Fall of the systolic and diastolic Blood pressure and collapse. Increasing metabolic acidosis.

30. 4 - Cardiogenic shock Treatment: Oxygen should be administered Treatment of the cause Inotropic drugs as Dubotamin Mechanical support by intra-aortic balloon pulsation device to elevate diastolic Bl.P, hence better filling of the coronary arteries and reduction of myocardial work.

31. 5 - Anaphylacic shock This type of shock occurs due to Antigen antibody reaction (allergic reaction) leads to release of large amount of histamine which causes capillary paralysis, dilatation and pooling. The best example is penicillin injection in a sensitized patient. Clinical pictures: Skin eruption, bronchospasm, laryngeal oedema and respiratory distress and collapse. Treatment: Immediate stop of further injection of the causing drug , give the patient corticosteroid injection ,adrenaline , antihistaminics and O 2 .

32. 6 - Endocrinal shock This may occur in patients with Addisons disease or those receiving continuous cortisone therapy if they are subjected to any stressful situation, as infection or surgery. The patient develops sever shock due to failure of release of corticosteroids necessary to cope with the stress from the suppressed adrenal cortex. The result will be a state of peripheral circulatory failure, hyponatraemia and hyperkalaemia. Treatment is essentially prophylactic. Any patient liable to this problem should receive an additional dose of hydrocortisone IV prior to any surgical procedure. The treatment of an established case needs large doses of IV hydrocortisone, saline infusions and treatment of the predisposing factors e.g., infection.

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