shock, definition, classification, anaphylaxis

shock, definition, classification, pathogenesis, pathophysiology, anaphylaxis, management in children

1. SHOCK By – Dr. Samruddhi S. Bengal MDS 1 st Year Dept of Pediatric and Preventive Dentistry

2. Contents Definition Classification and etiology of shock Pathogenesis of shock Pathophysiology of shock Morphological features Clinical features and complications Anaphylactic shock Management Dental consideration Conclusion References

3. Definition Shock is a life-threatening clinical syndrome of cardiovascular collapse characterized by: acute reduction of effective circulating blood volume (hypotension); inadequate perfusion of cells and tissues (hypoperfusion). If uncompensated, these mechanisms may lead to impaired cellular metabolism and death.

4. Classification and etiology of shock. 1. HYPOVOLAEMIC SHOCK etiology i ) Acute haemorrhage ii) Dehydration from vomitings , diarrhoea iii) Burns iv) Excessive use of diuretics v) Acute pancreatitis

5. 2. CARDIOGENIC SHOCK etiology i ) Deficient emptying e.g. a) Myocardial infarction b) Cardiomyopathies c) Rupture of the heart, ventricle or papillary muscle d) Cardiac arrhythmias ii) Deficient filling e.g. a) Cardiac tamponade from haemopericardium iii) Obstruction to the outflow e.g . a) Pulmonary embolism b) Ball valve thrombus c) Tension pneumothorax d) Dissecting aortic aneurysm

6. 3. SEPTIC SHOCK etiology Gram-negative septicaemia (endotoxic shock) e.g. Infection with E. coli, Proteus, Klebsiella, Pseudomonas and Bacteroides Gram-positive septicaemia ( exotoxic shock) e.g. Infection with streptococci, pneumococci

7. Other types Traumatic shock etiology a) Severe injuries b) Surgery with marked blood loss c) Obstetrical trauma Neurogenic shock etiology a) High cervical spinal cord injury b) Accidental high spinal anaesthesia c) Severe head injury

8. Hypoadrenal shock etiology a)Administration of high doses of glucocorticoids b) Secondary adrenal insufficiency (e.g. in tuberculosis, metastatic disease, bilateral adrenal haemorrhage, idiopathic adrenal atrophy)

9. Pathogenesis In general, all forms of shock involve following 3 derangements: 1. Reduced effective circulating blood volume. It may result by either of the following mechanisms: By actual loss of blood volume as occurs in hypovolaemic shock; or By decreased cardiac output without actual loss of blood as occurs in cardiogenic shock and septic shock. 2. Impaired tissue oxygenation. Following reduction in the effective circulating blood volume there is decreased venous return to the heart resulting in decreased cardiac output. This consequently causes reduced supply of oxygen to the organs and tissues and hence tissue anoxia, which sets in cellular injury.

10. i ) Activation of macrophage-monocytes. Lysis of Gram negative bacteria releases endotoxin, a lipopolysaccharide, into circulation where it binds to lipopolysaccharide binding protein (LBP). The complex of LPS-LBP binds to CD14 molecule on the surface of the monocyte/ macrophages which are stimulated to elaborate cytokines, the most important ones being TNF- α and IL-1. The effects of these cytokines are : a) By altering endothelial cell adhesiveness : This results in recruitment of more neutrophils which liberate free radicals that cause vascular injury . b) Promoting nitric oxide synthase : This stimulates increased synthesis of nitric oxide which is responsible for vasodilatation and hypotension. 3. T here is immune system activation and severe systemic inflammatory response to infection as follows :

11. ii) Activation of other inflammatory responses. Microbial infection activates other inflammatory cascades which have profound effects in triggering septic shock. These are :

12. Pathogenesis

13. 1. PATHOGENESIS OF HYPOVOLAEMIC SHOCK The major effects of Hypovolaemic shock are due to decreased cardiac output and low intracardiac pressure. The severity of clinical features depends upon degree of blood volume lost, haemorrhagic shock is divided into 4 types:

14. Accordingly, clinical features are : Increased heart rate (tachycardia), low blood pressure (hypotension) low urinary output (oliguria to anuria) A lteration in mental state. Nausea, Vomiting Diarrhea Cold extremities Blenching Dry skin

15. 2. PATHOGENESIS OF CARDIOGENIC SHOCK Cardiogenic shock results from a severe left ventricular dysfunction from various causes. The resultant decreased cardiac output has its effects in the form of decreased tissue perfusion and movement of fluid from pulmonary vascular bed into pulmonary interstitial space initially ( interstitial pulmonary oedema ) and later into alveolar spaces ( alveolar pulmonary oedema ).

16. 3. PATHOGENESIS OF SEPTIC SHOCK Septic shock results most often from Gram-negative bacteria entering the body from genitourinary tract, alimentary tract, respiratory tract or skin and less often from Gram-positive bacteria. In septic shock, T here is immune system activation and severe systemic inflammatory response to infection as : Activation of macrophage-monocytes. Activation of other inflammatory responses.

17. Pathophysiology (Stages of Shock) S hock has been divided arbitrarily into 3 stages: Compensated ( Initial ) Shock Progressive Decompensated Shock Irreversible Decompensated Shock

18. 1.Non progressive compensated shock In the early stage of shock, an attempt is made to maintain adequate cerebral and coronary blood supply by redistribution of blood so that the vital organs are adequately perfused and oxygenated. If the condition that caused the shock is adequately treated, the compensatory mechanism may be able to bring about recovery and re-establish the normal circulation; this is called compensated or reversible shock

19. Progressive compensated shock This is a stage when the patient suffers from some other stress or risk factors (e.g. pre-existing cardiovascular and lung disease) besides persistence of the shock condition; this causes progressive deterioration.

20. IRREVERSIBLE COMPENSATED SHOCK When the shock is so severe that in spite of compensatory mechanisms and despite therapy and control of etiologic agent which caused the shock, no recovery takes place, it is called decom pensated or irreversible shock.

21. MORPHOLOGIC FEATURES Eventually, shock is characterized by multisystem failure. The morphologic changes in shock are due to hypoxia resulting in degeneration and necrosis in various organs. The major organs affected are the brain, heart, lungs, kidneys, liver and other organs.

22. 1. HYPOXIC ENCEPHALOPATHY Cerebral ischaemia in compensated shock may produce altered state of consciousness. However, if the blood pressure falls below 50 mmHg brain suffers from serious ischaemic damage with loss of cortical functions, coma and a vegetative state. Grossly , the area supplied by the most distal branches of the cerebral arteries suffers from severe ischaemic necrosis . Microscopically , the changes are noticeable if ischaemia is prolonged for 12 to 24 hours. Neurons, particularly Purkinje cells, are more prone to develop the effects of ischaemia .

23. 2. HEART IN SHOCK Heart is more vulnerable to the effects of hypoxia than any other organ. Heart is affected in cardiogenic as well as in other forms of shock. There are 2 types of morphologic changes in heart in all types of shock: i ) Haemorrhages and necrosis . There may be small or large ischaemic areas or infarcts, particularly located in the subepicardial and subendocardial region. ii) Zonal lesions . These are opaque transverse contraction bands in the myocytes near the intercalated disc.

24. 3. LUNG in SHOCK Lungs due to dual blood supply are generally not affected by hypovolaemic shock but in septic shock the morphologic changes in lungs are quite prominent termed ‘ shock lung ’. Grossly, the lungs are heavy and wet. Microscopically, changes of acute respiratory distress syndrome (ARDS) are seen. Briefly, the changes include congestion, interstitial and alveolar oedema, interstitial lymphocytic infiltrate, alveolar hyaline membranes, thickening and fibrosis of alveolar septa, fibrin and platelet thrombi in the pulmonary microvasculature.

25. 4. KIDNEY IN SHOCK One of the important complications of shock is irreversible renal injury . The end-result is generally anuria and death. Grossly, the kidneys are soft and swollen. Sectioned surface shows blurred architectural markings. Microscopically, the tubular lesions are seen at all levels of nephron and are referred to as acute tubular necrosis (ATN) which can occur following other causes besides shock. If extensive muscle injury or intravascular haemolysis are also associated, peculiar brown tubular casts are seen.

26. 5. ADRENALS IN SHOCK The adrenals show stress response in shock. This includes release of : Aldosterone G lucocorticoids C atecholamines like adrenaline In severe shock, acute adrenal haemorrhagic necrosis may occur.

27. 6. HAEMORRHAGIC GASTROENTEROPATHY The hypoperfusion of the alimentary tract in conditions such as shock and cardiac failure may result in mucosal and mural infarction called haemorrhagic gastroenteropathy. Grossly, the lesions are multifocal and widely distributed throughout the bowel. The lesions are superficial ulcers, reddish purple in colour . The adjoining bowel mucosa is oedematous and haemorrhagic. Microscopically, the involved surface of the bowel shows dilated and congested vessels and haemorrhagic necrosis of the mucosa and sometimes submucosa. Secondary infection may supervene and condition may progress into pseudomembranous enterocolitis.

28. 7. LIVER IN SHOCK. Grossly , faint nutmeg appearance is seen. Microscopically , depending upon the time lapse between injury and cell death, ischaemic shrinkage, hydropic change, focal necrosis or fatty change may be seen. Liver function may be impaired. 8. OTHER ORGANS. Other organs such as lymph nodes, spleen and pancreas may also show foci of necrosis in shock. In addition, the patients who survive acute phase of shock succumb to overwhelming infection due to altered immune status and host defense mechanism. Nutmeg liver

29. Clinical features and complications The classical features of decompensated shock are characterized by depression of 4 vital processes: Very low blood pressure Subnormal temperature Feeble and irregular pulse Shallow and sighing respiration In addition, the patients in shock have pale face, sunken eyes, weakness, cold and clammy skin.

30. Life-threatening complications in shock are due to hypoxic cell injury resulting in immuno-inflammatory responses and activation of various cascades (clotting, complement, kinin). These include the following: 1. Acute respiratory distress syndrome (ARDS) 2. Disseminated intravascular coagulation (DIC) 3. Acute R enal Failure (ARF) 4. Multiple O rgan D ysfunction S yndrome (MODS) With progression of the condition, the patient may develop stupor, coma and death.

31. Anaphylactic shock

32. Etiology : •   The most common cause of anaphylaxis is the administration of penicillin. • The other causes include anesthesia, dextrans , serum injections, stings, consumption of shell fish. Pathophysiology: • The antigen combines with IgE on the mast cell & basophils releasing large amounts of histamine and slow releasing substances of anaphylaxis.

33. Clinical features: • It  manifests as bronchospasm, laryngeal edema, respiratory distress, chest tightness, hypoxia, dizziness, difficulty in swallowing, massive vasodilatation, wide spread redness, itchiness, hives, anxiety, confusion, weak pulse, hypotension and shock. • The mortality rate is 10%. • In the dental office this reaction can occur during or immediately following the administration of penicillin or LA to a previously sensitized patient.

34. 8. Management Immediate &  aggressive management is imperative if the patient is to survive. Step 1: Position the patient Place the patient in a supine position with the legs slightly elevated.  

35. Step 2: A-B-C-D-E(Airway, Breathing, Circulation, Disability and Exposure)

36. Compressions: Compression rate of 100-120 per minute, pushing hard and fast in chest center. Depth of 2" - 2.4” for adults (5-6cm). Children and infants: 1/3 depth of the chest (2” and 1.5”). Allow complete chest recoil between compression. Airway: Head tilt/chin lift: tilt victim's head back and lift the victim's chin to open the airway. Infant airway can be opened by placing the head in the “sniffing position.” Breathing: Give rescue breathing, mouth to mouth, in the apneic patient with a pulse. For effective breathing, watch for chest rise and avoid excessive ventilation. The ratio of chest compressions to breaths is 30 to 2, for a pulseless patient. 10 BREATHS should be delivered each minute, or one breath every six seconds. Each breath should be delivered over 1 second. Observe visible chest rise.

37. Management of Anaphylaxis (no signs of allergy) Recognize problem ↓ Discontinue dental treatment & Activate office emergency team ↓ P—Position patient supine with feet elevated slightly ↓ C → A → B—Assess and perform basic life support as needed ↓ D—Definitive management ↓ Activate emergency medical service Administer O2 Monitor vital signs ↓ Stabilization and transport of patient

38. Management of Anaphylaxis ( signs of allergy present) Recognize problem ↓ Discontinue dental treatment Activate office emergency team ↓ P—Position patient supine with feet elevated slightly ↓ C → A → B—Assess and perform basic life support as needed D—Definitive management ↓ Activate emergency medical service ↓ Administer epinephrine (IM, IV) Administer O2 Monitor vital signs ↓ Additional drug therapy: histamine-blocker, corticosteroid (IM, IV)

39. Administration of  epinephrine Adult dose 0.5 mg IM (=500 mcg = 0.5 mL of 1:1000) adrenaline (epinephrine). • >12 years: 500 mcg IM (0.5 mL) that is, the same as the adult dose. • 6-12 years: 300 mcg IM (0.3 mL). • <6 years: 150 mcg IM (0.15 mL). If the child is small or prepubertal 300 mcg (0.3 mL). IM adrenaline (epinephrine) should be repeated after 5 min if there is no clinical improvement. Patients requiring repeated IM doses may benefit from IV adrenaline (epinephrine).

40.   (B) Administration of oxygen • Deliver oxygen at a flow of 5-6 liters per minute by nasal hood or full face mask at any time during the episode. Hypovolemic, anaphylactic  and neurogenic shock are readily treatable and respond well to medical therapy. Perfusion of the brain may be the greatest danger during shock. Therefore urgent treatment is essential for a good prognosis

41. (C) Monitoring of  vital signs Monitoring the patients cardiovascular & respiratory status should be done continuously. Record blood pressure & heart rate at least every 5 minutes & start closed chest compression if cardiac arrest occurs. (D) Additional drug therapy • After the administration of epinephrine, the other drugs to be administered are : Antihistamines, Corticosteroids. • These drugs are administered only after clinical improvement is noted & are not be given during the acute phase as they are too slow in onset.

42. 9. PROGNOSIS OF SHOCK The prognosis varies with the origin of shock and its duration. 80%-90% of young patients survive hypovolemic shock with appropriate management. Cardiogenic shock associated with extensive myocardial infraction has mortality rate up to 75% Septic shock : (mortality rate up to 75%)

43. 11. CONCLUSION Shock can  present as a consequence of multiple causes & affect the body at cellular, visceral & systemic levels. Regardless of source, the fundamental primary treatment of shock remains recognition & prompt fluid replacement. The search for the underlying cause of the shock is only initiated after stabilization.

44. 12. References Davidson’s Principles And Practice Of Medicine – 22nd ed Essential Pathology – Harsh Mohan 3 rd ed Goto T. Management of Anaphylaxis in Dental Practice.  Anesth Prog . 2023;70(2):93-105. doi:10.2344/anpr-70-02-16 Nanavati RS, Kumar M, Modi TG, Kale H. Anaphylactic shock management in dental clinics: An overview. J Int Clin Dent Res Organ 2013;5:36-9

45. Thank you!!