Diagnosis, Investigations and Management of Shock

Diagnosis, Investigations and Management of Shock

1. DIAGNOSIS, INVESTIGATIONS AND MANAGEMENT OF SHOCK

2. CONTENTS Introduction Classification of shock Hypovolaemic shock Introduction Etiology Clinical Features Treatment Principles Treatment Cardiogenic Shock Etiology Investigations Management Septic Shock Introduction Etiology Stages of Septic Shock Investigations Treatment Neurogenic Shock Introduction Etiology Clinical features Management Endocrine Shock Etiology Anaphylactic Shock Introduction Clinical Features Treatment Severity Of Shock Mild Shock Moderate Shock Severe Shock

3. CONTENTS Effects of Shock on various organs Heart Lung Metabolic Cellular changes Brain Kidneys Blood Gastro – intestinal Tract Multiple Organ Dysfunction Syndrome Introduction Features related to MODS Management

4. SHOCK A systemic state of low tissue perfusion which is inadequate for normal cellular respiration.

5. HYPOVOLAEMIC SHOCK This is the most common type of shock out of all the varieties encountered in the emergencies of the hospitals.

6. ETIOLOGY

7. CLINICAL FEATURES

8. TREATMENT PRINCIPLES CONTROL ONGOING LOSS RAPID RE-EXPANSION OF THE CIRCULATING INTRAVASCULAR BLOOD VOLUME + GOAL : Restore blood volume & improve tissue perfusion and oxygenation

9. TREATMENT

10. CARDIOGENIC SHOCK It is defined as circulatory failure causing diminished forward flow of blood leading into tissue hypoxia with systolic blood pressure less than 90mm of hg for 30 minutes and raised pulmonary capillary wedge pressure (PCWP) more than 15mm of hg.

11. It is commonly seen in acute myocardial infarction (MI) with mortality more than 50%. Cardiogenic shock develops within 24 hours of MI. It occurs when 50% of left ventricular wall is damaged by infarction. It leads to pulmonary oedema and severe hypoxia. Ischaemic necrosis of left ventricular wall causes failure of pump thereby decreasing the stroke volume.

12. ETIOLOGY

13. INVESTIGATIONS

14. MANAGEMENT

15. SEPTIC SHOCK It is due to bacterial infection which release toxins leading to shock.

16. May be due to gram positive organisms, gram negative organisms , fungi, viruses or protozoal origin . Gram negative septic shock is called as endotoxic shock and it is caused by organisms like E. Coli , Klebsiella , pseudomonas and proteus .

17. ETIOLOGY Septic shock is typically a vasodilatory shock wherein there is peripheral vasodilatation causing hypotension which is resistant to vasopressors .

18. STAGES OF SEPTIC SHOCK HYPER DYNAMIC SHOCK (WARM SEPTIC SHOCK) This stage is reversible stage. Patient is still having inflammatory response and so presents with fever , tachycardia and tachypnoea . Patient should be treated properly at this stage . HYPO DYNAMIC HYPOVOLAEMIC SEPTIC SHOCK (COLD SEPTIC SHOCK) This stage is irreversible stage. Here inflammatory response is lost. Patient is in decompensated shock. This irreversible stage is associated with multi-organ dysfunction syndrome (MODS ), anuria (kidney failure), respiratory failure (cyanosis), liver failure ( jaundice), cardiac depression , hypotension , pulmonary oedema , hypoxia , drowsiness, eventually coma and followed by death.

19. INVESTIGATIONS

20. MANAGEMENT

21. MANAGEMENT

22. Neurogenic shock Occurs due to sudden shocking event or sudden painful stimuli or injury to spinal cord causing severe splanchnic vessel vasodilatation

23. ETIOLOGY

24. CLINICAL FEATURES

25. TREATMENT

26. ENDOCRINE shock It may present as a combination of hypovolaemic , cardiogenic and distributive shock. Causes of endocrine shock include : i . Hypothyroidism ii. Hyperthyroidism iii. Adrenal insufficiency

27. ETIOLOGY

28. ANAPHYLACTIC SHOCK It occurs due to Type I hypersensitivity Reactions. Various drugs including antibiotics, anaesthetic drugs , stings, venoms may be having antigens which may combine with IgE of mast cells and basophils of host body and release histamines and large amounts of slow releasing substance of anaphylaxis (SRS-A).

29. CLINICAL FEATURES MORTALITY RATE IS 10%

30. TREATMENT

31. SEVERITY OF SHOCK

32. SHOCK INDEX It is a ratio of pulse to blood pressure . Normal value is less than one . In shock the normal value is reversed that is it is more than one.

33. EFFECTS OF SHOCK ON VARIOUS ORGANS Heart Lung Metabolic Cellular changes Brain Kidneys Blood Gastro-intestinal tract

34. HEART L ow perfusion L ow venous return Decreased cardiac output Hypotension Tachycardia . Persistent shock causes hypoxia and release of myocardial depressants leading to further cardiac damage

35. LUNG Interstitial oedema D ecreased gaseous exchange Pulmonary arteriovenous shunting Tachypnoea Acute respiratory distress syndrome (ARDS ) Pulmonary oedema

36. METABOLIC Shock leads to hypoxia, which activates anaerobic metabolism leading to lactic acidosis. Antidiuretic hormone ( ADH) is released which increases the reabsorption of water from renal tubules Other hormones released are Adeno - cortico - trophic -hormone (ACTH ), bradykinin , prostaglandins, histamines and serotonins to compensate the effects of shock to increase the perfusion of vital organs like heart, brain, lungs

37. CELLULAR CHANGES Cellular changes occur in persistent shock due to release of lysosomal enzymes which alter the cell membrane permeability which in turn cause cell death.

38. BRAIN When the perfusion of the brain decreases, the patient becomes drowsy . Brain is the last organ to get under perfused in shock

39. KIDNEYS Glomerular filtration rate ( GFR) decreases and tubular reabsorption of salt and water increases for compensatory response. But in severe cases tubular necrosis sets in leading to irreversible damage

40. BLOOD Alterations in the cellular components of the blood including platelets leads to disseminated intravascular coagulation (DIC). It causes bleeding from all the organs

41. GASTRO – INTESTINAL TRACT Mucosal ischaemia develops causing bleeding from GIT with haematemesis and malaena . It is aggravated by disseminated intravascular coagulation

42. Multiple organ dysfunction syndrome It is the progressive irreversible damage and loss of functions of all vital organs like liver , lungs kidneys, GIT.

43. L ungs and liver are commonly involved (70%) Next organs to be involved are kidneys , GIT . Order of involvement of organs in Multiple Organ Dysfunction Syndrome is LUNGS > RIGHT VENTRICULAR FAILURE > LIVER > KIDNEY It occurs in critically ill patients after severe trauma, burns, bleeding , sepsis , pancreatitis etc. It is more common in elderly , diabetics , smokers, alcoholics , cirrhosis , malnutrition, uraemia cases , immunosuppressed patients, patients taking steroids and cytotoxic drugs

44. FEATURES RELATED TO MULTIPLE ORGAN DYSFUNCTION SYNDROME TypicalOliguria Jaundice Hypotension Drowsiness Respiratory distress are common findings on clinical examination Platelets micro aggregation Acute pulmonary hypertension (APH) Circulatory failure Acute respiratory distress syndrome (ARDS) Disseminated intravascular coagulation Impaired defense mechanism are the pathological features Respiratory, renal, hepatic, Circulatory , coagulative and cardiac failure occurs as end stage of MODS

45. MANAGEMENT OF MULTIPLE ORGAN DYSFUNCTION SYNDROME

46. TREATMENT OF THE CAUSE IF POSSIBLE MODS stage has got high mortality . ( Dobutamine raises cardiac output ) (Dopamine is preferred in hypotension cases)