shock_and_sirs in basic otolaryngology.pptx

Ent and head neck surgery

1. Shock and SIRS Dr. Subash Bhatta 1st Year, MS (ORL-HNS) GMSMA of ENT-HN Studies MMC-TUTH, IOM

2. Roadmap Definition Historical overview Brief introduction Pathophysiology Stages Classification Hypovolemic shock Cardiogenic shock Obstructive shock Distributive shock Septic shock and SIRS Neurogenic shock Anaphylactic shock

3. Shock Definition It is a condition produced by inability of the circulatory system to adequately nourish tissues or remove toxic metabolites. It is a condition of profound hemodynamic and metabolic disturbance characterized by failure of the circulatory system to maintain an appropriate blood supply to the microcirculation with consequent inadequate perfusion of vital organs. An acute medical condition associated with a   fall  in  blood pressure , caused by such events as loss of  blood , severe burns ,  allergic  reaction , or sudden emotional stress , and marked by cold, pallid skin, irregular breathing, rapid pulse, and dilated  pupils. Emergency medicine by R osen and Barkin 4 th edition Rubins pathology 4 th edition Oxford dictionary

4. Shock definition contd.. A  condition of acute peripheral circulatory failure due to  derangement of circulatory control  or loss of circulating  fluid, marked   by hypotension and   coldness of the skin , and often by  tachycardia  and  anxiety if untreated cab  be fatal. A life threatening  medical condition of low blood perfusion  to tissues resulting in cellular injury and inadequate tissue function , typical signs being low blood pressure, rapid heart rate, and signs of poor end-organ  perfusion. Wikipedia Dorland medical dictionary

5. H istory First resuscitation efforts by Ambroise Pare back in 1510 to 1590 Treatment of shock started back in Dec14, 1650 , By Dr. William ( king,s doctor, England) unknowningly revived a person declared dead after judicial hanging.

6. History contd.. First intravenous fluid therapy in 1830 by Herman for cholera Gross was the first to define the shock as Manifestation of a “rude unhinging of the machinery of life” Crile was the first to do blood transfusion on 1900 Later A lexis Carrel went on to study about blood group

7. Introduction Most common & most important cause of death among surgical patients. Death may be immediate as a result of profound shock or delayed due do organ ischemia or reperfusion injury. Shock is not a disease itself, its constellations of manifestations of various diseases and conditions. Sabiston textbook of surgery 17th ed “Transitions between a illness and death”

8. Introduction Most common cause of shock in Nepal is RTA. The recent earthquake was the major cause of the patient with shock in various part of the country Total death 7619 Total injured 14,454 Source: Nepal Police:www.nepalpolice.gov.np

9. Pathophysiology Circulatory system four part machine Pump  (the heart ) A  complex system of  flexible tubes   ( the blood  vessels) A   circulating fluid  ( the blood)   Fine  regulating system or  “computer” (the nervous system )

10. Pathophysiology contd.. Pic source internet

11. Pathophysiology contd..

12. Pathophysiology contd.. Enters vicious cycle Hypoxia Increased vascular permeability Loss of total blood volume Decreased blood to myocardium Myocardial injury Myocardial injury Reduced CO Reduced renal perfusion Reduced clearance of products Acidosis - ve ionotrophic Respiratory distress Aggravates shock Ion homeostasis Cell structure Electrical and mechanical fxn alters Hypoxia Not managed Cycle continues with more severity

13. Pathophysiology contd.. Various organ response Cellular level Aerobic to anaerobic cycle- lactic acid Disruption of cell membrane end stage in all form of shock Metabolic acidosis Tinnitus,vertigo . Visual disturbances Palpitations Chest pain arrythmias Cranial nerve palsies Headache Lethargy, stupor, and coma Mental confusion Dyspnea Hyperventilation Kussmaul respiration Nausea and vomiting Abdominal pain Diarrhea Polyphagia Generalized muscle weakness Bone pain Increased intracellular Ca Electric pump failure Increased intracellular Na Hypo calcemia Apoptosis

14. Various organ response contd Micro vascular Activation of complement and prime neutrophil Endothelial injury, increased permeability Edema Anasarca Systemic Cardiovascular Tachycardia Low BP Respiratory Increased rate Shallow breathing Renal Decreased urine output Endocrinological Release of catecholamine

15. Various organ response contd … Ischemia reperfusion injury Local inflammatory mediators get disseminated with increase in perfusion. Myocardial depression Vascular dilatation Endothelial injury in kidney and lungs Cause of delayed death after resuscitation in shock

16. Stages  Stage  I   compensated , or  nonprogressive  Stage  II   decompensated , or  progressive  Stage  III   irreversible Fast heart rate Vasoconstriction Slight decreased UO Treatment completely halt progression Compensatory methods begins to fail Symptoms more prominent Symptoms can be reversed Permanent damage done Heart failure Renal shutdown CNS dysfunction Cant be revived Death Mild Moderate Severe

17. Stages with clinical manifestations Parameters/stages Compensated Mild Moderate Severe Lactic acidosis + ++ +++ ++++ Urine output Normal Normal Reduced(<0.5ml/kg/ hr ) Anuric Consciousness level Normal Mild anxiety Drowsy Comatose Respiratory rate Normal Increased(>20 upto 30/minutes in adults) >30/minutes Shallow and labored Pulse rate 80 -100/min 100-130/min >130/min >130/min or not detected Blood pressure Normal Normal Mild hypotension Severe hypotension Short practice of baily and love 25 th edi

18. Stages with clinical manifestations various pitfalls Capillary refill Tachycardia Blood pressure Central venous pressure Hematocrit or hemoglobulin level So much variation No fixed universal value Can lead to

19. Classification First time in ninetienth century Cardiac cause Brain dysfunction Due to microorganisms Due to blood loss

20. Classification contd.. Emergency medicine by rosen and barkin 4 th edi H emorrhage Myocardial dyfxn Circulatory obstructiom hypovolemia AV fistula Sepsis Anaphylaxis dyshemoglubunemia Heat shock hypothermia

21. Classification contd.. Hypovolemic Cardiogenic Distributive O bstructive Bailey and Love 25 th edi

22. H ypovolemic shock Most common Shock is hypovolemic until diagnosed otherwise Some degree of component of all form of shock Hypovolemia Hypo Volume Reduction Body fluid Reduction in body fluid

23. Hypovolemic shock contd Definition Hypovolemic shock refers to a medical or surgical condition in which rapid fluid loss results in multiple organ failure due to inadequate circulating volume and subsequent inadequate perfusion . Vicious triad

24. Hypovolemic shock contd Total body fluid Intracellular fluid 40% Extracellular fluid 60% Interstitial 20% Plasma 40% 60% of total body weight Circulating blood Loss, main cause of hypovolemia

25. Hypovolemic shock etiology Causes Hemorrhage Hemorrhage H emorrhage 1 st , 2 nd and 3 rd Internal External RTA causig solid organ injury liver,spleen,lungs,GI tract Ulcers in GI tract Esophageal varices Dissection of aorta Hemoptysis B ronchogenic Ca Intra bronchial TB RTA Trauma due to any cause Gynaecological and obstetrics cause most common in Nepalese women Intraoperative bleeding ENT causes Bleeding diathesis DIC Blood on the floor, plus 4 more" = intrathoracic , intraperitoneal , retroperitoneal, pelvis/thigh

26. Hypovolemic shock etiology contd ENT bleeding producing shock Epistaxis Post tonsillectomy hemorrhage Intra and post operative bleedings Traumatic ENT bleedings

27. Hypovolemic shock etiology contd Causes other than hemorrhage Diarrhoea and vomiting Burns All kinds of burns Small bowel obstructions Hours of hyperglycemia (DKA) Tension pneumothorax Anaphylactic shock Fluid discharging lesions Dermal conditions

28. Hypovolemic shock stages Stages of hemorrhage Stage 1 (<15%, 750ml approximately) BP maintained Normal respiratory rate (12-20/min) Skin pale Normal mental status  to slight anxiet y Normal  capillary refill Normal urine output Stage 2( 15-30%, 750-1500ml approximately) Systolic blood pressure  maintained Increased  diastolic blood pressure Narrow  pulse pressure Tachycardia >100bpm Tachypnoea >20/min Pale , cold, and clammy skin Mildly anxious/Restless Delayed  capillary refill >2sec Urine output 20-30 ml/hour

29. Hypovolemic shock stages contd Stages of hemorrhage Stage 3( 30-40%, 1500-2000ml approximately) Systolic BP 100mmHg or less Marked  tachycardia >120 bpm Marked  tachypnea >30/min Confusion,  anxiety, agitation Sweating, cool, pale skin Delayed capillary refill >3sec Urine output 20 ml/hour Stage 4( >40%, >2000ml approximately) Tachycardia >140 Shallow respiration Systolic blood pressure of 70 mmHg or less Decreased consciousness , lethargy, coma Skin sweaty , cool, and extremely pale (moribund) Absent capillary refill Negligible urine output Survival is extremely unlikely

30. Hypovolemic shock contd Other clinical manifestations V ague symptoms like Lethargy Weakness Drowsiness Nausea,vomiting Abdominal pain Chest pain Difficult in respiration

31. Hypovolemic shock management Management algorithym Resuscitation History, clinical examination and investigations simultaneously ABC To find out The type of shock Doubt In the line of hypovolemic shock without delay Look for response Control of bleeder May require OT Done in ER With help of i.v. fluid therapy only after bleeding has stopped

32. Hypovolemic shock management contd i.v. fluid therapy Responders Transient Responders N on Responders When and how to administer the fluid Crystalloid Colloid Blood Best to replace the blood loss No O2 carrying capacity Hartman solution NS RL albumin

33. Hypovolemic shock management contd Long term critical care management and treat the primary . Use of vasopressors Phenylephrine Dobutamine adrenaline Never be used as primary method in hypovolemic shock Only when heart has something to pump i.e after fluid therapy Don’t flog the tired horse Monitoring Heart rate Noninvasive BP SPO2 Hourly UO ECG More invasive like CVP Cardiac output Systemic vascular resistance Preload Serious pts Systemic and Organ perfusion monitoring

34. Hypovolemic shock contd Systemic and Organ perfusion monitoring Urine output Level of conscious Base deficit/lactic acidosis Mixed venous oxygen saturation Less reliable More reliable End point in resusucitation Easily known when to start but slight difficult to decide when to stop Previously used Pulse BP Consciousness level Urine output Not that reliable Base deficit Mixed venous oxygen saturation Lactate

35. Obstructive shock Definition Form of shock associated with physical obstruction  of the great vessels or the heart itself causing the decreased blood supply and various manifestation leading progressively to multi-organ failure and ultimately death if not dealt properly. Pulmonary embolism Cardiac tamponade Tension pneumothorax Most common causes

36. Obstructive shock Obstructive shock has much in common with  cardiogenic shock , and the two are frequently grouped together. Some sources do not recognize obstructive shock as a distinct category, and categorize  pulmonary embolism  and  cardiac tamponade  under cardiogenic shock. Except for management of the underlying individual pathology the obstructive shock is similar to cardiogenic shock wikipedia Sabiston textbook of surgery 17th ed

37. Cardiogenic shock Life-threatening medical condition resulting from an inadequate circulation of blood  due to primary failure of the ventricles  of the heart to function effectively Characterized by systemic hypo perfusion due to severe depression of the cardiac index [<2.2 (L/min)/m 2 ] and sustained systolic arterial hypotension (<90 mmHg) despite an elevated filling pressure [ pulmonary capillary wedge pressure (PCWP) >18 mmHg ]. Ciculatory shock Insufficient  perfusion of tissue to meet the demands for oxygen and nutrients

38. Cardiogenic shock contd Highest mortality rate, 80% mortality More common in elderly More in patients with other comorbidities More in patients with STEMI Common in 2 nd episode of STEMI Common in patients with some intervention in the past LV failure accounts for ~80% of cases of CS complicating acute MI Leading cause of death of patients hospitalized with MI

39. Cardiogenic shock etiology Acute myocardial infarction/ischemia    LV failure   Papillary muscle/ chordal rupture— severe MR   Ventricular free wall rupture with sub acute tamponade   Hemorrhage   Excess negative inotropic or vasodilator medications    Prior valvular heart disease    Post-cardiac arrest Post- cardiotomy Refractory sustained tachyarrhythmias Acute fulminant myocarditis End-stage cardiomyopathy Most common

40. Cardiogenic shock etiology contd Left ventricular apical ballooning Hypertrophic cardiomyopathy with severe outflow obstruction Aortic dissection with aortic insufficiency or tamponade Pulmonary embolus Severe valvular heart disease Critical aortic or mitral stenosis Acute severe aortic or mitral regurgitation Toxic-metabolic Beta-blocker or calcium channel antagonist overdose

41. Cardiogenic shock pathophysiology

42. Cardiogenic shock contd Those at Special risk Acute MI Older age Female sex Prior MI Diabetes Anterior MI location Reinfarction soon after MI

43. Cardiogenic shock clinical signs and symptoms Continuing chest pain and dyspnea Appear pale, apprehensive, and diaphoretic Mentation altered , with somnolence, confusion, and agitation Pulse is typically weak and rapid (90–110 beats/min) or severe bradycardia due to high-grade heart block may be present

44. Cardiogenic shock clinical signs and symptoms contd Systolic blood pressure reduced (<90 mmHg) with a narrow pulse pressure (<30 mmHg) Tachypnea , Cheyne -Stokes respirations , and jugular venous distention may be present Precordium typically quiet , with a weak apical pulse S 1 soft and an S 3 gallop may be audible, systolic murmurs, Rales audible Oliguria (urine output <30 mL/h ) is common.

45. Cardiogenic shock management algorithym Treat the arrythmia

46. Laboratory Findings TLC elevated , left shift RFT initially normal , but BUN and creatinine rise progressively LFT deranged Anion-gap acidosis with elevation of the lactic acid level Cardiac markers markedly elevated Electrocardiogram Q waves and/or >2-mm ST elevation in multiple leads or left bundle branch block More than one-half of all infarcts associated with shock are anterior Global ischemia due to severe left main stenosis usually is accompanied by severe (e.g., >3 mm) ST depressions in multiple leads. Cardiogenic shock management algorithym contd

47. Cardiogenic shock management algorithym contd Chest Roentgenogram Pulmonary vascular congestion Pulmonary edema Heart size normal when CS results from a first MI but enlarged with a previous MI. Echocardiogram Left-to-right shunt Proximal aortic dissection with aortic regurgitation or tamponade Pulmonary embolism

48. Distributive shock M edical condition in which abnormal distribution of blood flow in the smallest blood vessels results in inadequate supply of blood to the body's tissues and organs. Types Septic shock most common Neurogenic shock Anaphylactic shock Blood accumulates

49. Septic shock & SIRS SIRS stand for “Systemic Inflammatory response syndrome ” Definition An exaggerated and generalized manifestation of a local immune or inflammatory reaction and is often fatal. Hyper metabolic state with two or more sign of systemic inflammation , such as fever, tachycardia, leukocytosis or leukopenia in a setting of known cause of inflammation . An   inflammatory state   affecting the whole body , frequently a response of the immune system to  infection , but not necessarily so, sometimes can be non-infectious. Rubin’s pathology 4 th edi Harrisson’s medicine 18th edi Wikipedia

50. Septic shock & SIRS Local response Systemic response rubor calor tumor dolor Functionolesia Fever or hypothermia Leukocytosis or leukocytopenia Tachycardia or bradycardia Systemic Inflammatory response syndrome Infectious Non infectious Mostly

51. Septic shock & SIRS Systemic Inflammatory response syndrome + Infection Sepsis Dysfunction of organ in the site distant from the site of infection with hypotension and hypo perfusion . Severe Sepsis + Hypotension and Hypo perfusion not corrected with fluid infusion for at least 1 h despite adequate fluid resuscitation Septic shock By consensus conference committee in 1992 and revised in 2001 +

52. Septic shock & SIRS Criteria of SIRS Fever more than 38°C (100.4°F ) or less than 36°C (96.8°F) Heart rate more than 90 beats per minute Respiratory rate Less than 20 breaths per minute or A rterial carbon dioxide tension ( PaCO   2 ) of less than 32 mm Hg Abnormal white blood cell count >12,000/µL or < 4,000/µL or > 10% immature band forms SIRS can be diagnosed when two or more of these criteria are present

53. Septic shock & SIRS Epidemiology Increase in incidence for last decade Good diagnostic facility Longevity of life among chronically diseased persons Wide spread use of immunosuppressive drugs indwelling catheters mechanical devices More in elderly and children No sex preponderance (M=F) Female more in developing countries due to Gynae /Obstetrics problems More in patients with chronic illness AIDS, DM, CKD

54. Septic shock & SIRS Some terms of special mention Bacteremia Presence of bacteria in blood, as evidenced by positive blood cultures Septicemia Presence of microbes or their toxins in blood Refractory septic shock Septic shock that lasts for >1 h and does not respond to fluid or pressor administration Multiple-organ dysfunction syndrome (MODS) Dysfunction of more than one organ, requiring intervention to maintain homeostasis

55. Septic shock & SIRS etiology Ischemia hemorrhage Complications of surgery Adrenal insufficiency Pulmonary embolism Complicated aortic aneurysm Cardiac tamponade Anaphylaxis Drug overdose NON INFECTIOUS

56. Septic shock & SIRS etiology contd

57. Septic shock & SIRS 20-40% of cases of severe sepsis 40-70% cases of septic shock Blood culture positive Approx. 80% Bacterial Fungi Mixture of other microbes

58. Septic shock & SIRS pathophysiology Most cases triggered by bacteria or fungi not causing systemic disease in immunocompetent hosts Some microbial pathogens, in contrast, can circumvent innate defenses because (1 ) lack molecules that can be recognized by host receptors ( 2) elaborate toxins or other virulence factors In both cases, the body can mount a vigorous inflammatory reaction resulting in severe sepsis yet fails to kill the invaders Septic response may also be induced by microbial exotoxins that act as superantigens (e.g ., toxic shock syndrome toxin 1 ) as well as by many pathogenic viruses .

59. Septic shock & SIRS pathophysiology Bacterial products CD14 TLR

60. Septic shock & SIRS clinical presentations How the patient presents ? In shock patient don’t present , rather he is presented by others. S E P S I S Shivering, fever or very cold Extreme pain and generalized discomfort Pale or discolored skin Sleepy, difficult to rouse, confused “I feel I might die” feeling of impending doom Shortness of breath

61. Septic shock & SIRS clinical presentations contd Superimposed on the symptoms and signs of the patient's underlying illness and primary infection. Rate at which severe sepsis develops may differ from patient to patient. some may be normo or hypothermic absence of fever most common in neonates in elderly patients in persons with uremia or alcoholism.

62. Septic shock & SIRS clinical presentations contd Hyperventilation Acrocyanosis and ischemic necrosis of digits Cellulitis , Pustules , bullae, or hemorrhagic lesions

63. Septic shock & SIRS clinical presentations contd Skin lesions may suggest specific pathogens occasionally Sepsis with cutaneous petechiae or purpura then N. meningitidis (or, less commonly, H. influenzae ) Patient bitten by a tick endemic area , petechial lesions suggest Rocky Mountain spotted fever Cutaneous bullous lesion, surrounded by edema, that undergoes central hemorrhage and necrosis almost exclusively in neutropenic patients is ecthyma gangrenosum , caused by P. aeruginosa . Hemorrhagic or bullous lesions with h/o eating raw oysters suggest V. vulnificus  bacteremia Generalized erythroderma in a septic patient suggests the toxic shock syndrome due to S. aureus or S. pyogenes .

64. Septic shock & SIRS clinical presentations contd Gastrointestinal manifestations Nausea , vomiting, diarrhea, and ileus Stress ulceration can lead to upper GI bleeding Cholestatic jaundice Hepatocellular or canalicular dysfunction

65. Septic shock & SIRS major complications Cardiopulmonary Complications Acute lung injury or ARDS in  50% cases Respiratory muscle fatigue hypoxemia and hypercapnia elevated pulmonary capillary wedge pressure (>18 mmHg) volume overload or cardiac failure Pneumonia caused by viruses or by Pneumocystis Sepsis-induced hypotension refractory hypotension Depression of myocardial function Death results from refractory shock or the failure of multiple organs rather than from cardiac dysfunction per se.

66. Septic shock & SIRS major complications contd Adrenal Insufficiency P lasma cortisol level of <15mcg/mL Hypotension that is refractory to fluid replacement and requires pressor therapy Renal Complications Oliguria A zotemia P roteinuria Nonspecific urinary casts Acute tubular necrosis G lomerulonephritis R enal cortical necrosis I nterstitial nephritis

67. Septic shock & SIRS major complications Coagulopathy Platelet counts are usually very low (<50,000/ microL ) DIC Immunosuppression Neurologic Complications Polyneuropathy Guillain-barré syndrome Motor weakness

68. Septic shock & SIRS management Investigations Blood investigations Leukocytosis or Leukopenia Thrombocytopenia becoming more severe with advanced disease Neutrophils may contain toxic granulations , Döhle bodies , or cytoplasmic vacuoles Prolongation of the thrombin time Decreased fibrinogen The presence of d-dimers Azotemia LFT deranged Active hemolysis suggests clostridial bacteremia , malaria , a drug reaction, or DIC DIC In the case of DIC , microangiopathic changes may be seen on a blood smear

69. Septic shock & SIRS management contd Arterial blood gas Respiratory alkalosis due to hyper ventilation Metabolic acidosis (with increased anion gap ) typically supervenes Hypoxemia initially correctable with supplemental oxygen, if refractoriness to 100% oxygen indicates right-to-left shunting Chest radiograph May be normal May show evidence of U nderlying pneumonia Volume overload Diffuse infiltrates of ARDS Electrocardiogram sinus tachycardia nonspecific ST–T-wave abnormalities.

70. Septic shock & SIRS management contd Sugar profile Hyperglycemia Hypoglycemia occurs rarely Severe infection may precipitate diabetic ketoacidosis that may exacerbate hypotension Serum albumin level declines as sepsis continues Hypocalcemia rare Urine R/E Hematuria Proteinuria Pus cells

71. Septic shock & SIRS management contd Diagnosis N o specific diagnostic test Diagnostically sensitive findings Fever or hypothermia Tachypnea or tachycardia Leukocytosis or leukopenia Acutely altered mental status Thrombocytopenia An elevated blood lactate level Hypotension

72. Septic shock & SIRS management contd Quite variable manifestation In one study( PGI chandigarh ) 33% had a normal temperature 44% had a normal respiratory rate 14% had a normal pulse rate 38% had normal white blood cell counts. Systemic responses of uninfected patients with other conditions may be similar to those characteristic of sepsis.

73. Septic shock & SIRS management contd Definitive etiologic diagnosis Culture Blood Local infection site Two blood samples From two different venipuncture sites Patient with an indwelling catheter one sample from each lumen and another via venipuncture Many negative Antibiotic administration Slow-growing or fastidious organisms Absence of microbial invasion Gram staining Polymerase chain reaction To identify microbial DNA in peripheral-blood or tissue samples Definitive Sometimes

74. Septic shock & SIRS management contd Examine skin and mucosa for lesions that might yield diagnostic information as described earlier. With overwhelming bacteremia Pneumococcal sepsis in splenectomized individuals Fulminant meningococcemia Infection with V. Vulnificus , B. Pseudomallei , or Y. Pestis Microorganisms are sometimes visible on buffy coat smears of peripheral blood .

75. Septic shock & SIRS management Personnel who are experienced in the care of the critically ill Urgent measures to treat the infection To provide hemodynamic and respiratory support To eliminate the offending microorganisms These measures should be initiated within 1 hour of the patient's presentation Rapid assessment and diagnosis are very essential

76. Septic shock & SIRS management contd A ntimicobials Resuscitation Hemodynamic, Respiratory, and Metabolic Support Removal of infection source S imultaneously General support

77. Septic shock & SIRS management contd Anti microbial agents Immunocompetent Piperacillin-tazobactam (3.375 g q4–6h) Imipenem-cilastatin (0.5 g q6h) Meropenem (1 g q8h) Cefepime (2 g q12h) If allergic to lactam agents C iprofloxacin (400 mg q12h) L evofloxacin (500–750 mg q12h) plus clindamycin (600 mg q8h) Vancomycin (15 mg/kg q12h) should be added to each of the above regimens

78. Septic shock & SIRS management contd Neutropenic (<500 neutrophils/L ) Imipenem-cilastatin (0.5 g q6h) or Meropenem (1 g q8h) or Cefepime (2 g q8h) Piperacillin tazobactam (3.375 g q4h) plus tobramycin (5–7 mg/kg q24h) Vancomycin (15 mg/kg q12h) should be added if indwelling vascular catheter has received quinolone prophylaxis has received intensive chemotherapy that produces mucosal damage Staphylococci are suspected Empirical antifungal therapy with an echinocandin or amphotericin B

79. Septic shock & SIRS management contd IV drug user Vancomycin (15 mg/kg q12h ) AIDS Cefepime (2 g q8h) or piperacillin-tazobactam (3.375 g q4h) plus tobramycin (5–7 mg/kg q24h) If the patient is allergic to lactam drugs C iprofloxacin (400 mg q12h) or levofloxacin (750 mg q12h) plus vancomycin (15 mg/kg q12h) plus tobramycin Splenectomy Cefotaxime (2 g q6–8h) or ceftriaxone (2 g q12h) Add vancomycin , If local prevalence of cephalosporin-resistant pneumococci high Patient allergic to lactam drugs vancomycin (15 mg/kg q12h) plus either moxifloxacin (400 mg q24h) or levofloxacin (750 mg q24h) or aztreonam (2 g q8h)

80. Septic shock & SIRS management Removal of the Source of Infection Drainage of a focal source of infection is essential lungs , abdomen and urinary tract Foley and drainage catheters should be replaced Indwelling IV or arterial catheters removed Tip rolled over a blood agar plate for culture New catheter should be inserted at a different site after initiation of antibiotic therapy The possibility of paranasal sinusitis for patient with nasal intubation .

81. Septic shock & SIRS management Hemodynamic, Respiratory, and Metabolic Support Primary goals to restore adequate oxygen and substrate delivery to the tissues to improve tissue oxygen utilization and cellular metabolism to make adequate organ perfusion, restore circulation General Support Nutritional supplementation by enteral delivery route Prophylactic heparinization to prevent deep venous thrombosis Prevention of skin breakdown, nosocomial infections, and stress ulcers . Tight control of the blood glucose concentration

82. Septic shock & SIRS management Prognosis 20–35 % of patients with severe sepsis and 40–60% of patients with septic shock die within 30 days, Others die within the ensuing 6 months. Late deaths poorly controlled infection immunosuppression complications of intensive care failure of multiple organs the patient's underlying disease Case-fatality rates similar for culture-positive and culture-negative severe sepsis With no known preexisting morbidity Case-fatality rate <10 % until 40 years of age , increases to exceed 35% in the very elderly Death is significantly more likely in severely septic patients with preexisting illness

83. Septic shock & SIRS management Prevention Best to reduce morbidity and mortality Most cases complications of nosocomial infections Reducing the number of invasive procedures undertaken Limiting the use (and duration of use) of indwelling vascular and bladder catheters Reducing incidence and duration of profound neutropenia (<500 neutrophils/L ) Aggressively treating localized nosocomial infections Avoid indiscriminate use of antimicrobial agents and glucocorticoids

84. Neurogenic shock Distributive  type of shock resulting in  low blood pressure , occasionally with a  slowed heart rate , that is attributed to the disruption of the autonomic pathways within the spinal cord . Low blood pressure due to decreased systemic vascular resistance  results in pooling of blood within the extremities lacking sympathetic tone . The slowed heart rate results from unopposed  vagal  activity and has been found to be exacerbated by  hypoxia and endo bronchial suction.

85. Neurogenic shock Peripheral pooling of blood makes less blood available for tissue perfusion, decreased venous return causing decreased cardiac output . Neurogenic shock can be a potentially devastating complication, leading to organ dysfunction and death if not promptly recognized and treated It is not to be confused with  spinal shock , which is not circulatory in nature .

86. Neurogenic shock etiology Blunt or penetrating trauma/injury to the spinal cord Rotation, dislocation, over- flexion/extension of the spinal cord. Motor vehicle accidents Sports injuries Falls, stab and gunshot wounds. Improper administration of regional anesthesia Drugs and medications which affect the autonomic nervous system can also cause neurogenic shock

87. Neurogenic shock clinical signs and symptoms Hypotension Bradycardia Hypothermia Difficulty in breathing and has rapid and deep shallow breathing. The skin feels warm to touch in contrast to hypovolemic and cardiogenic Facial pallor Dizziness, lightheadedness, fainting Nausea and vomiting

88. Neurogenic shock clinical signs and symptoms Faint and rapid pulse. Patient experiences weakness due to insufficient blood supply. Patient stares blankly at nothing. Feels anxious and there can be changes in mental state or disorientation. Does not respond to any stimuli. Has bluish discoloration of lips and fingers (cyanosis). Decreased or absent urine output. Sweats profusely. Considerable chest pain. Loss of consciousness.

89. Neurogenic shock diagnosis Complete physical examination and medical history Key to the diagnosis Various tests Blood Urine tests Imaging CT scan MRI scan X-rays Ultrasound Carried out to assess the patient's medical condition and the extent of injury or damage.

90. Neurogenic shock management protocol Assessment of general condition Stabilize the patient and prevent any irreversible tissue damage including revival of the patient Simultaneus resuscitation Airway pattern Breathing including the circulation Spinal immobilization is must Arterial blood pressure, through administration of IV fluids to restore the mean pressure Inotrophics Dopamine D obutamine Other inotropic agents may be infused in case of inadequate fluid resuscitation

91. Neurogenic shock management protocol Severe bradycardia IV infusion of atropine given 0.5mg to 1 mg every 5 minutes for a total dosage of 3.0 mg a pacemaker if necessary High dosage of methylprednisolone within 8 hours following the onset of neurogenic shock in cases where neurological deficit has already been present. Vitals stable Immediately transfer the patient to neuro tertiary unit for definitive management to prevent the permanent neurological deficit Rehabilitation of the patients who have permanent disability

92. Anaphylactic shock A widespread and very serious allergic reaction with symptoms including   dizziness, loss of consciousness, labored breathing, swelling of the tongue and breathing tubes, blueness of the skin, low blood pressure,  heart failure, and death . Is a systemic , type I hypersensitivity reaction that often has fatal consequences . Caused by a runaway histamine response to an allergic reaction F oreign matter of any type penetrates the skin, mucous membranes, or digestive system histamine Increased blood to affected area Swelling from edema and inflammation Restricts blood flow to the affected area Protective action Protective action Mosquito bite Bee sting Normally

93. Anaphylactic shock In some individuals the histamine response is triggered by substances that are not inherently harmful to the human body Normal histamine response is atypically aggressive Causing the normal symptoms associated with a histamine response to be somewhat more severe A llergy Mostly it is only annoying not distressing In some causes acutely distressing symptoms Anaphylacsis Anaphylactic shock

94. Anaphylactic shock causes

95. Anaphylactic shock pathophysiology

96. Anaphylactic shock signs and symptoms

97. Anaphylactic shock management algorithm

98. References Harrison's Principles of Internal Medicine 18th Ed Short practice of baily and love 25 th edition Pathology basis of diseases, Robbins and C otran 7 th edi and 8 th edi Rubins pathology 4 th edition Emergency medicine by Rosen and Barkin 4 th edition Sabiston textbook of surgery 17th ed Textbook of medical physiology guyton and hall 11 th edi Scott Brown 7th edition Otorhinolaryngology, Head & Neck Surgery Internet ( www.google.com ) Wikipedia Medscape