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![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)/m2] 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](https://image.slidesharecdn.com/jhhrn8gq8qmjqmi9sytt-shock-and-sirs-240509182821-ab9c1a90/75/shock_and_sirs-in-basic-otolaryngology-pptx-37-2048.jpg)
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- 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 Hypovolemicshock Cardiogenic shock Obstructive shock Distributive shock Septic shock and SIRS Neurogenic shock Anaphylactic shock
- 3. Shock Definition It isa 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 Rosen and Barkin 4th edition Rubins pathology 4th 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. History First resuscitationefforts 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.. Firstintravenous 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 Alexis 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 causeof 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 fourpart 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)
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- 12. Pathophysiology contd.. Enters viciouscycle 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 organresponse 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 responsecontd 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 responsecontd… 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, ornonprogressive 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 clinicalmanifestations 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 25th edi
- 18. Stages with clinicalmanifestations 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 inninetienth century Cardiac cause Brain dysfunction Due to microorganisms Due to blood loss
- 20. Classification contd.. Emergency medicineby rosen and barkin 4th edi Qualitative Quantitative Shock Hemorrhage Myocardial dyfxn Circulatory obstructiom hypovolemia AV fistula Sepsis Anaphylaxis dyshemoglubunemia Heat shock hypothermia
- 21.
- 22. Hypovolemic shock Mostcommon 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 Hypovolemicshock 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 Totalbody 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 Hemorrhage 1st,2nd and 3rd Internal External RTA causig solid organ injury liver,spleen,lungs,GI tract Ulcers in GI tract Esophageal varices Dissection of aorta Hemoptysis Bronchogenic 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 etiologycontd ENT bleeding producing shock Epistaxis Post tonsillectomy hemorrhage Intra and post operative bleedings Traumatic ENT bleedings
- 27. Hypovolemic shock etiologycontd 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 Stagesof hemorrhage Stage 1(<15%, 750ml approximately) BP maintained Normal respiratory rate(12-20/min) Skin pale Normal mental status to slight anxiety 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 stagescontd 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 Otherclinical manifestations Vague symptoms like Lethargy Weakness Drowsiness Nausea,vomiting Abdominal pain Chest pain Difficult in respiration
- 31. Hypovolemic shock management Managementalgorithym 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 managementcontd i.v. fluid therapy Responders Transient Responders Non 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 managementcontd 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 Systemicand 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 ofshock 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 shockhas 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 medicalcondition 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)/m2] 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 2nd 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 etiologycontd 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.
- 42. Cardiogenic shock contd Thoseat Special risk Acute MI Older age Female sex Prior MI Diabetes Anterior MI location Reinfarction soon after MI
- 43. Cardiogenic shock clinicalsigns 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 clinicalsigns 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 S1 soft and an S3 gallop may be audible, systolic murmurs, Rales audible Oliguria (urine output <30 mL/h) is common.
- 45. Cardiogenic shock managementalgorithym Treat the arrythmia
- 46. Laboratory Findings TLCelevated, 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 managementalgorithym 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 Medical conditionin 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 4th 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 Arterial 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 Plasma cortisol level of <15mcg/mL Hypotension that is refractory to fluid replacement and requires pressor therapy Renal Complications Oliguria Azotemia Proteinuria Nonspecific urinary casts Acute tubular necrosis Glomerulonephritis Renal cortical necrosis Interstitial 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 Underlying 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 No 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 Antimicobials Resuscitation Hemodynamic, Respiratory, and Metabolic Support Removal of infection source Simultaneously 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 Ciprofloxacin (400 mg q12h) Levofloxacin (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 Ciprofloxacin (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 typeof 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 poolingof 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 clinicalsigns 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 clinicalsigns 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 Completephysical 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 managementprotocol 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 Dobutamine Other inotropic agents may be infused in case of inadequate fluid resuscitation
- 91. Neurogenic shock managementprotocol 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 widespreadand 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 Foreign 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 Mosquito bite Bee sting Normally
- 93. Anaphylactic shock In someindividuals 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 Allergy Mostly it is only annoying not distressing In some causes acutely distressing symptoms Anaphylacsis Anaphylactic shock
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- 96. Anaphylactic shock signsand symptoms
- 97. Anaphylactic shock managementalgorithm
- 98. References Harrison's Principlesof Internal Medicine 18th Ed Short practice of baily and love 25th edition Pathology basis of diseases, Robbins and Cotran 7th edi and 8th edi Rubins pathology 4th edition Emergency medicine by Rosen and Barkin 4th edition Sabiston textbook of surgery 17th ed Textbook of medical physiology guyton and hall 11th edi Scott Brown 7th edition Otorhinolaryngology, Head & Neck Surgery Internet (www.google.com) Wikipedia Medscape
Editor's Notes
- #4 Differen books have different ways of defining the shock.
- #5 Despit many definitions.the main thing to occur in shock is tissue hypoxia leading to many manifestations.
- #6 First resusucitation by pare,Pare used enemas to administer fluid in rectum of bleedin patients. Treatment of shock started back in dec14,1650,by Dr. William ,during process of autopsy he put a pungent smellin oil(cordial) in her mouth,she coughed out.this was later classified as neurogenic shock.
- #7 First intravenous fluid therapy in 1830 by Herman for cholera,However his son died of the fluid he used.then he went in isolation. Rude unhinging of machinery of life -Since mitochondria are the ultimate consumer of oxygen in cells, mitochondria might indeed be the machinery of life rudely unhinged by shock, shock can result in inherent mitochondrial dysfunction as manifested by decoupling. This pathologic condition has been recently termed cytopathic hypoxia. Crile was first to do blood transfusion,but his blood transfusion killed many patients,later on alexis carrel went on to study about blood group which was immense help in treating bleeding patients.
- #8 Most common & most important cause of death among surgical patients. So surgeons must understand the pathophysiology and diagnosis of shock and hemorrhage as well as their priorities for management
- #9 Road traffic accident are very common in Nepal mostly due to the poor condition of road,resulting in many death and morbidity accounting for many cases of shock every year. Recent earthquake leaving about 7619 dead and 14454 injured with property loss of around 7billion usd was the major cause of shock.
- #10 Circulatory system can be considered as a machine consisting of 4 parts,If any defect occurs in any of this part of the device,that may lead to development of shock.
- #13 Cell maintains order through biosynthesis of high energy compounds which are used to make cell component and run the cell machinery,cell in this process utilizes various substrates but if their source is disrupted for long period of time,they enter a vicious cycle with one event aggravating the other.
- #14 Metabolic acidosis can result in a variety of nonspecific changes in several organ systems, including, but not limited to, neurologic, cardiovascular, pulmonary, gastrointestinal, and musculoskeletal dysfunction. Symptoms are often specific to and a result of the underlying etiology of the metabolic acidosis. Dysfunction of cell membranes is thought to represent a common end-stage pathophysiologic pathway in the various forms of shock. Normal cellular transmembrane potential falls, and there is an associated increase in intracellular sodium and water, leading to cell swelling that interferes further with microvascular perfusion. In a preterminal event, homeostasis of calcium via membrane channels is lost with flooding of calcium intracellularly and a concomitant extracellular hypocalcemia. There is also evidence for a widespread but selective apoptotic (programmed cell-death) loss of cells, contributing to organ and immune failure.
- #16 Local inflammatory mediators like potassium,acid and various cytokines collected in the local area gets dissiminated with the established perfusion causing various complications ,leading to multiorgan dysfunction.it is called ischaemia reperfusion injury and is the cause for delayed death after resuscitation in shock.
- #17 when low blood flow (perfusion) is first detected, a number of systems are activated in order to maintain/restore perfusion. The result is that the heart beats faster, the blood vessels throughout the body become slightly smaller in diameter, and the kidney works to retain fluid in the circulatory system. All this serves to maximize blood flow to the most important organs and systems in the body. The patient in this stage of shock has very few symptoms, and Treatment completely halt progression Next satge,due to continuing insult the compensatory mechanisms begin to fail with more prominent symptoms,but till now the symptoms can be reversed if urgent steps are taken.it can be of mild and moderate type. Then on further deterioration or pts in shock for about 12hrs he enters stage 3 or irreversible stage.from where pts cant be revived and death is the result. In Stage II of shock, these methods of compensation begin to fail. The systems of the body are unable to improve perfusion any longer,and the patient's symptoms reflect that fact. Oxygen deprivation in the brain causes the patient to become confused and disoriented,while oxygen deprivation in the heart may cause chest pain. With quick and appropriate treatment, this stage of shock can be reversed. In Stage III of shock, the length of time that poor perfusion has existed begins to take a permanent toll on the body's organs and tissues.The heart's functioning continues to spiral downward, and the kidneys usually shut down completely. Cells in organs and tissuesthroughout the body are injured and dying. The endpoint of Stage III shock is the patient's death.
- #19 Most pt in shock have pale and cold peripheries,however the actual capillary refill time varies so much in adults that it cant be taken as marker to differentiate stages properly for some normal value can be 3 bt in well built athelete it can be2 seconds in old people with wrinkling of skin it can normally be 5 sec Tachy cardia may not always accompany shock,esp in pts with Beta blockers and in pts with pacemakers,in patients with penetrating trauma but with little tissue damage but massive hemorrhage there may be paradoxical brady cardia rather than tachycardia for shocked state Blood pressure low BP is last stage of shock,children and fit young people can maintain BP until very last minute,they can be profound shock with normal BP.elderly pt who are normally hypertensive can have normal range BP in shock. There is ongoing debate as to the indications for using the CVP,Most patients in the ICU can be safely managed without the use of a CVP. However, in shock with significant ongoing blood loss, fluid shifts, and underlying cardiac dysfunction, a CVP may be useful, its value are aslo not fixed it may be normal for a lean and thin person to have CVP of 5cm h2o while 10cm of h20 can be normal in well built person.however recent guideline suggest change in CVP to be a reliable guideline. Even after acute hemorrhage, hemoglobin and hematocrit values do not change until compensatory fluid shifts have occurred or exogenous fluid is administered. Thus, an initial normal hematocrit does not disprove the presence of significant blood loss.
- #20 Multiple classification schemes have been developed in an attempt to explain dissimilar processes leading to shock. Strict adherence to a classification scheme may be difficult from a clinical standpoint because of the frequent combination of two or more causes of shock in any individual patient,
- #21 Many books have different classifications Qualitative interfering with cellular metabolism and hemostatic mechanisms while quantitative is due to reduced perfusion to larger percentage of body weight. Though classified differently most of the time they overlap each other.
- #22 For the ease of description it can broadely divided into 4 main types
- #23 Most common and all shock are considered hypovolemic until diagnosed otherwise,similarly it is also a component of all form of shock.
- #24 Hemorrhage leads to hypovolemic state causing inadequate perfusion leading to anaerobic metabolism leading to production of lactic acidosis causing coagulopathy which further increases the bleeding,also due to decreased blood supply the tissues cant maintain their temperature causing hypothermia which further causes coagulopathy.
- #26 Hemorrhage is the most common cause of shock,it is so common that its can be taken as first 2nd and third most common cause of shock.hemorrhage can be of 2 types Internal is bleeding from internal organs that may be visible outside or may not be visible outside,while external is the type of bleeding that is visible outside.external can be quantified and is less dangerous than it seems but since we cant quantify the internal loss it is more dangerous though it may not seem so,kills the patient silently. so look for obvious signs of external bleeding while remembering that people can bleed to death internally without any external blood loss. ("Blood on the floor, plus 4 more" = intrathoracic, intraperitoneal, retroperitoneal, pelvis/thigh).few causes bleeding diathesis hemophilia,vonwillebrand disease,platelet disorders,coagulation factors difficiency can cause both external and internal hemorrhage. Gynaecological obstretic bleeding are the most common killers of women in our country most common being pph and bleedin secondary to abortion
- #28 Diarrhoea and vomiting following gastroenteritis followed by burns of all kind flame burns,scald burns,electric burns(mostly cause cardiogenic but may also cause hypovolemic) are amongst the commonest non hemorrhagic cause of hypovolemic shock.
- #31 If the patient is complainin of these vague symptoms following the history of trauma or major event,through examination and evaluation has to be done coz sometimes these can be only features complained in the pts with shock specially in elderly,children and if pts are in disoriented stage.
- #32 For management multidiscipilary team of surgeons,physicians is required.prmary aim is to maintain the airway,breathing and circulation with side by side taking a concise history n doing the needed examinations and investigations.after ABC primary aim shud be to control the bleedin,fluid therapy shudnt be given prior to it coz it may lead to rise in BP and increase bleeding.the control of bleedin can be done in ER or sometimes the patients has to be transferred to OT.only once the bleedin has been controlled we can administer the fluid.
- #33 There is a ongoing debate abt the choice of the fluid but according baily and love 25 edi,its not choice of fluid that’s more imp it’s when and how to give the fluid that’s more imp.crystalloids and colloids have similar benefit with crystalloid being required 1,3 time than colloid for same volume of replacement.best replacement for blood loss is blood coz colloid and crystalloid donot have o2 carrying capacity.after the fluid therapy there are broadly 3 types of patients- responders who show improve in CVS status and that is sustained,there is no active bleeding but require filling to a normal volume status, next are transient responders showing improvements bt reverting to their previous statusover next 10 to 20 minutes,may have moderate on going blood loss. then there are non responders who have severe volume depletion with major ongoing loss of blood.
- #34 Vasopressor agents are not used as primary agents in hypovolemic shock as contrast to cardiogenic and distributive shock,they should only be used once fluid therapy has been done,otherwise they will cause more harm than benefit by the saying donot flog the tired horse .after that it requires a long term critical care management and treatment of the primary cause. throughout the management process there should be continuous monitoring with atleast pulse,BP,SPO2,hourly UO,ECG and in severe patients wit invasive methods like CVP and CO.no normal value of CVP is there,some pts require 5cmH2o while others may require 15cmH2O.normal CVP response is rise in CVP by2-5cm with infusion of 250-500 ml of fluid and returning back to normal in 10-20 mins.pts with no change in cvp are empty with fluids and require more fluid. Cardiac output may be used to differentiate various type of shock.now coming in evaluation of systemic and organ perfusion monitoring
- #35 For systemic and organ perfusion urine output and consciousness level are less reliable coz urine output is measured hourly so minute to minute monitoring is no possible,and for consciousness brain’s perfusion is maintained till last so it can sometimes be misleading to find the severity of shock While base deficit(with value>6 having much higher morbidity and mortality) and mixed venous oxygen saturation(normal value of 50-70%,<50 signifies inadequate oxygen delivery occurring in cardiogenic and hypovolemic shock while value >70 are more often consistent with septic shock,due to inappropriate utilization of oxygen at cellular level ) give good results. For end point for resuscitation previously pulse,BP,Consciousness level and urine output were used but these monitors the systems whose perfusion is maintained till very last,(GI,skin are under perfused with these value being normal causing reperfusion injury)so others investigations like base deficit,lactate level,mixed venous saturation are used to find out when to end resuscitation
- #37 So I will be discussing obstructive shock in the cardiogenic shock briefly
- #40 MI is the most important cause for cardiogenic shock,and the complications that occur after MI are mostly responsible for causing it.
- #42 LVEDP-LT ventricular end diastolic volume it is preload that is amt of blood in diastolic stage that stretches the heart.
- #51 Any infection has a local and systemic response,the infection with systemic features if not dealt in time leads to SIRS.which may be of both infectious and non infectious origin more commonly infectious though.
- #56 Etiology can be both infectious and non infectious.
- #57 The various bacterial infections causing SIRS and septic shock are represented in the figure.
- #60 Humans have exquisitely sensitive mechanisms for recognizing and responding to certain highly conserved microbial molecules. Recognition of the lipid A moiety of lipopolysaccharide is the best-studied example Bacterial products bind to dendritic cells which are the main antigen presenting cells, leading either to their destruction causing paralysis of antiviral response or deranging their function causing dysregulated costimulation leading to self harm. Mainly by gram negative bacteria through their lipopoly saccharides or by gram positive bacteria through their lipoteichoic acid.LPS with its lipid A binds to CD14 which is cluster differentiation) receptor on macrophage leading to toll like receptor(TLR) induction.TLR is primary sensor of innate immune system that recognize bacteria,fungi,virus and protozoa.leading to production of various mediators most important being TNF alfa,viral glycoprotein,interlukin 6,Tissue factor Bacterial products also acts on hepatocytes causing liver dysfxn and inhibition of clotting factor synthesis leading to hemorrhagic syndromes They invade adrenal cortical cells causing inhibiting its hormone release leading to hypotension and metabolic disorder .
- #61 Major clinical manifestations are.
- #63 Hyperventilation is often a early sign of a septic shock while lethargy,drowsiness,coma are not consistent with stage of shock may appear any time. Acrocyanosis and ischemic necrosis of peripheral tissues, most commonly the digits is due to Hypotension and DIC. Cellulitis, pustules, bullae, or hemorrhagic lesions may develop when hematogenous bacteria or fungi seed the skin or underlying soft tissue. Continuing with skin lesion
- #64 skin lesions may suggest specific pathogens occasionally. When sepsis is accompanied by cutaneous petechiae or purpura, infection with N. meningitidis (or, less commonly, H. influenzae) should be suspected; patient who has been bitten by a tick while in an endemic area, petechial lesions also suggest Rocky Mountain spotted fever. A cutaneous bullous lesion, surrounded by edema, that undergoes central hemorrhage and necrosis seen almost exclusively in neutropenic patients is ecthyma gangrenosum, usually caused by P. aeruginosa. Histopathologic examination shows bacteria in and around the wall of a small vessel with little or no neutrophilic response. Hemorrhagic or bullous lesions in a septic patient 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.
- #65 Gastrointestinal manifestations such as nausea, vomiting, diarrhea, and ileus may suggest acute gastroenteritis. Stress ulceration can lead to upper gastrointestinal bleeding. Cholestatic jaundice, with elevated levels of serum bilirubin (mostly conjugated) and alkaline phosphatase, may precede other signs of sepsis. Hepatocellular or canalicular dysfunction appears to underlie most cases, and the results of hepatic function tests return to normal with resolution of the infection.
- #71 Most diabetic patients with sepsis develop hyperglycemia. Severe infection may precipitate diabetic ketoacidosis that may exacerbate hypotension (Chap. 344). Hypoglycemia occurs rarely. The serum albumin level declines as sepsis continues. Hypocalcemia is rare.
- #88 Hypotension (low blood pressure) occurs as a result of decrease in the systemic vascular resistance, which causes pooling of blood within the extremities resulting in decreased sympathetic tone. Bradycardia is another primary sign of neurogenic shock. Nerve injury causes relaxation of the blood vessels walls resulting in decreased heart rate. Bradycardia in spinal cord injury is also found to be worsened by hypoxia or decreased blood supply. The resting heart rate in bradycardia is below 60 beats/ minute and can even go lower when the patient is in neurogenic shock. Hypothermia (decreased body temperature) can occur in neurogenic shock due to loss of sympathetic tone leading to decreased core circulation, excessive loss of heat and massive decrease in body temperature. Patient feels very cold, with warm limbs and the rest of the body is cold to touch in contrary to hypovolemic and cardiogenic shock.
- #91 Assessing the general condition of the patient is the initial step in managing neurogenic shock. The goal of treatment is to stabilize the patient and prevent any irreversible tissue damage including revival of the patient. The patient under neurogenic shock must be carefully assessed of their general condition giving importance to airway pattern and breathing including the circulation. Neurogenic shock is potentially a life-threatening situation that requires a medical emergency to preserve the life of the patient. Spinal immobilization is necessary to prevent further spinal cord damage. Arterial blood pressure should be given immediate attention through administration of IV fluids to restore the mean pressure. Dopamine and other inotropic agents may be infused in case of inadequate fluid resuscitation.
- #92 Severe bradycardia can be managed with IV infusion of atropine given 0.5mg to 1 mg every 5 minutes for a total dosage of 3.0 mg or a pacemaker if necessary. High dosage of methylprednisolone on the other hand may be given within 8 hours following the onset of neurogenic shock in cases where neurological deficit has already been present. Immediate transfer to the nearest hospital is necessary once the patient has been stabilized for further treatment and to further ensure the safety of the patient including life preservation.
- #94 However, for reasons that are not totally understood, in some individuals the histamine response is triggered by substances that are not inherently harmful to the human body or a normal histamine response is atypically aggressive, causing the normal symptoms associated with a histamine response to be somewhat more severe. This condition is known as an allergy. In most allergy sufferers, this histamine response is annoying, but not life threatening. For example, the sufferer may have an excessively runny nose, hives or a rash. However, in some individuals, the histamine response continues unabated. Body tissues swell up, blood vessels throughout the body become constricted, and the bronchial tubes in the lungs become inflamed, constricted and full of mucous. As a result, the individual's breathing starts to become labored and if left untreated the sufferer can die from suffocation. A panic attack is often mistaken for anaphylactic shock as it also presents as a seeming inability to breathe. However, injecting adrenaline for a panic attack will naturally make the symptoms worse. The two conditions can usually be distinguished by the fact that respiration and heartbeat become rapid in anaphylactic shock, while they remain close to normal in a panic attack despite the perception that the patient is having trouble breathing.