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SHOCK - PowerPoint PPT Presentation

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SHOCK. September 6, 2005 Andrew Filiatraut. In General. Shock Clinical syndrome defined as hypoperfusion Hypotension and Cellular Hypoxia Elevated lactate Oliguria Hepatic/GI dysfunction Mental status changes . In General. Four Classifications Hypovolemic Cardiogenic Obstructive

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September 6, 2005

Andrew Filiatraut

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In General

  • Shock

    • Clinical syndrome defined as hypoperfusion

      • Hypotension and Cellular Hypoxia

        • Elevated lactate

        • Oliguria

        • Hepatic/GI dysfunction

        • Mental status changes

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In General

  • Four Classifications

    • Hypovolemic

    • Cardiogenic

    • Obstructive

    • Distributive

      • Septic, Addison’s, Anaphylactic, Neurogenic, Thyrotoxicosis, Beriberi, Paget’s, Cirrhosis, Chroinc Anemia, Osler-Weber-Rendu

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  • 751,000 cases of severe sepsis /year

  • Up to half develop shock

  • Overall mortality rate of 45%

  • Cause

    • Gram+ 35-40%

    • Gram- 55-60%

  • Slightly higher incidence in men, older adults (55-60 yrs)

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  • Infection

    • Inflammation against microorganism

  • Bacteremia

    • Viable bacteria in blood

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  • SIRS

    • Evidence of inflammation NOT necessarily infection

    • 2 or more of the following

      • Temp>38 or <36

      • HR >90bpm

      • RR >20 or PaCo2 <32

      • WBC’s >12,000 or <4000 or >10% bandemia

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  • Sepsis

    • systemic inflammatory response as a result of infection

  • Severe Sepsis

    • sepsis associated with organ dysfunction

      • Lactic acidosis, oliguria, mental status change

  • Septic shock

    • sepsis-induced hypotension with presence of perfusion abnormalities

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  • Sepsis-induced hypotension

    • SBP<90 or reduction of 40mm Hg from baseline without other cause

  • Multiple Organ Dysfunction Syndrome

    • Altered organ dysfunction in acutely ill patient requiring intervention to maintain homeostasis

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  • Focus of infection

    • Pneumonia, UTI, cellulitits, abscess, indwelling device

    • ICU: catheters, sinusitis, acalculus cholecystitis, C. diff, resistant organism, fungal infection

  • Blood stream invasion or proliferation of organism at site

  • Exogenous toxin release

  • Activation of endogenous mediators

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Molecular Mediators in Pathophysiology

  • Three phases

    • Induction

    • Cytokine synthesis & secretion

    • Cascade

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Molecular Mediators in Pathophysiology

  • Induction

    • Interaction of microbial molecules with host

      • Mediators activated that amplify & transmit the microbial signal to other cells

      • Ex LPS binds to LPS binding protein which is detected by CD14 releasing TNF-alpha

      • Peptidoglycan & lipoteichoic acid of gram (+) induce similarly

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Molecular Mediators in Pathophys

  • Cytokine cascade

    • Activation & release of central mediators

      • TNF-alpha and IL-1

    • Release of secondary mediators

      • IL-6, IL-8, PAF, PG’s, leukotrienes

    • Activation of neutrophils, complement system, vascular endothelial cells

    • Synthesis of acute phase reactants

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Molecular Mediators in Pathophys

  • Parallel to SIRS is CARS

    • Compensatory Anti-inflammatory Response System

      • Attempts to down regulate the SIRS response

      • IL-4, IL-10, transforming growth factor beta, CSF, soluble receptors to TNF, antagonists to TNF-alpha and IL-1

      • If CARS reaction is severe it will manifest as anergy and infection susceptibility

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Vasoactive Mediators in Pathophys

  • Nitric Oxide

    • Produced by endothelium

    • Increased levels during shock

    • Actions at high levels

      • Mediator of vasodilation & hypotension

      • Direct cellular toxicity

      • Myocardial depression

      • Increased permeability

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Clinical Features

  • Constitutional

    • Hyper/hypothermia

    • Tachycardia

    • Tachypnea

    • Wide pulse pressure

    • Mental status change

      • Most likely obtunded

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Clinical Features

  • Cadiovascular

    • Early, vasodilators predominate

    • Cardiac output is increased with tachycardia

      • CO=SV x HR

      • i.e. Initially patients will have warm extremities

    • If not treated aggressively decompensation ensues

    • Typically hypotension is not reversible with fluids alone

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Clinical Features

  • Pulmonary

    • Sepsis is most common condition associated with ARDS

      • Lung edema from increased permeability

        • Alveolar edema dyspnea, hypoxemia, opacities on CXR

        • B/L infiltrates, wedge pressure <18

        • Endotoxin, TNF-alpha, IL-1, IL-6, IL-8, bactericidal/permeability-increasing (BPI) protein

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Clinical Features

  • Pulmonary

    • ARDS

      • B/L pulmonary infiltrates

      • PCWP <18 (non-cardiogenic pulm edema)

      • PaO2/FiO2 <200

        • If PaO2/FiO2 >200, but <300 then ALI

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Clinical Features

  • Renal

    • Acute renal failure w/ azotemia, oliguria, active urinary sediment

      • Hypotension/Dehydration, aminoglycosides, pigmenturia (e.g. myoglobinuria)

      • Immune complex deposition

        • IgG, IgM,C3, bacterial antigens & antibodies

      • Tubulointersitial disease

        • S. pneumoniae, S. pyogenes, Legionella, salmonellosis, brucellosis, diptheria

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Clinical Features

  • Gastrointestinal

    • Accelerated apoptosis of GI epithelial cells

      • Can lead to blood loss anemia

    • Cholestatic jaundice (most frequent abnormality)

      • Transaminase/Alkaline phosphatase 1-3x normal

      • Bilirubin concentrations, usually not >10mg/dL

        • Hemolysis of RBC’s, hepatocellular dysfunction due to endotoxin

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Clinical Features

  • Hematologic

    • Minor blood loss secondary to erosions in mucosal layer of stomach/duodenum

    • Accelerated apoptosis of lymphocytes

      • Possibly due to elevated glucocorticoids

    • Most frequent changes are neutrophilia or neutropenia, thrombocytopenia, DIC

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Clinical Features

  • Hematologic

    • Neutrophilia

      • Most common

      • Left shift

        • Demargination & release of less mature granulocytes from BM

          • C3a causes release of neutrophil releasing substance

      • Sustained neutrophilia is secondary to CSFs

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Hematologic continued


Increases mortality

Increased peripheral use of cells, damage to cells by bacterial byproducts, depression of marrow by inflammatory mediators

Morphological changes of WBC’s in sepsis

Toxic granulations, Dohle bodies, vacuolization

Functional changes of WBC’s

Increased phagocytic/cytotoxic activities

Clinical Features

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Clinical Features

  • Hematologic continued

    • RBC production & survival are decreased

      • Usually does not cause anemia unless infection is prolonged

    • Low serum Fe concentrations

      • Decrease by 50%

      • Influx into liver & other reticuloendothelial cells

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Clinical Features

  • Hematologic continued

    • Thrombocytopenia

      • Usual a consequence of DIC

      • May be early sign of bacteremia

        • Inhibition of thrombopoiesis, increased platelet turnover, increased endothelial adherence, increased destruction

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Clinical Features

  • DIC

    • Clotting & fibrinolytic systems activated

      • Consumption of coagulation factors & platelets

      • Clotting system activated through the extrinisic clotting system by bacteria, viruses, fungi, endo/exotoxins

      • Gram(-) precipitate DIC more readily than gram (+)

      • Fibrinolytic system is activated by tissue type plasminogen activator

        • As sepsis progresses, increase release of plasminogen activator inhibitor type 1

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Clinical Features

  • DIC continued

    • Two forms

      • Compensated

        • “slower” generalized activation

        • Bleeding prevented by increasing coagulation factor production in liver, release of platelets from reserve, synthesis of inhibitors at accelerated rate

      • Decompensated

        • Clinical bleeding and/or thrombosis

        • Thrombocytopenia, prolonged PT/PTT, decreased fibrinogen & antithrombin III, increased fibrin monomer/fibrin split products/D-dimer

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Clinical Features

  • Endocrine

    • Hyperglycemia

      • Increased catecholamines, cortisol, glucagon, peripheral insulin resistance, impaired glucose use, decreased insulin secretion

      • Significant risk for adverse outcome

        • Must maintain tight control w/insulin infusion to keep b/w 80-100 mg/dl (NEJM Nov 8, 2001; vol 345, #19)

    • Hypoglycemia

      • Assoc. w/S. pneumoniae, S. aureus, S. pyogenes, Listeria, Neisseria meningitidis, H. flu, Enterobacteriaceae

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Clinical Features

  • Acid/Base

    • Early in sepsis  resp alkalosis

    • Metabolic acidosis suggests inadequate perfusion, impaired hepatic clearance of lactate/pyruvate, increased glycolysis

    • Hypoxemia often present due to vent/perfusion mismatch

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Clinical Features

  • Cutaneous

    • Direct bacterial involvement

      • Cellulitis, erysipelas, fasciitis

    • Lesions as a consequence of sepsis/hypotension/DIC

      • Acrocyanosis & necrosis of peripheral tissue

    • Lesions secondary to intravascular infection

      • Microemboli &/or immune complex vasculitis

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  • Pt presents with

    • Hypotension not responsive to fluid bolus

    • Inadequate perfusion

    • Complaints attributable to a serious infection

    • Hot flushed skin

    • Mental obtundation or agitation

    • Widened pulse pressure

    • Hyperventilation

    • Dysthermia

    • **beware of the old, young, immunocompromised

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  • Differential Diagnosis

    • Other causes of shock

      • Cardiogenic

      • Neurogenic

      • Hypovolemic

      • Anaphylactic

      • Obstructive (PE, tamponade)

      • Endocrine (adrenal insufficiency, thyroid storm)

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  • H & P

  • Basic lab and x-rays are usually successful in identification of source

    • CNS

      • Meningitis (nuchal rigidity, MS change, petechiae)

      • Brain abscess, sub/epi dural empyemas

      • Viral CNS infections

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  • Pulmonary

    • Acute bacterial pneumonia

  • Intra-abdominal processes

    • Most common source of infection leading to sepsis

    • Acute pancreatits

    • Cholangitis

    • Septic abortion/endometritis/myometritis

    • Pyelonephritis

    • Occult Abscess

  • Skin

    • Cellulitis (S.aureus, S.pyogenes)

    • Decubitus ulcer(s)

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  • No obvious source

    • Endocarditis

    • Primary bacteremia

      • S.aureus, S.pneumoniae, N.meningitidis

      • Asplenia

        • Salmonella, H flu, S pneumo, N. meningitidis

      • IVD users, Pseudomonas & gram(-) bacteria

        • Skin abscess from “popping”

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  • Ancillary Studies

    • CBC

    • DIC panel (PT,PTT,fibrinogen,D-dimer, ATIII)

    • CMP (include Mag, Ca, Phosphate)

    • Lactate level

    • ABG

    • UA

    • CXR

    • Cultures (blood, urine)

    • If H&P suggest

      • LP, CT (abd . . .)

    • Consider

      • CRP, pro-calcitonin, IL-6 level

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Standard Treatment

  • ABC’s!

    • Maintain O2 sat’s above 90%

  • Hemodynamic Stabilization

    • Rapid fluid administration

      • Rate of 0.5L of NS every 5-10min

      • May require 2-6L in initial stabilization phase

      • Be careful with heart failure patients

      • Monitor response with BP, HR, RR, mental status, urine output (1cc/kg/hr), CVP, skin perfusion

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Standard Treatment

▪ Inotropic support

  • If no response to fluids or signs of fluid overload present

  • Goal is to keep MAP above 65 mm Hg

    • Dopamine 5-20 micrograms/kg/min

      • Beta-1, dopaminergic and alpha adrenergic activity

    • Norepinephrine

      • Beta-1 and alpha adrenergic stimulation

    • Short term vasopressin infusion (0.04 units/min for 4-16h)

      • Vasodilatory septic shock

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Standard Treatment

  • End points

    • Early goal directed therapy provides significant benefit & improves outcome

      • Rivers et al. NEJM vol. 345:1368, 2001

  • Maintain CVP b/w 8-12

  • Hct 30%

  • SVO2 >70%

  • Reduction in mortality from 44% in control group to 29% in intervention group

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Standard Treatment

  • Empiric Antimicrobial Therapy

    • Start ASAP

    • Try to get culture samples before

    • Select based on adequate coverage of potential pathogens

    • Should cover gram +/-

    • Give maximum dose allowed

    • Give IV

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Standard Treatment

  • Removal of Source of Infection

    • Indwelling catheters  send tip for culture

    • Replace Foley catheters

    • Intra-abdominal or soft tissue sites of pus require urgent drainage

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Standard Treatment

  • Initial Baseline Assessment & Continued Monitoring (again goal directed)

    • Some use serum lactate to monitor response

    • ABG’s to monitor ventilation & perfusion

    • 2 large bore IV’s

      • Consider central line early

    • If requiring vasoactive drugs consider pulm artery thermal-dilution catheter

    • Other monitoring gadgets

      • Sublingual capnography, gastric pH tonometry, muscle oximetry, bioimpedance determination of CO

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Innovative Therapy

  • Based in premise that neutralizing bacterial toxins, cytokines, & other mediators could stop or slow the syndrome

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Innovative Therapies

  • Corticosteroids

    • Meta-analysis has shown physiologic doses of hydrocortisone improves outcomes

      • (200-300mg/d) for 5-7 days

      • Then tapered for 5-7 days

        • Early studies (proir to 1989) used high doses and had increased mortality

        • Those published after 1997 (5)used lower doses and reported improved survival similar to that of Activated Protein C

          • Annal of Internal Med 2004;141:47-56

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Innovative Therapy

  • Activated Protein C (Xigris)

    • Inactivates Factors Va and VIIIa

    • Inhibits thrombin (decreases inflammation)

      • Inhibits platelet activation, neutrophil recruitment, and mast cell degranulation

    • Blocks cytokine production

    • Inhibits cell adhesion

    • Anti-apoptotic actions

      • Apoptosis (i.e. GI epithelial cell) induces anergy

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Innovative Therapy

  • Summary

    • To date the only treatments shown to produce benefit

      • Early goal directed hemodynamic stabilization

      • Tight control of blood glucose with insulin

      • Activated protein C

        • “Efficacy and Safety of Recombinant Human Activated Protein C for Severe Sepsis” NEJM 2001, vol. 344; 699-709

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Cardiogenic Shock

  • A state of decreased cardiac output(CO) producing inadequate tissue perfusion despite adequate or excessive circulating volume

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Cardiogenic shock

  • Etiology

    • AMI

      • Pump failure (40% of LV involved)

      • Mechanical complications (MR,VSD,free wall rupture)

      • RV infarction

    • Depression of contractility

      • Sepsis, myocarditis, contusion

    • Mechanical obstruction

      • AS, hypertrophic CM, MS, LA myxoma

    • Regurgitation of LV output

      • AI, chordal rupture

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  • AMI cell death loss of contractile function

  • Decreased CO/SV tachycardia/hypotension decreased coronary perfusion/diastolic filling time

  • Further ischemia SNS/Renin-Angiotension System activation

  • Increased SVR and myocardial O2 consumption

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Cardiogenic Shock

  • Clinical Features

    • PE

      • Hypoperfusion

        • Skin mottling, obtunded

      • +/-hypotension (SBP<90)

        • May be compensated (pulse pressure <20, ST) or pre-existing hypertension

      • Tachypnea, rales (clear if RV), JVD

      • Murmur

        • MR (chordae tendinea rupture): holosystolic at apex going to axilla

        • VSD: holosystolic at L parasternal

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Cardiogenic Shock

  • Ancillary Studies

    • ECG: ischemia/infarction,electrolyte abnormality,drug toxicity

    • CXR: helps r/o other causes (pneumonia, aortic dissection, pericardial effusion)

    • Labs: BNP, cardiac enzymes, ABG, lactate, electrolytes, serum drug levels

    • Echo: ventricular/valve dysfunction

    • HD monitoring (table 33-3): invasive vs bioimpedance

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Cardiogenic Shock

  • Differential Diagnosis

    • AMI

    • PE

    • COPD

    • Pneumonia

    • Aortic dissection

    • Tamponade

    • Acute valvular insufficiency

    • Hemorrhage

    • Sepsis

    • Drug OD of negative inotropic/chronotropic agent

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Cardiogenic Shock

  • Treatment

    • ABC’s first

    • IV access/cardiac monitor/art line/foley

    • Correct hypoxia/hypovolemia/rhythm disturbance/electrolyte abnormalities/acid-base alterations

    • Hypotension

      • Dopamine,dobutamine

      • Fluid bolus if RV involved

      • Acute MR consider dobutamine and nitroprusside

      • IABP

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Cardiogenic Shock

  • Treatment continued

    • Thrombolytic therapy

      • Better outcomes if followed by revascularization

    • Intraaortic balloon conterpulsion

      • Decreases afterload, increases diastolic BP

    • Early revascularization

      • Most important life saving intervention

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Cardiogenic Shock

  • Treatment continued

    • Inotropic agents

      • Dopamine

        • First line agent

        • 2.5-5 micrograms/kg/min beta-1

        • 5-10 alpha & beta-1

        • 10-20 alpha

      • Dobutamine

        • Use for signs of poor perfusion when SBP>90

        • 2-20micrograms/kg/min

      • Norepinephrine

        • Use only when inadequate response to other pressors

        • 2 micrograms/min and titrate to response

      • Milrinone

        • 50 microgram/kg bolus followed by 0.5microgram/kg/min infusion—watch BP!

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Anaphylactic Shock

  • Severe systemic hypersensitivity with multisystem involvement

  • Life-threatening release of mediators by mast cells and basophils

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Anaphylactic Shock

  • Pathophysiology

    • 4 classic mechanisms

      • 1. cross-linking of 2 IgE molecules on a mast cell or basophil by a multivalent antigen

      • 2. reaction of IgM & IgG to cell surface antigens

      • 3. soluble antigen-antibody complexes activating complement

      • 4. activation of T lymphocytes

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Anaphylactic Shock

  • Pathophysiology

    • Classic anaphylaxis

      • 2 separate exposures

        • First the antigen or hapten-protein complex is processed by macrophage & dendritic cells

        • Presented externally with MHC-2

        • T helper cells recognize and stimulate plasma cells to produce IgE

        • Second exposure recognized by these IgE antibodies triggers degranulation of mast cells and basophils

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Anaphylactic Shock

  • Pathophysiology

    • Complement mediated reaction

      • Occur after administration of blood products secondary to immune complexes

        • C3a & C5a cause degranulation

    • Non-immunologic anaphylaxis (anaphylactoid)

      • Exogenous substances directly degranulate mast cells

        • Radiocontrast dye, opiates, depolarinzing drugs, dextrans

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Anaphylactic Shock

  • Pathophysiology


      • Non-mast cell process

      • Modulate cyclooxygenase-arachidonic acid metabolism

    • Idiopathic anaphylaxis

      • Diagnosis of exclusion

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Anaphylactic Shock

  • Clinical Features

    • Diffuse urticaria & angioedema

    • +/- abd pain or cramping, N/V, diarrhea, bronchospasm, rhinorrhea, conjunctivitis, dysrhythmias, hypotension

    • c/o “lump” in the throat heralds life-threatening laryngeal edema

    • Usually begin w/in 60 minutes of exposure

      • Faster the onset the more severe the reaction

      • Biphasic phenomenon

        • Second release of mediators clinically evident 3-4h after the initial manifestations clear

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Anaphylactic Shock

  • Diagnosis

    • History and physical

      • 2 or more body systems involved

      • Differential

        • Vasovagal reaction, status asthmaticus, seizure, epiglottitis, hereditary angioedema, FB airway obstruction, carcinoid, mastocytosis, non-IgE drug reactions, AMI, dysrhythmias

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Anaphylactic Shock

  • Treatment

    • First Line

      • ABC’s

      • Epinephrine, oxygen, fluids (NS 1-2L)

        • Epi 0.1mg in 10cc NS over 5-10minutes IV if signs of CV collapse

          • If refractive start infusion: 1mg in 500ccD5W at 1-4 micrograms/min

        • Less severe, give 0.3-0.5 mg IM in the thigh

      • decontamination

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Anaphylactic Shock

  • Treatment

    • Second Line

      • Corticosteroids

        • Methylprednisolone 125mg IV

        • 2mg/kg in children

      • Antihistamines

        • Diphenhydramine (H1) 25-50mg IV

        • Ranitidine or cimetidine(H2)

          • Avoid cimetidine in elderly, renal/hepatic failure, or if patient is on beta blocker

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Anaphylactic Shock

  • Treatment

    • Second Line

      • Agents for bronchospasm

        • Albuterol

        • Ipratropium bromide

        • Magnesium 2g IV over 20-30minutes

          • 25-50mg/kg in children

      • Glucagon

        • 1 mg IV q 5min until response followed by infusion 5-15 micrograms/min if patient on beta blockers with refractive hypotension

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Anaphylactic Shock

  • Disposition

    • Unstable patients admit to ICU

    • If patient received epi-observe for 4h

      • Consider distance from care, someone to go home with, comorbidities, age

      • Good discharge instructions is a must

      • Send with epipen, short course of antihistamines and steroids

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Neurogenic Shock

  • Acute spinal cord injury

  • Disruption of sympathetic outflow

  • Hypotension & bradycardia

  • Majority caused by blunt trauma

    • MVA, falls, sports

    • Cervical region most commonly injured

    • Penetrating injury (10-15% of cases)

      • GSW’s and stab wounds

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Neurogenic Shock

  • Pathophysiology

    • 33 bony vertebrae

      • Anterior body, posterior arch, sup/inf articular processes, pedicles, laminae

    • Spinal cord is cylindrical arising from base of brain & covered by 3 layers of meninges & CSF

    • 31 pairs of spinal nerves exit the canal via intervertebral foramen

      • Spinal nerves are formed by ant/post nerve roots

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Neurogenic Shock

  • Pathophysiology

    • Spinal cord contains white & gray matter

      • White: nerve fibers running up & down in cord tracts

      • Gray: nerve cells

    • Autonomic Nervous System

      • Sympathetic

        • Outflow tracts in lateral gray horns of 1st thoracic to 2nd lumbar

        • Controlled by hypothalamus

        • Lateral hornanterior nerve rootganglia of paraspinal sympathetic trunktravel throughout the body

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Neurogenic Shock

  • Pathophysiology

    • Autonomic Nervous System

      • Parasympathetic

        • Cranial Nerves & 2-4th sacral segments (splanchnic nerves)

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Neurogenic Shock

  • Clinical features

    • Hypotensive with warm,dry skin

    • Bradycardic ususally

    • Hypothermic

    • These symptoms last 1-3 weeks

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Neurogenic Shock

  • Treatment

    • ABCDE’s

    • Investigate all other possible sources of hypotension & bradycardia

    • Infuse crystalloids rapidly

      • Attempt to keep MAP 85-90mm Hg for the first 7 days to minimize secondary cord injury

      • Dopamine & dobutamine may be helpful

    • Severe bradycardia can be treated with atropine or pacing

    • Steroids are not indicated in the treatment of neurogenic shock per se

      • Indicated in blunt injury with neuro deficits if started within 8h (30mg/kg bolus then 45 mins later infuse at 5.4mg/kg/h for 23h)

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  • 1. In cardiogenic shock the PCWP is

    • A. Decreased

    • B. Increased

    • C. Normal

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  • 2. SIRS is defined as inflammation secondary to infection

    • A. True

    • B. False

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Answers anaphylaxis

  • 1. B

  • 2. B

  • 3. B

  • 4. A

  • 5. C