Presented by: Dr. Mashfiqul HasanPresented by: Dr. Mashfiqul HasanEmOC (anaesthesia) traineeEmOC (anaesthesia) traineeICMH...
Shock is a state of wide spread tissueShock is a state of wide spread tissuehypo perfusion caused byhypo perfusion caused...
Shock caused by inadequate cardiacShock caused by inadequate cardiacoutputoutputCO = SV x HRCO = SV x HR
StrokeVolumeStroke VolumeStroke VolumeVolume of Blood pumped by eachVolume of Blood pumped by eachventricle during 1 card...
Heart rateHeart rateSever bradycardia due to any cause.Sever bradycardia due to any cause.
Shock due to ineffective circulatoryShock due to ineffective circulatoryblood volumeblood volumeBP = CO x SVRBP = CO x SVR
Stages of shockStages of shockNon progressive stageNon progressive stageProgressive stageProgressive stageIrreversible ...
Classification of shockClassification of shockHypovolemic shockHypovolemic shockCardiogenic shockCardiogenic shockDistr...
Hypovolemic shockHypovolemic shock Loss of blood:Loss of blood: External hemorrhage: trauma(accidental, surgical), GIExt...
Effect of hemorrhage on cardiacEffect of hemorrhage on cardiacoutput & blood pressureoutput & blood pressure100%100%50%50%...
What prevented fall of bloodWhat prevented fall of bloodpressure?pressure? Reflex sympathetic compensation:Reflex sympath...
Decreased cardiac outputDecreased cardiac outputDecreased arterial pressureDecreased arterial pressureDecreased systemic b...
Progressive shockProgressive shock
Classification of HaemorrhageClassification of Haemorrhage Class-I: Blood loss 15%Class-I: Blood loss 15% Normal pulse r...
DiagnosisDiagnosisHistoryHistoryPhysical signs of haemodynamic instabilityPhysical signs of haemodynamic instabilityThe...
MonitoringMonitoring Patients in shock require care in an intensivePatients in shock require care in an intensivecare uni...
Hemodynamic ParametersHemodynamic ParametersCVP & PCWP CO SVRCardiogenic High Low HighExtra-cardiacobstructive (Low) Low H...
Management of hypovoloemic shockManagement of hypovoloemic shock Irrespective of etiology the first treatment ofIrrespect...
Hypovolemic Shock - Fluid SelectionHypovolemic Shock - Fluid SelectionDistribution % IntravascularNormal saline Extracellu...
Distribution of fluidDistribution of fluid
Aims of therapyAims of therapyTo achieve and maintainTo achieve and maintainMAP of 70-80 mm of HgMAP of 70-80 mm of HgUr...
Further managementFurther management Continuing blood loss, with hemoglobinContinuing blood loss, with hemoglobinconcentr...
Cardiogenic shockCardiogenic shockMyocardial ischemia or infarction (pumpMyocardial ischemia or infarction (pumpfailure)f...
Cardiogenic Shock
Hemodynamic ParametersHemodynamic ParametersCVP & PCWP CO SVRCardiogenic High Low HighExtra-cardiacobstructive (Low) Low H...
ManagementManagementAdjusting volume status to a level thatAdjusting volume status to a level thatensures optimum LV fill...
Hemodynamic effects ofHemodynamic effects ofadrenoceptor subtypesadrenoceptor subtypesTypeType TissueTissue ActionsActions...
Effects of Inotropic AgentsEffects of Inotropic AgentsEpinephrineEpinephrine α ,βα ,β11 = β= β22 0.02 – 0.50.02 – 0.5Norep...
DopamineDopamineAn endogenous precursor of norepinephrine withAn endogenous precursor of norepinephrine withmultiple dose-...
Distributive shockDistributive shockSeptic shockSeptic shockAnaphylactic shockAnaphylactic shockNeurogenic shockNeuroge...
Septic shockSeptic shockSepsis with hypotension (arterial blood pressure <90Sepsis with hypotension (arterial blood pressu...
Features of Septic ShockHigh Cardiac OutputHigh Cardiac OutputLow Systemic Vascular ResistanceLow Systemic Vascular Resi...
General managementGeneral managementMeasure CVPMeasure CVP If CVP is <8 mm of Hg – fluid is infusedIf CVP is <8 mm of Hg –...
Neurogenic ShockNeurogenic Shock Neurogenic shock is caused by-Neurogenic shock is caused by- traumatic spinal cord inju...
Management of neurogenic shockManagement of neurogenic shock Treatment involves a simultaneous approach toTreatment invol...
Anaphylactic shockAnaphylactic shockAnaphylaxis is a potentially life-Anaphylaxis is a potentially life-threatening, syst...
Anaphylaxis: IgE-mediatedAnaphylaxis: IgE-mediatedmast cell degranulationmast cell degranulation FoodsFoods PeanutsPeanu...
Anaphylactoid, non-IgE-mediatedAnaphylactoid, non-IgE-mediatedmast cell degranulationmast cell degranulation DrugsDrugs ...
Management of anaphylaxisManagement of anaphylaxis Anaphylaxis is an acute medical emergency. TheAnaphylaxis is an acute ...
Obstructive shockObstructive shock Tension pneumothoraxTension pneumothorax Pericardial disease (temponade, constrictive...
THANKS TO EVERYBODYTHANKS TO EVERYBODY
Shock
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It was part of my anesthesia training in Matuail, ICMH. I presented in weekly CPD in front of Gynae & Paediatrics teachers.

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Shock

  1. 1. Presented by: Dr. Mashfiqul HasanPresented by: Dr. Mashfiqul HasanEmOC (anaesthesia) traineeEmOC (anaesthesia) traineeICMHICMH
  2. 2. Shock is a state of wide spread tissueShock is a state of wide spread tissuehypo perfusion caused byhypo perfusion caused byan inadequate cardiac output oran inadequate cardiac output orineffective circulatory blood volume,ineffective circulatory blood volume,leading to inadequate supply of oxygenleading to inadequate supply of oxygenand nutrients to the tissues and removal ofand nutrients to the tissues and removal ofmetabolic wastes from there to the organsmetabolic wastes from there to the organsof excretion.of excretion.What isWhat is shock ?shock ?What isWhat is shock ?shock ?
  3. 3. Shock caused by inadequate cardiacShock caused by inadequate cardiacoutputoutputCO = SV x HRCO = SV x HR
  4. 4. StrokeVolumeStroke VolumeStroke VolumeVolume of Blood pumped by eachVolume of Blood pumped by eachventricle during 1 cardiac cycle.ventricle during 1 cardiac cycle.What affects Stroke volume?HeartMuscleDamageBloodVolumeMechanicalObstructionMechanicalRhythmProblems
  5. 5. Heart rateHeart rateSever bradycardia due to any cause.Sever bradycardia due to any cause.
  6. 6. Shock due to ineffective circulatoryShock due to ineffective circulatoryblood volumeblood volumeBP = CO x SVRBP = CO x SVR
  7. 7. Stages of shockStages of shockNon progressive stageNon progressive stageProgressive stageProgressive stageIrreversible stageIrreversible stage
  8. 8. Classification of shockClassification of shockHypovolemic shockHypovolemic shockCardiogenic shockCardiogenic shockDistributive shockDistributive shockObstructive shockObstructive shock
  9. 9. Hypovolemic shockHypovolemic shock Loss of blood:Loss of blood: External hemorrhage: trauma(accidental, surgical), GIExternal hemorrhage: trauma(accidental, surgical), GIbleeding, PV bleedingbleeding, PV bleeding Internal hemorrhage: hemothorax, hemoperitoneum,Internal hemorrhage: hemothorax, hemoperitoneum,hematoma, haemorrhage due to pelvic bone fracture,hematoma, haemorrhage due to pelvic bone fracture,femur fracture, etc.femur fracture, etc. Loss of plasma: burn, exfoliative dermatitisLoss of plasma: burn, exfoliative dermatitis Loss of fluid & electrolytes:Loss of fluid & electrolytes: External: diarrhoea, vomiting, excessive sweating,External: diarrhoea, vomiting, excessive sweating,hyperosmolar state (DKA, HONKDC)hyperosmolar state (DKA, HONKDC) Internal: pancreatitis, ascites, bowel obstructionInternal: pancreatitis, ascites, bowel obstruction
  10. 10. Effect of hemorrhage on cardiacEffect of hemorrhage on cardiacoutput & blood pressureoutput & blood pressure100%100%50%50%00 1010 2020 3030 4040 5050ArterialArterial pressurepressureCardiac outputCardiac outputPercentage of total blood removedPercentage of total blood removed
  11. 11. What prevented fall of bloodWhat prevented fall of bloodpressure?pressure? Reflex sympathetic compensation:Reflex sympathetic compensation: Arterioles constrict, increasing peripheral resistanceArterioles constrict, increasing peripheral resistance Vein & venous reservoirs constrict (esp. skin &Vein & venous reservoirs constrict (esp. skin &splanchnic), thereby increasing the venous returnsplanchnic), thereby increasing the venous return Stimulation of the cardiac activityStimulation of the cardiac activity Activation of Renin-Angiotensin-AldosteroneActivation of Renin-Angiotensin-Aldosteronesystemsystem Formation and release of vasopressinFormation and release of vasopressin
  12. 12. Decreased cardiac outputDecreased cardiac outputDecreased arterial pressureDecreased arterial pressureDecreased systemic blood flowDecreased systemic blood flowDecreased nutrition of tissuesDecreased nutrition of tissues Intravascular clottingIntravascular clottingDecreased cardiac nutritionDecreased cardiac nutritionDecreased nutritionDecreased nutritionof vascular systemof vascular systemDecreased nutritionDecreased nutritionof the brainof the brainTissue ischemiaTissue ischemiaDecreased vasomotorDecreased vasomotoractivityactivityVascular dilatationVascular dilatationVenous poolingVenous poolingOf bloodOf bloodCardiac depressionCardiac depression Decreased venous returnDecreased venous returnIncreasedIncreasedCapillaryCapillarypermeabilitypermeabilityDecreasedDecreasedblood volumeblood volumeRelease ofRelease ofToxins/lactic acidosisToxins/lactic acidosisProgression of shockProgression of shock
  13. 13. Progressive shockProgressive shock
  14. 14. Classification of HaemorrhageClassification of Haemorrhage Class-I: Blood loss 15%Class-I: Blood loss 15% Normal pulse rate and blood pressureNormal pulse rate and blood pressure Tilt test +Tilt test + Class-II: Blood loss 20-25%Class-II: Blood loss 20-25% Tachycardia, TachypnoeaTachycardia, Tachypnoea Low systolic blood pressureLow systolic blood pressure Pulse pressure less than 30mmHgPulse pressure less than 30mmHg Delayed capillary fillingDelayed capillary filling Class-III: Blood loss 30-35%Class-III: Blood loss 30-35% Skin-cold, clammy and paleSkin-cold, clammy and pale Severe drop in blood pressureSevere drop in blood pressure Restlessness, oliguria, metabolic acidosisRestlessness, oliguria, metabolic acidosis Class-IV Blood loss 40-50%Class-IV Blood loss 40-50% Profound hypotensionProfound hypotension Carotid pulse may only be palpableCarotid pulse may only be palpable Irreversible shockIrreversible shock
  15. 15. DiagnosisDiagnosisHistoryHistoryPhysical signs of haemodynamic instabilityPhysical signs of haemodynamic instabilityThe diagnosis is more difficult when theThe diagnosis is more difficult when thesource of blood loss is occult, as into thesource of blood loss is occult, as into thegastrointestinal tract, fracture of femur,gastrointestinal tract, fracture of femur,pelvic fracture or when plasma volumepelvic fracture or when plasma volumealone is depleted.alone is depleted.
  16. 16. MonitoringMonitoring Patients in shock require care in an intensivePatients in shock require care in an intensivecare unit.care unit. Arterial pressure through an indwelling line,Arterial pressure through an indwelling line,pulse, and respiratory rate should be monitoredpulse, and respiratory rate should be monitoredcontinuously;continuously; A Foley catheter should be inserted to followA Foley catheter should be inserted to followurine flow;urine flow; Mental status should be assessed frequently.Mental status should be assessed frequently. Invasive monitoring: Pulmonary artery catheterInvasive monitoring: Pulmonary artery catheter(PAC, Swan-Ganz catheter).(PAC, Swan-Ganz catheter).
  17. 17. Hemodynamic ParametersHemodynamic ParametersCVP & PCWP CO SVRCardiogenic High Low HighExtra-cardiacobstructive (Low) Low HighHypovolemic Low Low HighSepsis Variable Variable LowToxic Shock (Low) (High) LowAnaphylaxis Low High Low
  18. 18. Management of hypovoloemic shockManagement of hypovoloemic shock Irrespective of etiology the first treatment ofIrrespective of etiology the first treatment ofshock is 100%Oshock is 100%O22 inhalation.inhalation. Initial resuscitation requires rapid re-expansionInitial resuscitation requires rapid re-expansionof the circulating intravascular volume andof the circulating intravascular volume andinterventions to control ongoing losses.interventions to control ongoing losses. Volume resuscitation is initiated with the rapidVolume resuscitation is initiated with the rapidinfusion of a balanced salt solution such asinfusion of a balanced salt solution such asRingers lactate or Normal saline through large-Ringers lactate or Normal saline through large-bore intravenous lines.bore intravenous lines. No distinct benefit from the use of colloid hasNo distinct benefit from the use of colloid hasbeen demonstrated & in some studies theybeen demonstrated & in some studies theyseem to be even harmful.seem to be even harmful.
  19. 19. Hypovolemic Shock - Fluid SelectionHypovolemic Shock - Fluid SelectionDistribution % IntravascularNormal saline Extracellular space 25-30%Lactated Ringer’s Extracellular space 25-30%5% DA Total body water space 8-10%Blood/ Colloids Intravascular space 100%
  20. 20. Distribution of fluidDistribution of fluid
  21. 21. Aims of therapyAims of therapyTo achieve and maintainTo achieve and maintainMAP of 70-80 mm of HgMAP of 70-80 mm of HgUrine output >0.5 ml/kg/hourUrine output >0.5 ml/kg/hourTreatment of the cause.Treatment of the cause.
  22. 22. Further managementFurther management Continuing blood loss, with hemoglobinContinuing blood loss, with hemoglobinconcentrations declining to 10 g/dL shouldconcentrations declining to 10 g/dL shouldinitiate blood transfusion, cross-matched wholeinitiate blood transfusion, cross-matched wholeblood.blood. In the presence of severe and/or prolongedIn the presence of severe and/or prolongedhypotension, inotropic support with dopamine,hypotension, inotropic support with dopamine,vasopressin, or dobutaminevasopressin, or dobutamine may bemay be required torequired tomaintain adequate ventricular performancemaintain adequate ventricular performanceafterafter blood volume has been restored.blood volume has been restored. Once hemorrhage is controlled and the patientOnce hemorrhage is controlled and the patienthas been stabilized, blood transfusions may nothas been stabilized, blood transfusions may notbe continued unless the hemoglobin is <~7g/dLbe continued unless the hemoglobin is <~7g/dL
  23. 23. Cardiogenic shockCardiogenic shockMyocardial ischemia or infarction (pumpMyocardial ischemia or infarction (pumpfailure)failure)Myocarditis, cardiomyopathyMyocarditis, cardiomyopathyArrhythmiaArrhythmiaAcute valvular dysfunctionAcute valvular dysfunction
  24. 24. Cardiogenic Shock
  25. 25. Hemodynamic ParametersHemodynamic ParametersCVP & PCWP CO SVRCardiogenic High Low HighExtra-cardiacobstructive (Low) Low HighHypovolemic Low Low HighSepsis Variable Variable LowToxic Shock (Low) (High) LowAnaphylaxis Low High Low
  26. 26. ManagementManagementAdjusting volume status to a level thatAdjusting volume status to a level thatensures optimum LV filling pressure.ensures optimum LV filling pressure.Use of ionotropic drugs.Use of ionotropic drugs.
  27. 27. Hemodynamic effects ofHemodynamic effects ofadrenoceptor subtypesadrenoceptor subtypesTypeType TissueTissue ActionsActionsAlphaAlpha Most vascular smoothMost vascular smoothmusclemuscleContractionContractionBeta 1Beta 1 HeartHeart Increases force & rate ofIncreases force & rate ofcontractioncontractionBeta 2Beta 2 Vascular smoothVascular smoothmusclemuscleRelaxationRelaxationD 1D 1 Smooth muscleSmooth muscle Dilates renal blood vesselsDilates renal blood vesselsAdrenalineAdrenaline NoradrenalineNoradrenaline DobutamineDobutamine DopamineDopamine
  28. 28. Effects of Inotropic AgentsEffects of Inotropic AgentsEpinephrineEpinephrine α ,βα ,β11 = β= β22 0.02 – 0.50.02 – 0.5NorepinephrineNorepinephrine αα11, β, β11 >>>> ββ22 0.05 – 0.50.05 – 0.5DopamineDopamine DD, β, β22, β, β11, α, α 2 -202 -20DobutamineDobutamine ββ11, β, β22 2 - 202 - 20Drug Receptor CO SVR Dose Range(µg/kg/min)1
  29. 29. DopamineDopamineAn endogenous precursor of norepinephrine withAn endogenous precursor of norepinephrine withmultiple dose-related effectsmultiple dose-related effectsLow Dose (0.5 - 5 mcg/kg/min)Low Dose (0.5 - 5 mcg/kg/min)ββ22 and dopaminergic (DR) effectsand dopaminergic (DR) effectsEnhanced blood flow to renal and splanchnicEnhanced blood flow to renal and splanchnicbedsbedsModerate Dose (5 -10 mcg/kg/min)Moderate Dose (5 -10 mcg/kg/min)Positive inotropic effectsPositive inotropic effectsHigh Dose (>10 mcg/kg/min)High Dose (>10 mcg/kg/min)αα-actions (vasoconstriction)-actions (vasoconstriction)
  30. 30. Distributive shockDistributive shockSeptic shockSeptic shockAnaphylactic shockAnaphylactic shockNeurogenic shockNeurogenic shockVasodilator drugsVasodilator drugsAcute adrenal insufficiencyAcute adrenal insufficiency
  31. 31. Septic shockSeptic shockSepsis with hypotension (arterial blood pressure <90Sepsis with hypotension (arterial blood pressure <90mmHg systolic, or 40 mmHg less than patients normalmmHg systolic, or 40 mmHg less than patients normalblood pressure) for at least 1 h despite adequate fluidblood pressure) for at least 1 h despite adequate fluidresuscitation;resuscitation;ororNeed for vasopressors to maintain systolic bloodNeed for vasopressors to maintain systolic bloodpressure 90 mmHgpressure 90 mmHg oror mean arterial pressure 70 mmHgmean arterial pressure 70 mmHg
  32. 32. Features of Septic ShockHigh Cardiac OutputHigh Cardiac OutputLow Systemic Vascular ResistanceLow Systemic Vascular ResistanceMyocardial DysfunctionMyocardial DysfunctionHypovolemia as Ongoing CirculatingHypovolemia as Ongoing CirculatingVolume Lost To Interstitial SpaceVolume Lost To Interstitial Space
  33. 33. General managementGeneral managementMeasure CVPMeasure CVP If CVP is <8 mm of Hg – fluid is infusedIf CVP is <8 mm of Hg – fluid is infusedto raise it to 8-12 mm of Hgto raise it to 8-12 mm of HgMeasure MAPMeasure MAP If MAP is still <65 mm of HgIf MAP is still <65 mm of Hg- use vasoactive agent- use vasoactive agentMaintain MAP >65 mm of HgMaintain MAP >65 mm of HgManagement of septic shockManagement of septic shock
  34. 34. Neurogenic ShockNeurogenic Shock Neurogenic shock is caused by-Neurogenic shock is caused by- traumatic spinal cord injury ortraumatic spinal cord injury or effects of an epidural or spinal anesthetic.effects of an epidural or spinal anesthetic. This results in loss of sympathetic tone with a reductionThis results in loss of sympathetic tone with a reductionin systemic vascular resistance and hypotension withoutin systemic vascular resistance and hypotension withouta compensatory tachycardia.a compensatory tachycardia. The extremities are often warm, in contrast to the usualThe extremities are often warm, in contrast to the usualvasoconstriction-induced coolness in hypovolemic orvasoconstriction-induced coolness in hypovolemic orcardiogenic shock.cardiogenic shock. Reflex vagal parasympathetic stimulation evoked byReflex vagal parasympathetic stimulation evoked bypain, gastric dilation, or fright may simulate neurogenicpain, gastric dilation, or fright may simulate neurogenicshock, producing hypotension, bradycardia, andshock, producing hypotension, bradycardia, andsyncope.syncope.
  35. 35. Management of neurogenic shockManagement of neurogenic shock Treatment involves a simultaneous approach toTreatment involves a simultaneous approach tothe relative hypovolemia and to the loss ofthe relative hypovolemia and to the loss ofvasomotor tone.vasomotor tone. Excessive volumes of fluid may be required toExcessive volumes of fluid may be required torestore normal hemodynamics if given alone.restore normal hemodynamics if given alone. A pure alpha-adrenergic agentA pure alpha-adrenergic agent(Ephedrine/phenylephrine) may be necessary to(Ephedrine/phenylephrine) may be necessary toaugment vascular resistance and maintain anaugment vascular resistance and maintain anadequate mean arterial pressure.adequate mean arterial pressure. In severe cases noradrenaline/adrenaline mayIn severe cases noradrenaline/adrenaline maybe used.be used.
  36. 36. Anaphylactic shockAnaphylactic shockAnaphylaxis is a potentially life-Anaphylaxis is a potentially life-threatening, systemic allergic reactionthreatening, systemic allergic reactioncaused by the release of histamine andcaused by the release of histamine andother vasoactive mediators.other vasoactive mediators.The most common allergens are foods,The most common allergens are foods,latex, insect venom and drugs.latex, insect venom and drugs.
  37. 37. Anaphylaxis: IgE-mediatedAnaphylaxis: IgE-mediatedmast cell degranulationmast cell degranulation FoodsFoods PeanutsPeanuts Tree nutsTree nuts Fish and shellfishFish and shellfish MilkMilk EggsEggs Soy productsSoy products Insect stingsInsect stings Bee venomBee venom Wasp venomWasp venom Chemicals, drugs and other foreign proteinsChemicals, drugs and other foreign proteins Penicillin and other antibioticsPenicillin and other antibiotics Intravenous anaesthetic agents, e.g. suxamethonium, propofolIntravenous anaesthetic agents, e.g. suxamethonium, propofol LatexLatex
  38. 38. Anaphylactoid, non-IgE-mediatedAnaphylactoid, non-IgE-mediatedmast cell degranulationmast cell degranulation DrugsDrugs OpiatesOpiates AspirinAspirin Radiocontrast mediaRadiocontrast media PhysicalPhysical ExerciseExercise ColdCold IdiopathicIdiopathic No cause can be identified in 30% of patients withNo cause can be identified in 30% of patients withanaphylaxisanaphylaxis
  39. 39. Management of anaphylaxisManagement of anaphylaxis Anaphylaxis is an acute medical emergency. TheAnaphylaxis is an acute medical emergency. Theimmediate management includes:immediate management includes: preventing further contact with the allergen (e.g. removal of beepreventing further contact with the allergen (e.g. removal of beesting)sting) ensuring airway patencyensuring airway patency administration of oxygenadministration of oxygen restoration of blood pressure (laying the patient flat, intravenousrestoration of blood pressure (laying the patient flat, intravenousfluids)fluids) prompt administration of adrenaline (epinephrine).prompt administration of adrenaline (epinephrine). Intravenous antihistamines (chlorphenamine 10-20 mg i.m. orIntravenous antihistamines (chlorphenamine 10-20 mg i.m. orslow i.v. injection), which limit ongoing inflammation.slow i.v. injection), which limit ongoing inflammation. Corticosteroids (hydrocortisone 100-300 mg) prevent late-phaseCorticosteroids (hydrocortisone 100-300 mg) prevent late-phasesymptoms in severely affected patients.symptoms in severely affected patients.
  40. 40. Obstructive shockObstructive shock Tension pneumothoraxTension pneumothorax Pericardial disease (temponade, constrictivePericardial disease (temponade, constrictivepericarditis)pericarditis) Disease of pulmonary vasculature (massiveDisease of pulmonary vasculature (massivepulmonary emboli, pulmonary hypertension)pulmonary emboli, pulmonary hypertension) Cardiac tumor (atrial myxoma)Cardiac tumor (atrial myxoma) Left atrial mural thrombusLeft atrial mural thrombus Obstuctive valvular disease (aortic or mitralObstuctive valvular disease (aortic or mitralstenosis)stenosis)These are medical emergencies requiring prompt diagnosis & treatmentThese are medical emergencies requiring prompt diagnosis & treatment
  41. 41. THANKS TO EVERYBODYTHANKS TO EVERYBODY

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