DR.FARZANA NAZNIN LECTURER DEPARTMENT OF PATHOLOGY BANGLADESH MEDICAL COLLEGE

DEFINATION Shock give rise to systemic hypoperfusion caused by reduction

either in cardiac output or in effective circulatory blood volume. End results are : Hypotension

Tissue hypoperfusion

Cellular hypoxia

Reversible injury

Irreversible injury with persistent of shock

End organ dysfunction

Death

TYPES OF SHOCK

Hypovolumic shock Cardiogenic shock Septic shockAnaphylactic shockNeurogenic shock

HYPOVOLUMIC SHOCKHypovolumic shock occurs due to rapid reduction in

blood volume or plasma volume.

Causes of hypovlumic shock :

1. Hemorrhage 2. Severe dehydration-severe vomiting, severe

diarrhea 3. Severe burn 4. Abdominal ascities 5. Acute pancreatitis 6. Diabetes mellitus 7. Over use of Diuretics

HYPOVOLUMIC SHOCK Pathophysiology of hypovolumic shock :

Dehydration, Hemorrhage

Reduction in intravascular blood volume

Decreased pre-load

Decreased stroke volume & CO

Systemic hypoperfusion

Compensatory vasoconstriction

Tissue ischemia, hypoxia

Cellular & organ dysfunction

CARDIOGENIC SHOCKCardiogenic shock is characterized by reduced

pumping ability of heart due to intrinsic myocardial damage or extrinsic or obstruction to out flow. It is most commonly occurs in association with and as a direct result of acute myocardial ischemia.

Incidence: -Cardiogenic shock occurs in 8.6% of patient with ST segment elevation. -Myocardial ischemia with 29% of those presenting to the hospital already in shock. -2% of non ST segment elevation MI.

CARDIOGENIC SHOCKRisk factor : -Pre existing myocardial damage -Diabetes Mellitus -Advanced age -Previous MI -Dysarythmia

CARDIOGENIC SHOCKCauses of Cardiogenic shock :

MIVulvular regurgitationAcute myocarditisCardiomyopathyCardiac tamponadePulmonary embolismAcute vulvular dysfunctionCardiac dysarythmiaRupture ventricular aneurysmBeta-blocker overdoseCa-channel blocker overdose

CARDIOGENIC SHOCKPathophysiology of cardiogenic shock : Myocardial Infraction

Myocardial ischemia or injury Myocardial dysfunction

Systemic inflammatory response Decreased CO & stroke volume

Increased NO synthesis Systemic hypoperfusion Hypotension

Vasodilatation Decreased coronary perfusion

Compensatory vasoconstriction Cardiac & other end organ damage

Progressive myocardial dysfunction

Death

SEPTIC SHOCKSepsis is a clinical state that accompanies

infection either confined to a local site from which toxin are absored or associated with invasion of organism in to the blood stream.

Causes of septic shock: -Overhelming microbial infection-Gram +ve septicemia-Endotoxic shock (Gram –ve septicemia)-Fungal sepsis-Super antigen

SEPTIC SHOCK

SEPTIC SHOCK

SEPTIC SHOCKMicrobiology :

Gm +StaphylococcusStreptococcus

Gm -E.ColiKlebsiellaProteus

OtherFungi

SEPTIC SHOCKPathophysiology of septic shock :

Bacterial infection

Endotxin ( LPS ) & other microbial products

Binds to LPS binding protein in serum

Binds to CD14 receptors on mononeuclear cells

CD14 binds to TLR4

Release of chemical mediators

SEPTIC SHOCKPathophysiology of septic shock :

SEPTIC SHOCKPatho-physiology of septic shock : In septic shock systemic vasodilatation and

pooling of blood in the periphery leads to tissue hypo perfusion and though the cardiac out put is preserved this is accompanying widespread endothelial cell activation and often leads to hablypercoagulable state that can manifest DIC.Septic shock is associated with change in metabolism that can directly suppress cellular function. The net effect is hypo perfusion and dysfunction of multi-organ.

SEPTIC SHOCKMajor factors contributing to the pathophysiology of septic

shock are following. Inflammatory mediators;

Various microbial cell wall contains lipopolysaccaride are released when the cell wall are degraded. Free LPS bind to circulatory LPS.This complex then binds to a cell surface receptor CD14 on macrophage, mononuclear paghocytic cell, endothelial cell.CD14 binds to the signal transducing protein TLR-4.Upon activation cascade of cytokines mediators TNF,TL-1,IL-8,INF- .The compliment cascade are activated directly or through proteolytic activity of plasmin resulting in production of anaphylotoxins C3a&C5a,chemotatctic factor C5a causes vasodilatation & increases vascular permeability.Activated endothelial cell and macrophage release NO contribute to pro-inflammatory state.

SEPTIC SHOCKEndothelial cell activation and injury:

Endothelial cell activation by microbial products or inflammatory mediators produced by leukocytes. Has 3 major sequele-thrombosis,increase vascular permiability,vasodilation

Pro-inflammatory cytokines result in increased tissue factor production by endothelial cell and monocyte.The production of endothelial anti-coagulant factor-tissue factor pathway inhibator,thrombomodulin and protein-C reduced.Reduced blood flow at the level of small vessels' produce stasis that reduce the wash out of activated coagulation factor results in deposition of fibrin rich thrombi in small vessels, that lead to tissue hypoperfusion..

In DIC increase consumption of coagulation factor & platelet leads to bleeding & hage.

Increase vascular permiability leads exudation of fluid in to interstitum causing oedema.

Endothelium increase the relase of NO.

SEPTIC SHOCKMetabolic abnormalities:Septis patient exhibit

insulin resistance and hypoglycemia. Cytokines such as TNF & IL-1,stress induced hormone(glucagon,catecholamines)all drive gluconeogenesis.At the same time the pro-inflammatory cytokines suppress insulin release while simultaneously promoting insulin resistance in the liver & other tissue, by surface expression of glucose transporter. Hyperglycemia reduced neutrophil function & bactericidal activity. Sepsis also related with adrenal insufficiency & factional deficency of glucocortcoid.

SEPTIC SHOCKImmuno suppression:

hyper inflammatory state activate immuno-suprssion mechanism which involve both innate & adaptive immunity by production of anti-inflammatory mediators(soluable TNF receptors,IL-recepor antagonist& IL-10).

Organ dysfunction:Systemic hypotension, interstitial edema, small vessels thrombosis reduce the delivery of oxygen &to the tissue.

SEPTIC SHOCK

High level of cytokines, secondary mediators reduces myocardial contractility & CO. Increase vascular permeability & endothelial injury acute respiratory distress syndrome ultimately cause multiple organ failure.

Toxic shock syndrome:Toxic shock syndrome is a potentially fatal

illness caused by bacterial toxin(super antigen) released by –Staphylococcus aureus & Streptococcus pyogens.

Streptococcal TSS associated with recent soft tissue injury like surgery,pharyngitis,NSAID drug use.

Staphylococcal TSS observe mostly among menstruating women, but also associated with cutaneous infection, post-partum & C/S wound infection & focal staphylococcal infection like abscess,empyma,pneumonia.

NEUROGENIC SHOCK

Neurogenic shock occurs in the setting of anesthetic

accident or spinal cord injury causes loss of vascular

tone and peripheral pulling of blood.

ANAPHYLACTIC SHOCK

In Anaphylactic shock,decreased systemic vascular resistance due primarily to massive histamine release from mast cell after activation of IgE mediated hypersensitivity reaction as well as increase synthesis of prostaglandin. That leads to vasodilatation and increase vascular permiability.Ultimate results are systemic hypotension, tissue perfusion and cellular anoxia.

ANAPHYLACTIC SHOCKCauses of anaphylactic shock:

1.Iatrogenic( drug)2.Accidental exposure to an allergen and co-

exiting respiratory complaints(wheezing & dyspnea)& or purities.

Systemic inflammatory response in anaphylactic shock:Respiratory distressWheezingUrticarial rash Angioedema.

STAGES OF SHOCK

1.An initial non progressive phage

2.A progressive stage

3.An irreversible stage

An initial non progressive phage:In this phage a varieties of neuro-hormonal

& haemostatic mechanism helps to maintain cardiac out-put & blood pressure. These includes:

- Baro-receptor reflex mechanism- Release of catecholamine's- Activation of Renin-angiotension axis - Anti-diuretic hormone release -Generalized sympathetic activation

Net effects are- 1.Tachycardia 2.Peripheral vasoconstriction 3.Renal conservation of fluid

Resulting in restoration of circulation and tissue perfusion.

Progressive phase: If the compensatory mechanism fails to

restore circulation, vital organ shows the effects of hypoxia.Persistant oxygen deficiency leads to intra cellular anaerobic glycolysis with lactic acidosis,thus reduce tissue pH and vasomotor response. Resulting reduce cardiac output and anoxic injury to endothelial cell leads to DIC.

Irreversible stage: When there is failure to restore

circulation either by compensatory mechanism or by therapeutic intervention,the process of shock enters the irreversible stage. Wide spread cell injury is reflected in lysosomal enzyme lekage,nitric oxide reduced myocardial contractility,acute tubular necrosis ultimately death.

MORPHOLOGY OF SHOCKSince shock is characterized by failure of multi-organ

systems, the cellular changes may appear in any tissue.

Brain: ischemic encephalopathy.Heart: coagulative necrosis or subendocardial hemorrhage or contraction band necrosis.Kidney: acute tubular necrosis.Lung: diffuse alveolar damage develop shock lung. Gastrointestinal tract: Hemorrhagic enteropathy.

Adrenal gland: cortical cell lipid depletion may occur.Liver: fatty change, central hemorrhagic necrosis.

CLINICAL PRESENTATION OF SHOCKAltered mental status-

Restless,confusion,stupor,coma,agitationPatient may unconscious or semi-consciousPallorIncrease sweatingCold clammy skin. Warm in septic shock Pulse-Tachycardia, rapid weak thready pulse Respiration-Tachypnia, slow and regularBlood pressure-low blood pressure Temperature may or may not be raisedDehydration Reduce urine output

DIAGNOSIS OF SHOCKHistory takingGeneral and physical examinationVital sign assessment

LAB DIAGNOSIS CBCBiochemical test-serum electrolyte,ramdom

blood sugar,s.creatinineECGChest x-rayBlood culture, urine R/M/E & C/S,sputum for

gram stain & C/S Blood grouping & Cross matchingCardiac enzymeArterial blood gas analysis

MANAGEMAENT OF SHOCK

Admitted in intensive care unitEnsure ABC

Clear airway, adequate breathing, assessment of circulation-pulse,BP,urine volume.

Position of the patientTrendelenburg or supine position to increase cerebral blood flow.

Oxygenation-High flow oxygen should be delivered.Establish IV accessRestore circulatory blood volume-blood in case of

bleeding,crystalioid(n/s,ringer’ s lactate )

cont..

Vasoactive drugsDopamine with or with out dobutamine provide ionotropic support increasing perfusion of the ischemic myocardium &all body tissue.

Surgical intervention if needed.Insulin therapy in case of hyperglycemiaTreatment of underlying cause:

Broad spectrum antibiotic coverage in case of infection.Cardiogenic shock-treatment according to cause such as MI or left ventricular failure.Hypovolumic shock-adrenalin I/m Hydrocortisone

In acute adrenal insufficiency-Corticosteroid use as life saving drug.

Activated protein-C can be use in severe sepsis.

The prognosis varies with the origin of shock and its duration.

80%-90% of young with hypovolumic shock survive with appropiate management.

Cardiogenic shock associated with extensive myocardial infraction mortality rate up to 75%

Septic shock -mortality rate up to 75%

PROGNOSIS OF SHOCK