Shock : hypovolemic, septic and neurogenic

27,520 views 33 slides Feb 25, 2014
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SHOCK Part II Bethelhem Berhanu

Shock Cardiogenic Hypovolaemic Anaphylactic Distributive Neurogenic Classification of Shock Septic

Hypovolemic Shock most common reduced circulating volume Hemorrhagic shock Non Hemorragic hypovolemic shock Vomiting Diuresis Diarrhoea Burns External or Internal

Pathophysiology of Hypovolemic shock Hypovolemia ↓Venous Return Multiorgan failure Organ dysfunction Perfusion failure & Tissue hypoxia Hypotension ↓Cardiac output ↓Preload BP = CO x TPR CO = SV x HR

Bodily responses Physiologic responses- sympathetic activity – tachycardia and SVR Hyperventilation collapse of venous capacitance vessels stress hormones Attempt to replace intravascular volume loss The body will prioritize – Brain and heart Severity ~ magnitude and the rate of fluid loss

“TENNIS STAGING” 15,15-30,30-40,40 American College of Surgeons, 1989 Postural Drop

Clinical Manifestations Anxiety - lethargy Tachypnea Tachycardia – weak, thready pulse Normal → Orthostatic drop → Hypotension Delayed Capillary refill Cool clammy skin Oliguria Thirst

Mild (<20% Blood Volume) Moderate (20–40% Blood Volume) Severe (>40% Blood Volume) Cool extremities Increased capillary refill time Diaphoresis Collapsed veins Anxiety Same, plus: Tachycardia Tachypnea Oliguria Postural changes Same, plus: Hemodynamic instability Marked tachycardia Hypotension Mental status deterioration (coma)

Treatment principles: Hypovolemic Shock control ongoing loss rapid reexpansion of the circulating intravascular blood volume GOAL : restore blood volume and improve tissue perfusion and oxygenation

Control bleeding Direct pressure on the site of wound, Gauze Elevation Pressure points - Tourniquets - Surgical Methods Artery forceps (Spencer Well’s forceps) Ligation Cauterisation Splenectomy – splenic rupture, Hysterectomy for post partum bleeding

Treatment contd. ABC … Supplemental Oxygen Endotracheal intubation Secure a large bore IV line for fluid resuscitation Median cubital vein, saphenous vein and sometimes the internal jugular and subclavian veins In pediatric patient - intraosseus line

Re-expansion of Intravascular volume Fluid Therapy Crystalloid solutions – 0.9% saline Ringer Lactate Colloid solutions – 5% albumin, gelatins, hetastarch 20 ml/kg in 5 – 15 minutes – repeat upto 60 ml/kg Blood transfusion – 1 unit of blood in 20 minutes >40% of blood loss (class IV) If the patient is anemic ( Hg < 8g/dl) We may need to supplement fresh frozen plasma and platelates

Treatment contd. Improved perfusion : Warmth Strong pulses Better capillary refill improved mental status Lower HR BP – ideally 90+(agex2) higher Urine output.

Septic Shock Septicemia - Presence of microbes or their toxins in blood Sepsis – Systemic inflammatory response syndrome ( SIRS ) that has a proven or suspected microbial etiology Severe sepsis – Hypoperfusion with signs of organ dysfunction – Lactic acidosis, oliguria etc. Septic shock - Sepsis + hypotension (ABP<90 mmHg systolic, or 40 mmHg less than patient's normal BP) for at least 1 hr despite adequate fluid resuscitation; Sepsis Severe Sepsis Septic shock MODS Death Sepsis and organ dysfunction, hypoperfusion , or hypotension Sepsis-induced hypotension

Septic, contd. Importance?? The most common of the distributive types, The leading cause of Deaths in ICU in the US. Increasing in occurrence Increased life support for high risk patients Increase in invasive procedures Growing number of the immunocompromised HIV Chemotherapy

PREDISPOSING FACTORS - examples Extended hospitalization Advanced age Debilitating illness Immunodeficiency disorder Disseminated malignancy Septic, contd.

Septic, contd. Focus of infection Pneumonia, UTI, Meningitis, skin and soft tissue infections, GI infections, etc. Gram – ve bacteria (70%) – LPS – Lipid A Peptidoglycan & lipoteichoic acid of gram + ves Polysaccharide surface of Candida

Septic, contd. LPS LBP LPS ENDOTHELIAL CELL Bacteria LPS LBP LPS CD 14 MONOCYTE, MACROPHAGES NEUTROPHILS soluble CD 14 TNF-A IL-1 Cellular chemotaxis Endotherlial injury Activation of coagulation cascade

Septic, contd. The syndrome of septic shock Systemic vasodilation (hypotension) Diminished myocardial contractility Widespread endothelial injury and activation, causing systemic leukocyte adhesion and pulmonary alveolar capillary damage ( ARDS) Activation of the coagulation system, culminating in DIC

Septic Shock Hemodynamics Warm ( hyperdynamic ) shock hypotensive tachycardia tachypnea bounding pulse warm, well perfused extremities skin flushed, moist Cold ( hypodynamic ) shock hypotensive tachycardia tachypnea narrow, thready pulse cold, poorly perfused extremities skin pale, dry

Principles of treatment: Septic shock Ventilatory support IV fluids – crystalloids or colloids - Fill the tank Vasoactive agents – Norepinephrine , Dopamine etc. Draw blood for culture – before Antibiotics Remove septic focus – Resect a gangrenous bowel, Drain an abscess Early empirical antibiotic therapy

Neurogenic Shock Cause – high spinal cord injury , spinal anaesthesia Pathophysiology - Interruption of sympathetic vasomotor input extremities are warm Rx – IV fluids norepinephrine or a pure -adrenergic agent ( phenylephrine )

Hypovolemic shock History – Trauma tearing type of chest pain hematemesis , melena , severe diarrhea P/E – Obvious bleeding Cool clammy skin sweating Narrow pulse pressure Delayed capillary refill Anxious, confused

Cardiogenic shock History - chest pain, shortness of breath, diaphoresis, syncope etc. Symptoms of Hypoperfusion plus Raised JVP gallop Rales – Basal creptations Beck’s triad

Septic shock History – Sx of underlying infection P/E Evidences of Infection Warm extermities Bounding pulse Wide pulse pressure Brisk capillary refill Obtunded

References Harrison’s principles of internal medicine- 18 th edition ACS surgery: principles & practice Mannipal manual of surgery Robbin’s basic pathology Shwartz principles of surgery Davidson’s principles and practice of medicine World Wide Web

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