MEKELLE UNIVERSITY Collage of health science School of public health Department of public health officer seminar on management of shock Date 30/09/2016 E.C
Presented by Mulubrhan Abrha Hayelom Gebremedhin Tekle Muez Tsegay Gebremariam Adugna Tsegay Modulator : D.r Rovel Date 30-09-2016 E.C
Introduction shock : is an acute syndrome characterized by inadequate organ and tissue perfusion. It is inadequate delivery of oxygen and nutrients to maintain normal tissue and cellular function. It is a state of oxygen demand becoming higher than oxygen supply and life threatening medical condition that needs immediate intervention.
Epidemiology It occurs approximately in 2% of all hospitalized children and adults. It is a clinical syndrome with mortality rate of 20-50%. Most patients die in acute hypotensive state. Infants(esp. premature infants) have the highest mortality. The mortality rate is higher in developing countries since they lack adequate pediatric life support.
Etiology Inadequate blood volume(GI loss, hemorrhage, burn) Sepsis(endotoxins of staph.aures and strep.pneumoniae) Defects of the heart Abnormality within vascular bed anaphylaxis -allargic reactions
Pathophysiology Fluid loss, peripheral vasodilation, decreasing cardiac contractility and circulatory obstruction Insufficient systemic circulation Inadequate tissue and organ perfusion (shock) Systemic tissue perfusion is determined by CO and SVR CO is the product of heart rate and stroke volume Stroke volume is related to preload, myocardial contractility and afterload
Inadequate tissue perfusion is initially reversible but prolonged oxygen deprivation leads to cellular hypoxia and derangement of critical biochemical processes like - ion pump dysfunction - intracellular edema - leakage of intracellular contents - disruption of intracellular PH
The organ and tissue perfusion of our body has 4 essential components - heart (the pump) - blood vessels - blood ( transport medium of oxygen) - oxygen Any fault in those components will result in inadequate organ and tissue perfusion(shock) Hence our body tries to compensate this by different physiological mechanisms to maintain BP and preserve tissue perfusion. These responses include increase in heart rate, stroke volume and vascular smooth muscle tone
Intra vascular fluid leaks in to the interstitial extracellular space because of vascular endothelial cell injury and loss of tight junctions. Maintenance of vascular volume is facilitated by - activation of renin angiotensin aldosterone axis - synthesis of cortisol and catecholamines - secretion of anti diuretic hormone (ADH)
Stages of shock Since it is the process of oxygen demand becoming greater than oxygen supply it is a continuous condition i.e. it has stages Stage 1 (compensatory stage ): - initiation of body's compensatory mechanisms through - hormonal - biochemical - neural - vital organ function is maintained - BP remains normal - no change in mental status -
- the baroreceptors in the arteries detect the hypotension and release epinephrine and norepinephrine which cause increasing heart rate and increase vasoconstriction and maintain BP. - activation of renin angiotensin aldosterone axis (RAAS) and secretion of ADH causes vasoconstriction of kidneys, GI tract and other organs to divert blood to the vital organs(heart, lung and brain). But this no longer act if no treatment is introduced. The compensatory mechanism fail and develop decompensated stage.
Stage 2 (decompensated stage): -Occur when the compensatory mechanism over whelmed -The prolonged vasoconstriction compromise vital organs due to reduced perfusion. - sign and symptoms of organ dysfunction appear. -oliguria - confusion - respiratory distress - hypotension also develops
Stage 3 (irreversible or refractory): At this stage the vital organs have failed and the shock can no longer be reversed Brain damage and cell deaths are occurring Death will occur immediately
Types of shock Shock can be categorized in to 4 broad classifications based on the underlying cause 1 , Hypovolemic shock : is caused due to a decrease in blood volume. causes of hypovolemic shock include A, hemorrhage (blood loss) - GI bleed(PUD) - AAA (rupture could cause a huge amount of blood loss) - trauma -PPH - ectopic pregnancy - hemoptysis
B,non bloody fluid loss - third degree burn - excessive vomiting and diarrhea -excessive sweating
2 , Cardiogenic shock : shock due to defective contractility of the heart or pumping ability of hurt is affected. causes of cardiogenic shock - myocarditis -multiple MI’s -arrythmia -dilated cardiomyopathy -congenital heart diseases
3, Obstructive shock : is due to obstruction of blood flow outside of the heart. causes of obstructive shock - tension pneumothorax - cardiac tamponade - pulmonary embolism - aortic stenosis
4 Distributive shock : it is due to inability to maintain vascular tone which leads to maldistribution of fluid and capillary leak. Examples of distributive shock a, septic sock : is caused by amplified systemic infection. b, anaphylactic shock : due to severe allergic reaction. c, neurogenic shock: due to acute spinal cord injury.
Shock can be classified in to 3 based on clinical manifestations 1 . mild shock : Initially with tachycardia, tachypnea , mild decrease in urine output Cold extremity, weak pulse, but normal BP Patient may exhibit anxiety and sweating
2 . moderate shock: Patient becomes drowsy and mildly confused Urine output less than 0.5ml/kg/hr. BP starts to fail
3. Severe shock : Profound tachycardia and hypotension Patient becomes anuria, unconscious with respiratory distress Patients experience seizure
Complications of shock Ignorance of immediate intervention could result in - multi organ damage -coagulation disorder -respiratory failure - coma and death
History and physical examination Symptoms History that suggests the cause Volume loss, infection, trauma, cardiac illness, anaphylaxis Orthostatic light headedness Weakness 27
Cont. Signs Vital signs PR Usually elevated (bradycardia in neurogenic shock) Decrease in pulse volume Pulsus paradoxus Decrease in SBP with inspiration (Present in cardiac tamponade) BP Orthostatic hypotension Fall in DBP >15 to 20 mm Hg when the patient is sitting or standing It is almost always abnormal, especially if accompanied by an increase in pulse rate greater than 20 to 30 beats per minute Hypotension Shock may occur with a normal BP, and hypotension may occur without shock Shock index (HR/SBP): elevated in volume loss and LV dysfunction (normal is 0.5 to 0.7) RR Elevated Temperature Hypothermia or fever 28
Clinical manifestations Cold extremities Weak pulse Low BP Low urine out put Confusion Central and peripheral cyanosis Delayed or absent capillary refill High pulse rate
Cont. Respiratory system Tachypnea Increased MV and dead space Respiratory failure ARDS Cardiovascular system Neck veins…..distended or flattened Tachycardia and week pulse Decreased capillary refill (>2 sec) Muffled heart sounds Arrhythmias Murmurs 31
Cont. Cont. Skin Pallor Duskiness/cyanosis Sweating Altered temperature MSS Ischemia/gangrene CNS Restlessness, disorientation, confusion, coma 32
Cont. 33
Investigations CBC RBS Blood culture Chest x-ray ECG Echo Urine analysis Blood group Stool examination Serum electrolyte etc. ….
Management of shock The primary goal of management is restoration of adequate organ perfusion and tissue oxygenation To active tis -the vasculature must have blood kept within it - the blood must have enough oxygen
General principles of management ABC of life IV fluid therapy Oxygen supplement Blood transfusion Catheterize
1 management of hypovolemic shock Control bleeding : identify source and site of bleeding apply pressure on it and stop the bleeding IV fluid administration: according to the degree of deficit, size of the person and amount of lost(20 ml/k of fluid as starting bolus and repeat if needed) Early blood transfusion( for every 1 ml of estimated blood lost give 3ml of fluid )
2, Management of obstructive sock Rapid and definite care must be taken to the specific cause because it is acute life threatening condition A, cardiac tamponade – pericardial drainage B, tension pneumothorax – needle decompression c, pulmonary embolism – anti coagulant or thrombolysis
3, Management of distributive shock Increasing IV volume is the initial management and then specific therapy is taken to specific cause 1,septic: aggressive IV fluid wit broad spectrum IV antibiotics ( IV Ampicili n and Gentamicin) 2, anaphylactic: IV or IM vasoconstrictors (epinephrine and adrenaline) with NS, corticosteroids 3, neurogenic: this is challenging since injury to ANS (sympathetic path way) if no response to fluid therapy give systemic vasopressant (norepinephrine , dopamine ) to restore blood flow to the pressure dependent areas (brain and heart)
4,Manaement of cardiogenic shock Restoring contractility of heart is the primary goal of therapy. Unlike other types of sock the first line management is IV or IM medications tat increase cardiac contractility - dopamine IV 2 -20 mcg/kg/min diluted with NS -dobutamine IV 2 -15mcg/kg/min diluted with dextrose solution If necessary 5 – 10 ml/kg Ringers lactate solution IV can be administered with effective care
Summary Shock is inadequate blood flow that results cells and organ not to get enough oxygen and nutrient to function properly. it is global tissue hypoperfusion and life threatening condition,that needs immidate intervention. Unless immidate treatment is introduced it gets worse rapidly and many organs can be dameged.Specially the brain.
References 1)Nelson text book of pediatrics,20th edition 2) Fanos pediatrics 2022GC edition 3) pediatric and child health lecture note for health science students