The shock

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The shock


Objectives

At the end of this session the participants will be able to: • Recognize signs of compensated and decompensated shock • Know the main treatments

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General assessment

• General aspect: consciousness and relationship with the environment • Respiratory work: distress or insufficiency • Circulation: color, skin temperature and peripheral and central pulses

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Compensated shock

• First phase and compensatory mechanisms: increased arterial resistance, reduction of flow to less noble organs, reduction of vascular bed and tachycardia • Subtle signs: irritability, mild confusion, cold extremities, pale skin, tachycardia, peripheral and central temperature difference, capillary refill, normal systolic and elevated diastolic

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Decompensated shock

• Compensation mechanisms become ineffective • Increased anaerobic metabolism resulting in metabolic acidosis • Reduction of tissue perfusion and consequent multi organ failure • BP reduction, capillary refill time increase, tachycardia, cold mottled skin, oliguria, altered state of consciousness

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Foundations in the treatment of shock

• Optimization of the oxygen content in the blood • Improved cardiac output volume and distribution • Reduce oxygen demand • Correct metabolic alterations

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The shock

Shock classification

Causes

Hypovolaemic

Hemorrhage Diarrhea/vomiting Burns Periptonitis

Distributive

Sepsis Anaphylaxis Spinal cord injury Drug poisoning

Cardiogenic

Congenital heart disease Arrhythmias Cardiomyopathies

Obstructive

Hypertensive pneumothorax Hemo-pneumothorax Cardiac tamponade Pulmonary embolism

Dissociative

Severe amnesia Carbon monoxide poisoning Methemoglobinemia

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Specific treatment of hypovolemic shock

• Identify the type of leak (hemorrhagic or non-hemorrhagic) • Replacement of intra and extra vascular deficit • Prevent further loss • Restoration of acid-base balance • Correct metabolic alterations

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Specific treatment of distributive shock

• Replacement of intra and extra vascular deficit • Broad spectrum antibiotic therapy • Restoration of acid-base balance • Identify and Correct metabolic alterations • Pharmacological treatment: vasopressors and hydrocortisone • Diagnostic insights

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Specific treatment of cardiogenic shock

• Give liquids with caution • Pharmacological support • Diagnostic insights: laboratory and nonlaboratory tests

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Specific treatment of obstructive shock

• Correction of the cause of cardiac output obstruction • Restoration of tissue perfusion

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Specific treatment of dissociative shock

• Correction of the cause of poor oxygenation • Replacement or chelating therapies

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Particular situations

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Such as

• • • • • • •

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Septic shock Hypovolemic shock Trauma Single Ventricle Pulmonary Hypertension Children with special care needs Intoxications

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Septic shock • Isotonic Fluids (Crystalloids) (Class IIa, LOE C) • Protocols (Early Goal Directed Therapy): ScvO2 ≥ 70% (Class IIb, LOE B) • Assisted ventilation (Target EGDT) • Etomidate: (Class III, LOE B) inhibition of the adrenal response -> worsening of the prognosis

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Hypovolemic shock • Crystalloids (SF or RL) (Class I, LOE A), no added benefit from colloids • Bolus of 20 ml/kg of crystalloids in the presence of signs of shock even with normal blood pressure (Class IIb, LOE C) • Continue with boluses (20 ml/kg) if perfusion does not improve • Insufficient data on the hypertonic solution

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Trauma #1 Common errors in the resuscitation of the pediatric trauma patient: • Inability to maintain an adequate airway • Inappropriate administration of fluids • Failure to recognize occult bleeding Early involvement of an experienced trauma surgeon and early referral to an experienced pediatric trauma center is desirable

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Trauma #2

• Avoid head and neck movements and use jaw thrust to open and maintain an open airway • If the airway cannot be opened with jaw thrust, use “head tilt – chin lift” because a patent airway is a priority anyway • It may be useful to place a pad under the back and shoulders • Avoid hyperventialtion • Short-term hyperventilation (moderate or controlled hypocapnia) may be used if signs of herniation are present (increased ICP if measured, unilateral non-lightresponsive mydriasis, bradycardia, and hypertension)

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Trauma #3 • Always think about chest injuries in systemic trauma (Pneumothorax, hemothorax and pulmonary contusion impairment of B and C) • In the presence of craniofacial trauma or in the suspicion of a skull base fracture, it is preferable not to insert the SNG (Class IIa, LOE C) • In particular situations of cardiac arrest (penetrating trauma) there may be an indication for thoracotomy (Class IIb, LOE C) • Always consider internal bleeding, pneumothorax hypertension, cardiac tamponade, and spinal injuries as causes of shock The shock

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Single Ventricle • • • • •

Increase pulmonary flow Heparin Oxygen with 80% SaO2 target ETCO2 not reliable Newborns in periarrest: PaCO2 50-60 mmHg • Systemic vasodilators (alpha-lytic eg. phenoxybenzamine, milrinone, nipride) • ScvO2 (central venous blood O2 saturation) monitoring • In patients undergoing Stage procedure it is reasonable to consider ECMO (Fontan-type Physiology or BDG) The shock

 venous blood (poor in oxygen)  Arterial blood (rich in oxygen)  Mixture of venous and arterial blood Pulmonary stenosis Single ventricle

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Pulmonary Hypertension • • • •

Standard PALS Correct hypercapnia Fluids to maintain the preload Inhaled nitric oxide or nebulized prostacyclin to reduce pulmonary vascular resistance • Alternatively, intravenous prostacyclin can be used • ECMO useful if used early in resuscitation

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Children with special care needs • Know the techniques for maintaining a clear and open airway, repositioning the tracheostomy tube, and performing CPR using the main airway • If the lung does not expand after aspiration, mouth-stoma or bagstoma ventilations can be performed • If the upper airways are patent, it is possible to ventilate with a bag and mask, keeping the tracheostomy manually occluded

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Post-resuscitation treatment

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Objectives

• Preserve neurological function • Prevent secondary damage • Diagnose and treat the underlying disease • Ensure transportation to an expert pediatric center • Reevaluate frequently

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Respiratory function Hyperoxemia increases the oxidative damage following reperfusion Use minimum O2 flow necessary to maintain SaO2 ≥ 94% and ≤ 99% Check the resolution of the metabolic acidosis and the reduction of lactates and the normalization of venous O2 saturation End-tidal CO2 detected with capnography Control the pain with analgesics and sedatives Monitor PETCO2 especially in case of transport and during diagnostic procedures Insert an SNG to prevent gastric distension

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Circulation • Monitor FC and PA, and diuresis • 12-lead ECG • Remove I.O. access (if present) when at least 2 peripheral venous accesses have been positioned • Chest x-ray, Lactates, ScvO2 • Myocardial dysfunction (post-cardiac arrest) is quite common in this phase

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Circulation - Drugs

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Adrenaline: large inter-individual variability, titrate dose to desired effect • Low dose (< 0.3 mcg/kg/min) beta adrenergic action • High dose (> 0.3 mcg/kg/min) alpha adrenergic action

Norepinephrine: very useful in shock with reduction of peripheral vascular resistance (septic, anaphylactic, spinal or vasodilator)

Dopamine: 2-20 mcg/kg/min

Dobutamine: selective effect on ß1 and ß2 receptors. It improves myocardial contractility and can lower peripheral resistance

Nitroprusside: reduction of peripheral vascular resistance and improvement of CO. Useful in association with inotropes

Inodilators: CO improvement with little effect on O2 consumption. In highly complex settings to treat myocardial dysfunction in the presence of increased peripheral or pulmonary resistance. They have a long half-life with some delay in reaching effect after dosage changes (from 18 hours with inamrinone to 4.5 hours with milrinone). In case of toxicity, prolonged effects even after suspension. 27


Nervous system

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Avoid hyperventilation. It has no benefit and many damage the CNS by reducing CO cerebral perfusion

Con trolled hypothermia (32-34 °C) may be considered for children who remain comatose after cardiac arrest (Class IIb, LOE C ) especially if witnessed (Class IIa, LOE C)

Monitor temperature and aggressively treat fever when > 38°C (Class IIa, LOE C)

Aggressively treat epileptic seizures

Avoid too rapid heating from 32 to 34 °C (> 0.5°C/2h)

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Unexpected death in the pediatric age

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Unexpected death in the pediatric age

Incidence (USA) • 0.6-6.2/100.000 subjects without heart disease • 20-25% during sport • 100/100.000 patients with heart disease

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Unexpected death in the pediatric age

2010 (New argument): in the event of sudden cardiac death with no apparent cause in a child or young adult, a personal and family medical history should be obtained (including list of episodes of syncope, epileptic seizures, drownings/accidents with no apparent cause or sudden and unexpected deaths < 50 years of age), as well as review previous ECGs. Infants, children and young adults suffering sudden and unexplained death should, where resources permit, undergo a full and unrestricted autopsy, preferably by a pathologist trained and experienced in cardiovascular pathology. Tissues should also be preserved for genetic analysis to establish the presence of channelopathy.

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Unexpected death in the pediatric age

Motivation: as evidenced by a growing body of evidence, some cases of sudden death of infants, children and young adults may be associated with genetic mutations that cause defects in cardiac ion transport, known as channelopathies. Such defects can cause fatal arrhythmias and correctly diagnosing them can be of great importance to the victims’ living relatives.

Possibility of diagnosis in survivors!!!

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Guidelines 2010 New considerations on pediatric MI

• The doctor’s task does not end with the resuscitation phase • In cases of MI, refer to the acquisition of data/information to exclude genetic diseases • Shockable rhythms in pediatric arrest: not so rare

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