Shock in children

47,453 views 56 slides Dec 22, 2014
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About This Presentation

shock in pediatrics ,nelson , pals , shock in children , hypovolemic , cardiogenic , obstructive , distributive


Slide Content

SHOCK IN CHILDREN - Dr.Apoorva.E PG,DCMS

“ ACUTE CIRCULATORY FAILURE “ with inadequate or inappropriately distributed tissue perfusion resulting in generalized cellular hypoxia

Body’s inability to deliver adequate oxygen to meet the metabolic demands of the tissues. Initially compensated Continued presence of an inciting trigger + body’s exaggerated response lead to progression of shock if untreated,irreversible tissue injury irreversible shock

CLASSIFICATION 5 major types of shock 1.HYPOVOLEMIC 2.CARDIOGENIC 3.OBSTRUCTIVE 4.DISTRIBUTIVE 5.SEPTIC

HYPOVOLEMIC SHOCK Characterized by fluid loss ( internal / external ) Decreased preload Water/electrolyte plasma blood loss loss loss

CARDIOGENIC SHOCK Poor myocardial contractility leading to cardiac pump failure Due to : CHD Myocarditis Cardiomyopathies Arrhythmias

OBSTRUCTIVE SHOCK Decreased cardiac output secondary to restriction of all cardiac chambers Due to : Tension pneumothorax Pericardial tamponade Pulmonary embolism Anterior mediastinal masses Coarctation of aorta

DISTRIBUTIVE SHOCK Caused by inadequate vasomotor tone Capillary leak Maldistribution of fluid into interstitium Post-spinal cord or brainstem injury Anaphylaxis Poisonings

SEPTIC SHOCK Complex interaction of distributive,cardiogenic and hypovolemic shock Bacterial/Viral/Fungal

Hypovolemic shock – blood VOLUME problem Cardiogenic shock - blood PUMP problem Distributive shock – blood VESSEL problem

PATHOPHYSIOLOGY

COMPENSATORY MECHANISMS >> Heart rate >> Stroke volume >> Vascular smooth muscle tone >> O2 extraction from the blood Redistributing blood flow to brain,kidneys,adrenals and heart at the expense of skin and GIT

To compensate for the metabolic acidosis , - >> RR with >>CO2 elimination - Renal excretion of hydrogen ions - Retention of bicarbonate ions To maintain intravascular volume , - Sodium regulation through RAAS - ADH secretion - Cortisol and catecholamine synthesis and release

CLINICAL MANIFESTATIONS Tachycardia Tachypnoea Decreased urine output Poor peripheral pulses Alteration of mental status Low BP

COMPENSATED Confusion Tachycardia Normal or mild tachypnoea >> CFT U/o-adequate BP normal

UNCOMPENSATED Drowsiness Marked tachycardia Tachypnoea and acidosis Very slow CFT Oliguria / Anuria Hypotension

HYPOTENSION FORMULA Ages – 1 to 10 years Hypotension is defined as SBP < 70mmHg + [age in years X 2] mmHg

IRREVERSIBLE Child is unresponsive Bradycardia Apnoea Cold cyanotic skin Anuria Unrecordable BP

DIAGNOSIS Thorough history and physical exam Lab findings : thrombocytopenia prolonged PT and apTT reduced serum fibrinogen level >> fibrin split products anemia neutrophilia left shift of leukocytes electrolyte disturbances

HYPOVOLEMIC SHOCK << intravascular volume << venous return and preload << decreased ventricular filling << decreased stroke volume << CO << tissue perfusion PATHOPHYSIOLOGY

ASSESSMENT OF FLUID LOSS

TREATMENT 1.Assess airway 2.Administer oxygen 3.Establish IV access 4.Fluid bolus of 20ml/kg isotonic fluid given 5.Continue fluid boluses (maximum of 3) until perfusion improves or hepatomegaly develops 6.In case of shock refractory to fluids,start inotrope (dopamine) GOAL – RESTORE CIRCULATING VOLUME AND TISSUE PERFUSION , CORRECT THE CAUSE

CARDIOGENIC SHOCK Impaired pumping ability of LV Inadequate systolic emptying of LV >>LV filling pressure << Stroke volume >>Left atrial pressure << CO >>Pulmonary capillary pressure Pulmonary interstitial and intralveolar edema PATHOPHYSIOLOGY

CLINICAL PRESENTATION Tachycardia Low volume pulse Cold clammy extremities >>CFT Pulmonary edema,Crackles,RD,Tachypnoea Jugular venous distension Hepatomegaly Hypotension Oliguria,changes in mental status

TREATMENT GOAL - >> CO, treat reversible causes, << myocardial workload 1.Assess airway , administer oxygen/mechanical ventilation 2. IV access 3. Inotropic agents ,vasoactive drugs to >> cardiac contractility and to decrease systemic vascular resistance

4.Cautious administration of fluids (5-10ml/kg boluses over longer time) 5. Morphine to decrease preload and anxiety 6. Vasodilators for afterload reduction 7.Short acting beta blockers for refractory tachycardia

OBSTRUCTIVE SHOCK PATHOPHYSIOLOGY Physical obstruction to blood flow << CO << Tissue perfusion Compensatory >> in systemic vascular resistance

CLINICAL PRESENTATION Muffled heart sounds Distended neck veins Pulsus paradoxus ( << in SBP by more than 10mmHg on inspiration ) Signs of right heart failure plus cyanosis,tachycardia,hypotension PERICARDIAL EFFUSION PULMONARY EMBOLISM

TREATMENT Pericardial drainage in case of pericardial effusion Immediate needle decompression then thoracostomy for chest tube in case of tension pneumothorax Anticoagulants or embolectomy for pulmonary embolism

DISTRIBUTIVE SHOCK Maldistribution of blood flow Some tissues inadequately Some tissues perfused over perfused ( splanchnic circulation) (skeletal muscle, skin) PATHOPHYSIOLOGY

<< Systemic vascular >> Systemic vascular resistance & resistance & >> blood flow to skin << blood flow to skin Warm extremities, Cold extremities, bounding peripheral weak pulses pulses WARM SHOCK COLD SHOCK

CLINICAL PRESENTATION Tachypnoea without increased work of breathing Hypotension/ Normotension Bounding pulses/Weak pulses Brisk/delayed CFT Warm flushed skin/cold pale skin

TREATMENT 1. ANAPHYLACTIC SHOCK – Airway, IV epinephrine, Antihistaminics , Corticosteroids, Withdrawal of Ag , Vasopressors,Inotropes , Cautious fluid administration

2. NEUROGENIC SHOCK – Cautious fluid administration, Vasopressors,Inotropes , Correct hypothermia, Treat bradycardia with atropine, Observe and prevent DVT (due to peripheral pooling of blood)

SEPTIC SHOCK PATHOPHYSIOLOGY

DEFINITIONS SIRS Requires 2 of the following 4 features to be present: Temperature  >38.5° or <36.0° C Tachypnea  >2SD ABOVE NORMAL FOR AGE Tachycardia  >2SD ABOVE NORMAL FOR AGE WBC  ELEVATED OR DEPRESSED FOR AGE/>10% IMMATURE NEUTROPHILS

INFECTION Suspected or proven infection or a clinical syndrome associated with high probability of infection SEPSIS SIRS plus a suspected or proven infection

SEVERE SEPSIS Sepsis plus organ dysfunction,hypoperfusion or hypotension (including but not limited to lactic acidosis,oliguria,acute mental status changes)

Identifying Acute Organ Dysfunction as a Marker of Severe Sepsis Tachycardia Hypotension  CVP  PAOP Jaundice  Enzymes  Albumin  PT Altered Consciousness Confusion Psychosis Tachypnea PaO 2 <70 mm Hg SaO 2 <90% PaO 2 /FiO 2 300 Oliguria Anuria  Creatinine  Platelets  PT/APTT  Protein C  D- dimer

MODS Presence of altered organ function such that homeostasis cannot be maintained without medical intervention

WORK UP Laboratory studies CBP Comprehensive chemistry panel (serum elec,abg,BUN,serum creat,GRBS,LFT,serum lactate) Coagulation studies Blood & urine cultures Imaging studies Chest radiography Abdominal radiography Others according to the suspected cause.

DRAW SAMPLE FOR BLOOD C/S AND START EMPERICAL ANTIBIOTIC

Antibiotics should be administered within the first hour of recognition of septic shock Selection of antibiotic agents is empirically based on an assessment of patient's immunity the potential source of infection the most likely responsible organisms. Antibiotic choice must be broad spectrum , covering gram-positive, gram-negative, and anaerobic bacteria when the source is unknown Regimen for septic shock of unknown cause is Gentamicin 3 rd generation cephalosporin if pseudomonas is suspected, ceftazidime

Vancomycin must be added if resistant staphylococci or enterococci are suspected. If there is an abdominal source, a drug effective against anaerobes should be included “ metronidazole ” Antibiotics are continued for at least 5 days after shock resolves and evidence of infection subsides Abscesses must be drained and necrotic tissues ( eg , infarcted bowel) surgically excised.

DRUGS USED IN SHOCK

1. Dopamine - ionotrope at low dose - peripheral vasoconstriction at >10mcg/kg/min - 3-20mcg/kg/min - arrythmia at higher doses

2. Epinephrine >> HR and >> cardiac contractility Potent vasoconstrictor 0.05 – 3 mcg/kg/min << renal perfusion at higher doses,arrythmia at higher doses 3. Norepinephrine Potent vasoconstrictor No significant effect on cardiac contractility 0.05 to 1.5 mcg/kg/min

4. Dobutamine >> cardiac contractility Peripheral vasodilator 1-10 mcg/kg/min 5. Phenylephrine -potent vasoconstrictor -0.5 to 2 mcg/kg/min ->> O2 consumption -can cause sudden hypertension

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