Shock states in children


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  • Teachers’ Guide:
    (This represents hypovolemic shock.)
    Example questions and examples of acceptable answers:
    What is your assessment?
    15 year-old post-operative patient with sudden tachycardia and borderline low blood pressure with impaired peripheral perfusion. Suggests hypovolemic shock.
    2) What stage of shock?
    Compensated … for now, given his lack of hypotension by strict definition. Given rapidity of onset, be extremely cautious for rapid decline.
    3) What classification of shock? If uncertain, what additional information would you want to obtain to decide?
    Hypovolemic shock, likely due to blood loss related to surgery; less likely septic shock (though you would be suspicious of this given the nature of his wounds) due to his physical exam findings.
    What is your initial management.
    Again, ABCDs, fluid resuscitation with 20 ml/kg crystalloid as needed to restore perfusion and blood pressure. Ensure a type and screen/cross match has been done and order PRBCs to the bedside in the event that bleeding continues. Stat baseline hemoglobin/hematocrit with repeat every 4 hrs until stable.
    MAIN TEACHING POINT: Hypovolemic shock is often first manifest by tachycardia and decreased peripheral perfusion. Hypotension is a late finding and indicates uncompensated shock.
  • Teachers’ Guide:
    (This represents distributive (most likely septic) shock.)
    Example questions and examples of acceptable answers :
    What is your assessment?
    6 year-old with altered mental status and oliguria, with hypotension and peripheral vasodilation after 1 day fever, bloody diarrhea. Likely septic shock.
    2) What stage of shock?
    Uncompensated, given hypotension accompanying altered mental status and oliguria.
    3) What classification of shock?
    Likely septic shock, given vasodilation in setting of what sounds like infection.
    What is your differential for the etiology?
    (not exhaustive differential) For fever and bloody diarrhea: Infectious causes -- salmonella, shigella, e-coli-0517, yersenia, c-diff, e. histolitica; Rheumatologic causes: IBD; Food allergies/intolerances less likely.
    What is your initial management?
    ABCDs, fluid resuscitation with 20 ml/kg crystalloid as needed to restore perfusion and blood pressure. Given the likelihood of septic shock, the goal is to give broad spectrum antibiotics within the first 15-30 minutes. Good antibiotic choices in a critically ill normal host would cover most gram negatives, gram positives (including MRSA) and anaerobes (in this case, since the likely source is intestinal): Ceftriaxone or cefotaxime, plus vancomycin, plus metronidazole is an example of an acceptable combination. If the patient were not clearly septic but if dehydration were more likely responsible for her findings, one should consider that antibiotics increase the likelihood of HUS with e-coli and increase the duration of salmonella carriage.
    Regarding escalation of care, this patient, in uncompensated shock, should require at least ICU monitoring. Discuss the protocol in your institution for instituting a higher level of care immediately.
    MAIN TEACHING POINT: Distributive shock is often marked by increased peripheral vasodilation. Sepsis is the most common cause of distributive shock; if suspected broad-spectrum antibiotics should be delivered in the first 15-30 minutes.
  • Teachers’ Guide:
    (This represents cardiogenic shock.)
    Example questions and examples of acceptable answers:
    What is your assessment?
    4 mo old with subacute onset of decreased desire to feed, emesis in setting of viral symptoms and possibly decreased urine output. Afebrile on exam with tachycardia and signs of hypoperfusion and liver distension and gallop. Suggests cardiogenic shock.
    2) What stage of shock?
    Answer is unclear given lack of available BP reading, but exam with impaired perfusion (and weak cry possibly indicating altered mental status) would suggest progression toward uncompensated shock.
    3) What classification of shock? If uncertain, what additional information would you want to obtain to decide?
    Likely cardiogenic, given decreased desire to feed, emesis, impaired perfusion, distended liver, and S4. Additional information could be gained through CXR looking for cardiac enlargement and pulmonary edema, stat echo, lactate, possibly chemistry looking for acidosis due to hypoperfusion and electrolyte imbalances due to emesis, +/- BNP.
    What leads your differential for the etiology?
    Given recent viral illness, viral cardiomyopathy possible cause.
    What is your initial management?
    ABCDs, continuing to monitor blood pressure closely and ensuring sufficient access, 10 ml/kg bolus (repeated with caution and constant monitoring for worsening heart failure, as needed) to restore perfusion if altered mental status or other signs of end organ dysfunction. Stat cardiac echo (or at least bedside ultrasound). Dopamine stat to the bedside. Stat cardiology consultation.
    MAIN TEACHING POINT: Cardiogenic shock is marked by decreased peripheral perfusion due to decreased cardiac output. Despite increased preload in cardiogenic and obstructive shocks, fluid boluses may be needed to restore perfusion if signs of end organ dysfunction. Howerver, because patient may worsen with these boluses the volume should be small and re-evaluation should occur after each intervention.
  • Shock states in children

    1. 1. Pediatric Shock Recognition, Classification and Initial Management Ramin Nazari MD Pediatric Critical Care Fellow St. Christopher Hospital for Children December 2012
    2. 2. Introduction    Shock is a syndrome that results from inadequate oxygen delivery to meet metabolic demands Oxygen delivery (DO2 ) is less than Oxygen Consumption (< VO2) Untreated this leads to metabolic acidosis, organ dysfunction and death
    3. 3. Oxygen Delivery  Oxygen delivery = Cardiac Output x Arterial Oxygen Content (DO2 = CO x CaO2)  Cardiac Output = Heart Rate x Stroke Volume (CO = HR x SV) – SV determined by preload, afterload and contractility  Art Oxygen Content = Oxygen content of the RBC + the oxygen dissolved in plasma (CaO2 = Hb X SaO2 X 1.34 + (.003 X PaO2)
    4. 4. Figure 1. FACTORS AFFECTING OXYGEN DELIVERY Hgb CaO2 A-a gradient DPG Acid-Base Balance Blockers Competitors Temperature Influenced By Oxygenation DO2 Influenced By Drugs Conduction System HR CO EDV SV CVP Venous Volume Venous Tone Ventricular Compliance Influenced By ESV Contractility Influenced By Afterload Temperature Drugs Metabolic Milieu Ions Acid Base Temperature Drugs Toxins Blockers Competitors Autonomic Tone
    5. 5. Stages of Shock Compensated – Vital organ function maintained, BP remains normal. Uncompensated – Microvascular perfusion becomes marginal. Organ and cellular function deteriorate. Hypotension develops. Irreversible
    6. 6. Clinical Presentation  Early diagnosis requires a high index of suspicion  Diagnosis is made through the physical examination focused on tissue perfusion  Abject hypotension is a late and premorbid sign
    7. 7. Initial Evaluation: Physical Exam Findings of Shock     Neurological: Fluctuating mental status, sunken fontanel Skin and extremities: Cool, pallor, mottling, cyanosis, poor cap refill, weak pulses, poor muscle tone. Cardio-pulmonary: Hyperpnea, tachycardia. Renal: Scant, concentrated urine
    8. 8. Initial Evaluation: Directed History  Past medical history – heart disease – surgeries – steroid use – medical problems  Brief history of present illness – exposures – onset
    9. 9. Differential Diagnosis of Shock   Hypovolemic  Myocardial dysfunction  Dysrrhythmia  Congenital heart  Hemorrhage  Fluid loss  Drugs  Distributive  Analphylactic  Neurogenic  Septic Cardiogenic disease  Obstructive  Pneumothorax, CardiacTamponade, Aortic Dissection  Dissociative  Heat, Carbon monoxide, Cyanide  Endocrine
    10. 10. Differential Diagnosis of Shock    Precise etiologic classification may be delayed Immediate treatment is essential Absolute or relative hypovolemia is usually present
    11. 11. Neonate in Shock: Include in differential: Congenital adrenal hyperplasia Inborn errors of metabolism Obstructive left sided cardiac lesions: – Aortic stenosis – Hypoplastic left heart syndrome – Coarctation of the aorta – Interrupted aortic arch
    12. 12. Management-General  Goal: increase oxygen delivery and decrease oxygen demand: For all children: ○ Oxygen ○ Fluid ○ Temperature control ○ Correct metabolic abnormalities Depending on suspected cause: ○ Antibiotics ○ Inotropes ○ Mechanical Ventilation
    13. 13. Management-General  Airway If not protected or unable to be maintained, intubate.  Breathing Always give 100% oxygen to start Sat monitor  Circulation Establish IV access rapidly CR monitor and frequent BP
    14. 14. Management-General Laboratory studies: – ABG – Blood sugar – Electrolytes – CBC – PT/PTT – Type and cross – Cultures
    15. 15. Management-Volume Expansion     Optimize preload Normal saline (NS) or lactated ringer’s (RL) Except for myocardial failure use 1020ml/kg every 2-10 minutes. Reasses after every bolus. At 60ml/kg consider: ongoing losses, adrenal insufficiency, intestinal ischemia, obstructive shock. Get CXR. May need inotropes.
    16. 16. Fluid in early septic shock Carcillo, et al, JAMA, 1991 Retrospective review of 34 pediatric patients with culture + septic shock, from 1982-1989. Hypovolemia determined by PCWP, u.o and hypotension. Overall, patients received 33 cc/kg at 1 hour and 95 cc/kg at 6 hours. Three groups: – 1: received up to 20 cc/kg in 1st 1 hour – 2: received 20-40 cc/kg in 1st hour – 3: received greater than 40 cc/kg in 1st hour No difference in ARDS between the 3 groups
    17. 17. Fluid in early septic shock Carcillo, et al, JAMA, 1991 Group 1 Group 2 Group 3 Hypovolemic at 6 hours (n = 14) 6 (n = 11) 2 (n = 9) 0 -Deaths Not hypovolemic at 6 hours 6 8 2 9 0 9 -Deaths Total deaths 2 8 5 7 1 1
    18. 18. Fluids Solution NS LR  Na+ 154 130 Cl154 109 K+ 0 4 Ca++ 0 3 Mg++ Buffer 0 None 0 Lactate Inotropic and vasoactive drugs are not a substitute for fluid, however... Can have various combinations of hypovolemic and septic and cardiogenic shock May need to treat poor vascular tone and/or poor cardiac function 18
    19. 19. Inotropes and Vasopressors   Lack of history of fluid losses, history of heart disease, hepatomegaly, rales, cardiomegaly and failure to improve perfusion with adequate oxygenation, ventilation, heart rate, and volume expansion suggests a cardiogenic or distributive component. Consider Appropriate inotropic or vasopressor support.
    20. 20. Case 1  15-year-old previously well boy is freshly from the PICU, POD #3 from partial small bowel resection after multiple gunshot wounds to the abdomen. The nurse pages because his HR has increased in the last hour from 90 to 130, despite pain score of 1/10 on morphine drip. On exam, he is afebrile, HR is 140, BP 80/50. Cap refill is >3 seconds in his cool extremities and pulses are 1+.  What is your assessment? What is the stage of shock? What is the classification of shock? What is your initial management?   
    21. 21. Hypovolemic Shock Most common form of shock world-wide Results in decreased circulating blood volume, decrease in preload, decreased stroke volume and resultant decrease in cardiac output. Etiology: Hemorrhage, renal and/or GI fluid losses, capillary leak syndromes
    22. 22. Hypovolemic Shock Clinically, history of vomiting/diarrhea or trauma/blood loss Signs of dehydration: dry mucous membranes, absent tears, decreased skin turgor Hypotension, tachycardia without signs of congestive heart failure
    23. 23. Hemorrhagic Shock Most common cause of shock in the United States (due to trauma) Patients present with an obvious history (but in child abuse history may be misleading) Site of blood loss obvious or concealed (liver, spleen, intracranial, GI, long bone fracture) Hypotension, tachycardia and pallor
    24. 24. Hypovolemic/Hemorrhagic Shock: Therapy Always begin with ABCs Replace circulating blood volume rapidly: start with crystalloid Blood products as soon as available for hemorrhagic shock (Type and Cross with first blood draw) Replace ongoing fluid/blood losses & treat the underlying cause
    25. 25. Septic Shock SIRS/Sepsis/Septic shock Mediator release: exogenous & endogenous Maldistribution Cardiac of blood flow dysfunction Imbalance of oxygen supply and demand Alterations in metabolism
    26. 26. Septic Shock: “Warm Shock”   Early, compensated, hyperdynamic state Clinical signs Warm extremities with bounding pulses, tachycardia, tachypnea, confusion.  Physiologic parameters widened pulse pressure, increased cardiac ouptut and mixed venous saturation, decreased systemic vascular resistance.  Biochemical evidence: Hypocarbia, elevated lactate, hyperglycemia
    27. 27. Septic Shock: “Cold Shock”   Late, uncompensated stage with drop in cardiac output. Clinical signs Cyanosis, cold and clammy skin, rapid thready pulses, shallow respirations.  Physiologic parameters Decreased mixed venous sats, cardiac output and CVP, increased SVR, thrombocytopenia, oliguria, myocardial dysfunction, capillary leak  Biochemical abnormalities Metabolic acidosis, hypoxia, coagulopathy, hypoglycemia.
    28. 28. Septic Shock Cold Shock rapidly progresses to mutiorgan system failure or death if untreated Multi-Organ System Failure: Coma, ARDS, CHF, Renal Failure, Ileus or GI hemorrhage, DIC More organ systems involved, worse the prognosis Therapy: ABCs, fluid Appropriate antibiotics, treatment of underlying cause
    29. 29. Case 2  6-year-old previously well girl is admitted to your ward directly from clinic with fever, bloody diarrhea x 1 day. She’s had no urine x 24 hrs and is becoming harder to awaken. On exam, her HR is 150, BP 72/30, temp 103. She’s sleepy but arousable. She’s flushed with capillary refill <1 second.  What is your assessment? What is the stage of shock? What is the classification of shock? What is your differential for the etiology? What is your initial management? If a higher level of care is needed, how would you obtain it?    
    30. 30. Cardiogenic Shock Etiology: – Dysrhythmias – Infection (myocarditis) – Metabolic – Obstructive – Drug intoxication – Congenital heart disease – Trauma
    31. 31. Cardiogenic Shock Differentiation from other types of shock: – History – Exam: Enlarged liver Gallop rhythm Murmur Rales – CXR: Enlarged heart, pulmonary venous congestion
    32. 32. Cardiogenic Shock Management: – Improve cardiac output:: Correct dysrhthymias Optimize preload Improve contractility Reduce afterload – Minimize cardiac work: Maintain normal temperature Sedation Intubation and mechanical ventilation Correct anemia
    33. 33. Case 3  4-month-old boy ex-term, previously well boy presents to ED with decreased desire to feed x 2 days with 2 times daily emesis, following what sounds like viral URI. Urine output has been 3 wet diapers daily. He is afebrile with HR 180; BP has not been obtained. He has a weak cry, is mottled with 3-second capillary refill, pulses 1+ in all extremities. Liver is palpable 4 cm below RCM. S4 is present without murmur.  What is your assessment? What is the stage of shock? What is the classification of shock? What is your differential for the etiology? What is your initial management?    
    34. 34. Distributive Shock Due to an abnormality in vascular tone leading to peripheral pooling of blood with a relative hypovolemia. Etiology – – – – Anaphylaxis Drug toxicity Neurologic injury Early sepsis Management – – Fluid Treat underlying cause
    35. 35. Obstructive Shock Mechanical obstruction to ventricular outflow Etiology: Congenital heart disease, massive pulmonary embolism, tension pneumothorax, cardiac tamponade Inadequate C.O. in the face of adequate preload and contractility Treat underlying cause.
    36. 36. Dissociative Shock Inability of Hemoglobin molecule to give up the oxygen to tissues Etiology: Carbon Monoxide poisoning, methemoglobinemia, dyshemoglobinemias Tissue perfusion is adequate, but oxygen release to tissue is abnormal Early recognition and treatment of the cause is main therapy
    37. 37. Hemodynamic Variables in Different Shock States Hypovolemic Cardiogenic Obstructive Distributive Septic: Early Septic: Late CO ↑ ↓↓ ↓ ↑↑ ↑↑↑ ↓↓ SVR ↑ ↑↑↑ ↑ ↓↓↓ ↓↓↓ ↑↑ MAP ↔ Or ↔↓Or ↔↓Or ↔↓Or ↔↓Or ↓ ↓↓ Wedg e ↓↓↓ ↑↑ ↑↑ ↔ Or ↓ ↓ ↑ CVP ↓↓↓ ↑↑ ↑↑ ↔ Or ↓ ↓ ↑ or ↔
    38. 38. Final Thoughts      Recognize compensated shock quickly- have a high index of suspicion, remember tachycardia is an early sign. Hypotension is late and ominous. Gain access quickly- if necessary use an intraoseous line. Fluid, fluid, fluid - Administer adequate amounts of fluid rapidly. Remember ongoing losses. Correct electrolytes and glucose problems quickly. If the patient is not responding the way you think he should, broaden your differential, think about different types of shock.
    39. 39. Take-Home Points  Shock is a progressive process.  Intervene early.  Identifying the stage and classification of shock is important.  Stage: Compensated, uncompensated, or irreversible?  Classification: Hypovolemic, distributive, cardiogenic, or obstructive?  Management should be directed at normalizing tissue perfusion and blood pressure.  Consider using the consensus-based goal-directed algorithm for shock management.