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Copied from the AAP Textbook of Pediatric Care
Shock can be classified by cause and mechanism: hypovolemic, cardiogenic, and distributive. Again, the primary clinician should recall that despite complexities of cause, the early stages of shock are easy to recognize, and the treatments are straightforward.[13]
Shock from loss of blood volume caused by trauma, diarrhea, burns, and 3rd spacing (as in peritonitis) is the most common form of shock in children. Loss of fluid leads to low intravascular volume and preload to the heart is decreased. If such losses (up to 30% of circulating blood volume) occur over days, then patients can compensate by increasing thirst, heart rate, and retention of fluid by concentrating urine. Large volumes of fluid loss that occur acutely lead to decompensation represented by diminished mental status, tachycardia, poorly perfused skin with prolonged capillary refill, oliguria, and, eventually, hypotension.
Nonhemorrhagic shock is seen in diarrhea, vomiting, urinary losses, evaporative losses, 3rd spacing of fluid (peritonitis, edema), and burns. The causes of hypovolemic shock are seen in BOX 358-2.
Physical signs in hypovolemic shock occur as a result of decreased venous return to the heart, which leads to diminished cardiac output. Catecholamines are released, which produces the hallmark vasoconstriction in skin, muscle, and splanchnic blood vessels. The renin-angiotensin system is activated, promoting the retention of salt and water. Fluid resuscitation restores preload, and cardiac output is increased with resolution of symptoms. Physical signs in dehydration reliably indicate the percentage of body fluid compartment losses (Table 358-3). In hemorrhagic shock, physical findings correlate to the amount of blood loss[15] (Table 358-4).
Cardiac shock can be caused by mechanical obstruction or muscle (pump) failure. In obstructive cardiogenic shock, air and fluid in the pericardium or pleural spaces (rarely) can impede venous return to the heart and decrease systolic ejection. Common causes are listed in BOX 358-3. These patients usually exhibit distended neck veins because of increased jugular venous pressure and hypotension. Massive pulmonary embolus, rare in children, can obstruct flow from the right to the left side of the heart. In coarctation of the aorta, hypoplastic left heart syndrome, and left ventricular outflow tract stenosis, cardiac output is compromised.
The heart can fail as a mechanical pump from a variety of causes (BOX 358-4). Patients with cardiac failure have low cardiac output resulting in the clinical signs of altered mental status, tachycardia, decreased capillary refill, and evidence of venous congestion (hepatomegaly, rales). Children with pericardial effusion may have muffled heart tones.
Septic shock is the most common and certainly best-studied cause of cardiovascular collapse the primary caregiver will encounter.[9] The causes of bacterial septic shock have changed since vaccination against Haemophilus influenzae type b was instituted in 1988. If sepsis in the (increasingly common) immunocompromised patient is excluded, meningococci and streptococci are then the most frequently encountered bacterial causes of sepsis.
Patients with infections caused by Staphylococcus aureus, Pseudomonas aeruginosa, Candida species, and Streptococcus pyogenes have higher mortality rates compared with patients with infections caused by coagulase-negative Staphylococcus and Acinetobacter species.[16]
Studies of children who have meningococcemia highlight important issues in the care of children in septic shock (see Chapter 353, Meningococcemia). Mortality remains high despite modern advances in critical care.[17] An unfortunate characteristic of meningococcal disease is its rapid progression in fatal cases. Characteristics of cases rapidly progressing to death include young age, absence of meningitis, thrombocytopenia, leukopenia, multiorgan failure, and severity of petechiae.[17] Invasive meningococcal disease is most common in children younger than 4 years. Meningitis and sepsis occurs in 1.3:100,000 in the United States, but incidence in Ireland is 15:100,000.[17] Clinicians who encounter these clinical stigmata in primary care settings should recognize the importance of early stabilization, the need for referral for definitive therapy, and the high mortality despite aggressive intervention.
Children and adults exhibit developmental differences in the hemodynamic response to sepsis. In adults, mortality is caused by a pressor and volume resistant state characterized as vasomotor paralysis. Myocardial dysfunction is common in adults, but cardiac output is maintained by tachycardia and ventricular dilatation.[7] [18]
In pediatric septic shock, low cardiac output, not vasodilatation, is associated with mortality.[19] In children, oxygen delivery is the major determinant of oxygen consumption, whereas in adults, oxygen used by tissues (oxygen extraction) is more important. Survival correlates to the restoration of cardiac output and oxygen delivery.[8] [20]
Some patients with severe septic shock may develop a hypoadrenal response to shock. This scenario is clinically characterized as patients who are in refractory shock (see Table 358-2) who are, by definition, unresponsive to volume resuscitation, the addition of 2 catecholamine drugs, and normalization of acid base, glucose, and calcium homeostasis. Infants and children at risk include those with septic shock and purpura, those with known or suggested adrenal abnormalities, and children who have received a therapeutic course of steroids in the 6 months before the onset of sepsis.[21]
In patients whose shock state is refractory to volume, dopamine or dobutamine, and the addition of epinephrine or norepinephine (catechol resistant shock), empirically initiating stress-dose steroids (hydrocortisone at stress doses of 50 to 100 mg/m[2]/day would be reasonable. If time and condition allow it, a baseline serum cortisol level is drawn, followed by a 250 microgram dose of corticotropin, and a repeat cortisol level is drawn at 30 minutes. The response (or absence of) will determine the presence of a hypoadrenal state and the need for continued steroid administration. A baseline serum cortisol of less than 18 Tg/dL and a poststimulation increment of less than 9 Tg/dL indicate a hypoadrenal state.[9] [21] If a stimulation test cannot be done, then continued steroid therapy for 3 to 5 days should be based on clinical response.
In distributive shock disorders, global disorder in vasomotor control is present, resulting in maldistribution of blood flow and oxygen to tissue. Anaphylaxis and spinal cord injury are the 2 types most likely to be encountered in primary care. Cardiac output may be normal or increased. These patients lose sympathetic control of the vascular system, which reduces peripheral vascular tone. This circumstance produces pooling of blood in the periphery, which, in turn, leads to decreased venous return to the heart.
In anaphylactic shock, the inciting agent should be removed if possible. These patients uniformly respond well to volume administration, epinephrine infusion, antihistamines that include an H2-receptor blocker, and steroid therapy.
March 29, 2009, Dr Cooper Pediatric Circulatory Emergencies PAT Is he in shock? Volume or Cardiogenic, assess vitals, mentation, etc, (BP last indicator) Peds, who present with dysrhythmias, present like they are in shock. They won’t tell you that they have palpitations, etc, do not presume that if a child is in shock you always give fluid…must rule out cardiogenic causes. Shock- failure of circulation to meet the metabolic demands of the tissues (energy) Hypoperfusion – inability of circulation to deliver blood to tissues, results in hypoxia Hypotension – not enough pressure to deliver blood to core organs Compensated shock – inability to meet needs of peripheral tissues Decompensated shock – inability to meet metabolic demands of core organs Cardiopulmonary failure – moribund state resulting in from total respiratory and/or circulatory collapse Preload – tension in ventricle wall at end diastole – corresponds with RAP/LAP (potential amount of force that can be generated by the ventricle based upon the amount of stretching by the muscle fibers – determined by end diastolic volume Afterload- tension in ventricular wall at end systole (covaries with PVR peripheral vascular resistance) (pressure head against which the heart has to squeeze) Contractility – force developed by the ventricular wall during systole Pediatric Hemodynamic changes Blood Loss Heart rate immediately increases and only drops at around 45% loss BP maintains until about 30% loss and then drops severely (soft arteries can constrict much better than adults) CO starts dropping immediately and also drops severely of at 30% loss Shock – A Hydraulic Solution Pump Failure (cardiogenic) Electrical dysrhythmias (defib cardiovert) Mechanical – cardiomyopathy (inotrope, vasopressor) Pipe Failure Distributive –(anaphylaxis, neurogenic – decreased vascular tone) (volume resuscitation MAST, Epi, contain the spread) Obstructive (Pneumothorax, Tamponade) (decompress tension pneumo) Prime Failure Hypovolmic dehydration, hemorrhage, GI Dissociative –CO poisoning (o2 specific antidote) Kids have proportionally larger blood volume but absolute volume is smaller Softer more compliant vessels – capable of intense vasoconstriction Smaller heart ventricles less compliant – less stretch per Starling’s Law – cannot really increase contractility – more dependent on rate to increase CO Pulse higher than 150 – (5x age in years) is tachycardia, BP <70 +2 x age is lowest BP Hypovolemic shock most common is peds, then septic, then cardiogenic Hypovolemic – mostly dehydration, then hemorrhagic, GI Septic –more common endotoxin vs extotoxin – (results in inability for cells to extract o2) Cardiogenic – usually electrical (SVT VFIB) Kids don’t usually get clammy unless cardiogenic, mottled in Hypovolemic Simultaneous palpation of proximal and distal pulses (eg. femoral vs Pedal) big diff indicates compensated shock Fluid Doses 20ml/kg of NS or LR – does it help? See study…Bottom line – maybe not be effective in short transport times. Focus on maintaining airway. 2 attempts or 90 sec, AC or saphenous at ankle. Then try IO. IO must be injected under pressure, gravity drip will not work Pediatric Trauma Immature anatomy Different mechanisms Long term sequela Age specific equipment Larger heads, softer skulls – will fall head first, will decompensate quickly due to head trauma, soft tissue obstruction due to decrease tone leading to hypoxemia, ICP, cerebral edema, Proportionally smaller torso yet larger organs Impact – smaller total body mass More often hit by cars than unrestrained passengers (abdomen and L spine from improper seat belt position) Waddell’s Triad 1. Femur fracture2. Intra-abdominal or intrathoracic injury3. Head injury Falls from height Fall from bike – head – unhelmeted bike riders 2nd leading cause of head injury death in US kids (#1 MVA) Normoventilate(30) for resp failure, decomp shock, traumatic coma Hyperventilate (35)– single dilated pupil, fixed dilated, apneic spells SCIWORA Syndrome: (Spinal Cord Injury w/o Radiologic Abnormality) Head Trauma – …. Neck Trauma …… Chest Trauma – soft bone structure – Abdominal Trauma – upper organs are lower, lower organs are higher (liver not well protected), thinner walled, abdominal viscera less protected MSK Trauma, lose less blood, growth plate involvement, incomplete fractures, vascular injury common ABCDEF – Airway Breathing Circulation Disability (pupils and GCS), E exposure, (but keep warm) F (focused physical on stable patient) El Physiocontrol Lifepak 12, así como muchos otros tipos de equipos médicos usados se pueden comprar en línea por mucho más barato que comprar nuevos.
March 29, 2009, Dr Cooper
Pediatric Circulatory Emergencies
PAT
Is he in shock? Volume or Cardiogenic, assess vitals, mentation, etc, (BP last indicator)
Peds, who present with dysrhythmias, present like they are in shock. They won’t tell you that they have palpitations, etc, do not presume that if a child is in shock you always give fluid…must rule out cardiogenic causes.
Shock- failure of circulation to meet the metabolic demands of the tissues (energy)
Preload – tension in ventricle wall at end diastole – corresponds with RAP/LAP (potential amount of force that can be generated by the ventricle based upon the amount of stretching by the muscle fibers – determined by end diastolic volume
Afterload- tension in ventricular wall at end systole (covaries with PVR peripheral vascular resistance) (pressure head against which the heart has to squeeze)
Contractility – force developed by the ventricular wall during systole
Pediatric Hemodynamic changes
Shock – A Hydraulic Solution
Pump Failure (cardiogenic)
Pipe Failure
Prime Failure
Kids have proportionally larger blood volume but absolute volume is smaller
Softer more compliant vessels – capable of intense vasoconstriction
Smaller heart ventricles less compliant – less stretch per Starling’s Law – cannot really increase contractility – more dependent on rate to increase CO
Pulse higher than 150 – (5x age in years) is tachycardia, BP <70 +2 x age is lowest BP
Hypovolemic shock most common is peds, then septic, then cardiogenic
Hypovolemic – mostly dehydration, then hemorrhagic, GI
Septic –more common endotoxin vs extotoxin – (results in inability for cells to extract o2)
Cardiogenic – usually electrical (SVT VFIB)
Kids don’t usually get clammy unless cardiogenic, mottled in Hypovolemic
Simultaneous palpation of proximal and distal pulses (eg. femoral vs Pedal) big diff indicates compensated shock
Fluid Doses 20ml/kg of NS or LR – does it help? See study…Bottom line – maybe not be effective in short transport times. Focus on maintaining airway.
2 attempts or 90 sec, AC or saphenous at ankle. Then try IO. IO must be injected under pressure, gravity drip will not work
Pediatric Trauma
Normoventilate(30) for resp failure, decomp shock, traumatic coma
Hyperventilate (35)– single dilated pupil, fixed dilated, apneic spells
SCIWORA Syndrome: (Spinal Cord Injury w/o Radiologic Abnormality)
Head Trauma – ….
Neck Trauma ……
Chest Trauma – soft bone structure –
Abdominal Trauma – upper organs are lower, lower organs are higher (liver not well protected), thinner walled, abdominal viscera less protected
MSK Trauma, lose less blood, growth plate involvement, incomplete fractures, vascular injury common
ABCDEF – Airway Breathing Circulation Disability (pupils and GCS), E exposure, (but keep warm) F (focused physical on stable patient)
El Physiocontrol Lifepak 12, así como muchos otros tipos de equipos médicos usados se pueden comprar en línea por mucho más barato que comprar nuevos.
3/25/09 Dr Cooper Pediatric Airway Management Bag and drag, get control of lungs and heart will follow – get control of airway and move Start with PAT – Appearance – example, seesaw respirations – upper airway obstruction. Snoring; soft tissue, gurgling; secretions, stridor; croup FBAO, epiglottis. Hoarseness; laryngeal trauma Mandibular block, needs to be moved forward– use OPA or Jaw thrust Larynx, higher and more forward in the throat, airway is funnel shaped, particulate matter can get wedged below cords but above cricoid ring. Size of Infant airway= drinking straw. Adult=Garden hose Management Non- rebreather Pulse Oximeter of 90-95%, GCS 14, AVPU of V , compensated shcok – SBP 70-90 + 2x age BVM, Spo2 <90%, SBP <70 + 2x age (decompensated shock), Traumatic Coma, AVPU P or U, GCS 8 or less – disable pop-off valve, watch the chest just rise, Size the mask, completely cover nose and mouth, face mask cannot press against eye, causes profound vagal response in baby EC Clamp OPA – teeth to angle of mandible NPA – nares to tip of earlobe Positioning Medical – Sniffing plus Trauma – Neutral airway position Squeeze – relax, 20 times per minute Do not hyperextend neck in either case Infant – pad entire body (or use a backboard with a hole for head). Head is too high and padding aligns plane of face to be parallel with stretcher. Disproportion ends around 8 years of age. Older child may need a shoulder roll. Steeles rule of three, spinal cord is only one third of spinal canal. Hard to add further injury as long as you keep some degree of caution, a little movement won’t injure, May have to remove C collar in order to intubate Technique for high pressure ventilation- Sniff plus, jaw thrust up into mask, two thumbs on side of mask ETT – respiratory failure decompensated shock, traumatic coma Miller Blade to lift floppy epiglottis (less than 8 years) Uncuffed tube – allows for larger diameter tube, and cuff pressure may cause pressure on tracheal mucosa Pass tube just below where black mark disappears 4 Ps Prepare – suction o2 scope and tube Position patent and operator – eye level of airway – Preoxygenate Perform intubation _ don’t persist longer than you can hold your own breath Smaller mouth, developing dentition, etc avoid levering, suction avoid prying RSI where used – GCS 5-9 Confirm placement primarily and secondary (wave form capnography) Neonatal Intubation – very delicate maneuver DOPE for common ETT problems Displacement – re-auscultate Obstruction – suction Pneumothorax – absent sounds on one side Equipment failure – Don’t screw around, bad tube – remove Nasogastric Intubation Straight back into nares will follow curve of throat, measure from nares, around ears down to xyphoid process ETT vs BVM – No significant mortality differences, true for medical and trauma patients. BVM the single most important skill to master (TUBE TOOLS – CD Rom) The Physiocontrol Lifepak 12 as well as many other types of used medical equipment can be purchased online for much cheaper than buying new. ___________________ Respiratory Problems Respiratory distress – increased effort but enough to compensate for tissue hypoxia – due to mild hypoxemia (days) Respiratory failure increased or decreased effort not enough to compensate for tissue hypoxia – due to sever hypoxemia (hours) Respiratory arrest – if uncorrected leads to cardiopulmonary arrest (2 minutes) Upper airway obstruction – extrathoracic Lower airway disease – intrathoracic Grunting = PEEPing Peripheral mottling – circulatory problem; central mottling- respiratory problem Sniffing and tripod – severe distress, head bobbing or grunting – respiratory failure Oxyhemoglobin dissociation curve – kid won’t turn blue until o2 is dangerously low Pediatric Respiratory volumes -Kids have smaller oxygen cushion than adults, will deteriorate more quickly. Higher o2 requiements Upper Airway Obstructions Croup FBAO Bacterial Tracheitis Least common.epiglottitis rare due to vaccine Lower Airway Asthma –reactive airway disease Bronchiolitis – caused by RSV Pneumonia – lung tissue disease FB – small FB lodged in lower airway – generally caused resorbtion atelectasis Pediatric Airway Assessment – determine degree of problem – altered mental status very worrying sign, indicates respiratory failure – BVM – if the baby accepts the mask he needs the mask. Treatment – o2 always primary – everything else is adjunct
3/25/09 Dr Cooper
Pediatric Airway Management
Bag and drag, get control of lungs and heart will follow – get control of airway and move
Start with PAT – Appearance – example, seesaw respirations – upper airway obstruction. Snoring; soft tissue, gurgling; secretions, stridor; croup FBAO, epiglottis. Hoarseness; laryngeal trauma
Management
Technique for high pressure ventilation- Sniff plus, jaw thrust up into mask, two thumbs on side of mask
ETT – respiratory failure decompensated shock, traumatic coma
ETT vs BVM – No significant mortality differences, true for medical and trauma patients.
BVM the single most important skill to master
(TUBE TOOLS – CD Rom)
The Physiocontrol Lifepak 12 as well as many other types of used medical equipment can be purchased online for much cheaper than buying new.
___________________
Respiratory Problems
Grunting = PEEPing
Peripheral mottling – circulatory problem; central mottling- respiratory problem
Sniffing and tripod – severe distress, head bobbing or grunting – respiratory failure
Oxyhemoglobin dissociation curve – kid won’t turn blue until o2 is dangerously low
Pediatric Respiratory volumes -Kids have smaller oxygen cushion than adults, will deteriorate more quickly. Higher o2 requiements
Upper Airway Obstructions
Lower Airway
Pediatric Airway Assessment – determine degree of problem – altered mental status very worrying sign, indicates respiratory failure – BVM – if the baby accepts the mask he needs the mask.
Treatment – o2 always primary – everything else is adjunct
Pediatric Assessment, Dr Cooper 3/23/09 See www.cpem.org Planning: Triage & transport – Needs vs. resources – enroute, review and plan Arrival: General Impression: Pediatric Assessment Triangle (PAT) – Hands off assessment – ABC Appearance, Work of Breathing, Circulation to skin Initial Assessment: Rapid cardiopulmonary assessment – Hands on Focused History: pertinent negatives, relevant findings Pediatric Assessment Triangle Appearance Alertness Distractibility Consolibility Eye contact Quality of cry Spontaneous movement (All critical to whether brain is perfused properly) Work of Breathing Chest rise Rocking motions Retractions Nasal flailing Head bobbing Grunting Snoring Stridor (C)Circulation Pallor Mottled Blue Grey Initial Assessment: Rapid cardiopulmonary assessment – Hands on Airway –clear? Maintainable?, stable? Breathing – ventilation, oxygenating, stable? In peds rates and effort are not necessarily related like adults, effort much more important! Circulation: Shock? Cardiogenic?, stable? Shock: inability of blood to meet metabolic needs of the tissues- Mental status, pulse rate and character; distal vs. proximal, skin color, BP. Cardiogenic shock: Dysrhythmias, other , compensated, decompensated, cardiopulmonary failure (cardiogenic shock not initially treated with fluid) Focused History: pertinent negatives, relevant findings Why peds don’t have heart attacks: no CAD, atherosclerosis, etc –congenital heart diseases are rare. Adults drop dead, kids droop dead (secondary to respiratory arrest, etc) Anatomic & Physiologic differences Child airway – funnel shaped, narrowest part is at crichoid ring- adult s cylinder, narrowest at glottis Small jaw, large tongue, prone t soft tissue obstruction – reposition Immature immune system. lack of specific antibodies, protective mucus layer Infants are nasal breathers, keep clear Floppy omega shaped epiglottis Narrow subglottic area Remember if suspected C spine injury, stabilize c spine before/while maintaining airway Breathing anatomy Adult – diagonal ribs, stiff cartilage, stronger muscles Ped – horizontal ribs, soft cartilage, weaker muscles – diaphragmatic breathers, much less alveoli – faster o2 depletion. Susceptible to barotraumas, high risk of Pneumothorax, bag until chest rise, no more. (head bobbing grunting – near end resp failure)young tissue – high elastin content– shift mediastinum -easily Breathing assessment requires an open Airway! – ASSESS A, THEN FIX A! THEN GO ON TO B! Is ventilation adequate – inspect chest rise – capability Auscultation – air entry (Missed slide) Always consider hypoxia first as cause for AMS Auscultate in armpits, small chest, sounds travel ETT only of BVM ineffective Consider NG/OG if abdominal distention Circulation Adults, big hearts large chambers and thin walls, Starlings Law (like a spring, recoil helps CO) peds – small chambers thick walls – can’t vary CO well with heart walls, CO depends only on HR Adults – stiff vessels – vigorous response to hypovolemia and hypothermia Peds – soft vessels – more compliant vessels Smaller blood volume, lose lager percentage compared to adult Smaller fat mass – larger relative blood volume Bleeding control – direct pressure – retain systemic o2 Shock assessment – cause assessment – cardiogenic etc – Simultaneous palpation of central and peripheral pulses – strong central weak peripheral – compensated – everything weak; decompensated shock Tachycardia = 150 – 5x age in year Kids get mottled – not clammy Cap refill – use warm extremities Minimum systolic BP: 80 + 2x age Adrenaline makes you stupid – use a Broselow Tape
Pediatric Assessment, Dr Cooper
3/23/09
See www.cpem.org
Pediatric Assessment Triangle
(C)Circulation
Initial Assessment: Rapid cardiopulmonary assessment – Hands on
Focused History: pertinent negatives, relevant findings
Why peds don’t have heart attacks: no CAD, atherosclerosis, etc –congenital heart diseases are rare. Adults drop dead, kids droop dead (secondary to respiratory arrest, etc)
Anatomic & Physiologic differences
Child airway – funnel shaped, narrowest part is at crichoid ring- adult s cylinder, narrowest at glottis
Remember if suspected C spine injury, stabilize c spine before/while maintaining airway
Breathing anatomy
Breathing assessment requires an open Airway! – ASSESS A, THEN FIX A! THEN GO ON TO B!
Always consider hypoxia first as cause for AMS
Circulation
Bleeding control – direct pressure – retain systemic o2
Shock assessment – cause assessment – cardiogenic etc – Simultaneous palpation of central and peripheral pulses – strong central weak peripheral – compensated – everything weak; decompensated shock
Adrenaline makes you stupid – use a Broselow Tape
