Pediatric Shock
Apr 27th, 2009 by
RH-111
Print This Post
Chapter 358: Shock
Copied from the AAP Textbook of Pediatric Care
Chapter 358: Shock
Monika Gupta, MD; Joseph R. Custer, MD
CLASSIFICATION OF SHOCK
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]
HYPOVOLEMIC SHOCK
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 ).
BOX 358-2: Causes of Hypovolemic Shock
Gastrointestinal losses
Excess urine output, diuretic agent administration
Mannitol administration
Hypoalbuminemia
Burns
3rd space fluid losses (peritonitis, edema)
Traumatic blood loss
Table 358-3: Physical Signs in Dehydration
Percentage of Dehydration
Physical Signs
5% (mild)
Dry skin, mild tachycardia, concentrated urine
10% (moderate)
Lethargy, poor perfusion
15% (severe)
Obtundation, tachycardia, hypotension, very poor perfusion to skin
Table 358-4: Physical and Vital Signs in Hemorrhagic Shock
Blood Volume Lost (%)
Signs
<15%
Minimal tachycardia, normal respiratory rate, blood pressure, and capillary refill
15-30%
Tachycardia, tachypnea, decreased pulse pressure, normal systolic pressure, prolonged capillary refill, anxiety
30-40%
Hypotension, decreased urine output, mental status changes
>40%
Hypotension, loss of consciousness
CARDIOGENIC SHOCK
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.
BOX 358-3: Causes of Obstructive Cardiogenic Shock
Tamponade (air, blood, or effusion)
Coarctation of the aorta
Aortic valve stenosis or atresia
BOX 358-4: Pump Failure
Arrhythmia
Hypoplastic left heart syndrome
Decreased contractility acquired in sepsis syndrome or shock of any cause
Myocardiopathy
Myocarditis
Anomalous coronary artery
Cardiac contusion
Storage disease—glycogen storage disease
SEPTIC SHOCK
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.
DISTRIBUTIVE SHOCK
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.
Pediatrics 3
Mar 29th, 2009 by
RH-111
Print This Post
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
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.
Pediatrics 2
Mar 25th, 2009 by
RH-111
Print This Post
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
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
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
Pediatrics 1
Mar 23rd, 2009 by
RH-111
Print This Post
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
Work of Breathing
Chest rise
Rocking motions
Retractions
Nasal flailing
Head bobbing
Grunting
Snoring
Stridor
(C)Circulation
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
