History and Physical Examination
History
Newborns may present with signs of infections such as lethargy, poor feeding, and—rarely—with fever. A gistory of acute blood loss or fluid loss may be present in hypovolemic shock.
Physical examination
Clinical manifestations of hypotension include prolonged capillary refill time, tachycardia, mottling of skin, cool extremities, and decreased urine output. Carefully observe heart sounds, peripheral pulses, and breath sounds. If hypotension is left untreated, neurologic signs with altered sensorium and signs of other organ damage may ensue.
The physical examination should accurately assess blood pressure, existence of any heart murmurs, and presence of the femoral pulses. Measurement of neonatal blood pressure can be completed directly through invasive techniques or indirectly through noninvasive techniques. Invasive methods include direct manometry using an arterial catheter or the use of an in-line pressure transducer and continuous monitor. Noninvasive methods include manual oscillometric techniques and automated Doppler techniques.
A good correlation is observed between the systolic blood pressure measured by Doppler, and pressure as assessed by direct manometry using an intra-arterial catheter.
Hypovolemic shock
Clinical signs of hypovolemic shock depend on the degree of intravascular volume depletion, which is estimated to be 25% in compensated shock, 25-40% in uncompensated shock, and more than 40% in irreversible shock.
Cardiogenic shock
Global myocardial ischemia reduces contractility and causes papillary muscle dysfunction with secondary tricuspid valvular insufficiency. Clinical findings suggestive of cardiogenic shock include peripheral edema, hepatomegaly, cardiomegaly, and a heart murmur suggestive of tricuspid regurgitation.
Septic shock
The most common form of maldistributive shock in the newborn is septic shock; this is a source of considerable mortality and morbidity. In sepsis, cardiac output may be normal or even elevated, but it may still be too small to deliver sufficient oxygen to the tissues because of the abnormal distribution of blood in the microcirculation, leading to decreased tissue perfusion. [9] In septic shock, cardiac function may be depressed (the left ventricle is usually affected more than the right ventricle).
The early, compensated phase of septic shock is characterized by an increased cardiac output, decreased systemic vascular resistance, warm extremities, and a widened pulse pressure. If effective therapy is not provided, cardiovascular performance deteriorates and cardiac output falls, and peripheral vasoconstriction leads to cold shock. Even with normal or increased cardiac output, shock develops. The normal relationship between cardiac output and systemic vascular resistance breaks down, and hypotension may persist as a result of decreased vascular resistance.
Newborns, who have little cardiac reserve, often present with hypotension and a picture of cardiovascular collapse. These critically ill infants represent a diagnostic and therapeutic challenge, and sepsis must be presumed and treated as quickly as possible.
As previously stated, shock is a progressive disorder and can generally be divided into three phases: compensated, uncompensated, and irreversible. Each phase has characteristic clinicopathologic manifestations and outcomes; however, in the neonatal setting, distinguishing them may be impossible. It is therefore important to initiate aggressive treatment in all cases where shock is suspected.
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Shock and Hypotension in the Newborn. Determinants of cardiac function and oxygen delivery to tissues. Adapted from Strange GR. APLS: The Pediatric Emergency Medicine Course. 3rd ed. Elk Grove Village, Ill: American Academy of Pediatrics; 1998:34.
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Shock and Hypotension in the Newborn. Assisted ventilation newborn – intubation and meconium aspiration. Video courtesy of Therese Canares, MD, and Jonathan Valente, MD, Rhode Island Hospital, Brown University.
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Shock and Hypotension in the Newborn. Presumed effects of commonly used cardiovascular drugs in neonatal intensive care. X-axis (effect on vascular tone): The more to the right, the more vasodilatory effects; the more to the left, the more vasoconstrictory effects. Y-axis (inotropic properties): The higher on the Y-axis, the more inotropic characteristics. The larger the size of the (semi-)circle, the more chronotropic effects. It should be noted that the effect on vascular tone depends on the used dosage that determines which adrenergic receptors are activated (e.g., dopamine and epinephrine). Courtesy of Springer Nature [de Boode WP et al. The role of neonatologist performed echocardiography in the assessment and management of neonatal shock. Pediatr Res. 2018 Jul;84(suppl 1):57-67. Online at: https://www.nature.com/articles/s41390-018-0081-1. PMID: 30072807.].
Tables
Agent Type |
Agent |
Initial Dosage |
Additional Factors |
Volume expanders |
Isotonic sodium chloride solution |
10-20 mL/kg intravenous (IV) |
Inexpensive, available |
Albumin (5%) |
10-20 mL/kg IV |
Expensive |
|
Plasma |
10-20 mL/kg IV |
Expensive |
|
Lactated Ringer solution |
10-20 mL/kg IV |
Inexpensive, available |
|
Isotonic glucose |
10-20 mL/kg IV |
Inexpensive, available |
|
Whole blood products |
10-20 mL/kg IV |
Limited availability |
|
Reconstituted blood products |
10-20 mL/kg IV |
Use type O negative |
|
Vasoactive drugs |
Dopamine |
5-20 mcg/kg/min IV |
Never administer intra-arterially |
Dobutamine |
5-20 mcg/kg/min IV |
Never administer intra-arterially |
|
Epinephrine |
0.05-1 mcg/kg/min IV |
Never administer intra-arterially |
|
Hydralazine |
0.1-0.5 mg/kg IV every 3-6 h |
Afterload reducer |
|
Isoproterenol |
0.05-0.5 mcg/kg/min IV |
Never administer intra-arterially |
|
Nitroprusside |
0.5-8 mcg/kg/min IV |
Afterload reducer |
|
Norepinephrine |
0.05-1 mcg/kg/min IV |
Never administer intra-arterially |
|
Phentolamine |
1-20 mcg/kg/min IV |
Afterload reducer |
|
Milrinone |
22.5-45 mcg/kg/h continuous IV infusion (ie, 0.375-0.75 mcg/kg/min) |
Afterload reducer in cardiac dysfunction; reduce the dose in the setting of renal impairment |
