Shock and Hypotension in the Newborn Clinical Presentation
- Author: Samir Gupta, DM, MRCP, MD, FRCPCH, FRCPI; Chief Editor: Ted Rosenkrantz, MD more...
Clinical manifestations of hypotension include prolonged capillary refill time, tachycardia, mottling of the skin, cool extremities, and decreased urine output. Carefully observe heart sounds, peripheral pulses, and breath sounds.
The physical examination should accurately assess blood pressure, the existence of any heart murmurs, and the presence of 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 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 as measured by Doppler and this pressure as assessed by direct manometry using an intra-arterial catheter.
Hypovolemic shock is caused by perinatal blood loss in newborn infants. 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 usually occurs following severe intrapartum asphyxia, structural heart disease, or arrhythmias. 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.
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 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. In septic shock, cardiac function may be depressed (the left ventricle [LV] is usually affected more than the right).
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. 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 but can generally be divided into 3 phases: compensated, uncompensated, and irreversible. Each phase has characteristic clinicopathologic manifestations and outcomes; however, in the neonatal setting, distinguishing them may be impossible. Initiate aggressive treatment in all cases in which shock is suspected.
In compensated shock, derangement of vital signs, such as heart rate, respiratory rate, blood pressure, and temperature, is absent or minimal. Clinical signs at this time include pallor, tachycardia, cool peripheral skin, and prolonged capillary refill time. As these homeostatic mechanisms are exhausted or become inadequate to meet the metabolic demands of the tissues, the uncompensated stage ensues.
Clinically, patients with uncompensated shock present with falling blood pressure, very prolonged capillary refill time, tachycardia, cold skin, rapid breathing (to compensate for metabolic acidosis), and reduced or absent urine output. If effective intervention is not promptly instituted, progression to irreversible shock follows.
A diagnosis of irreversible shock is actually retrospective. Major vital organs, such as the heart and brain, are so extensively damaged that death occurs despite adequate restoration of the circulation. Early recognition and effective treatment of shock are crucial to prevent inevitable progression to this stage.
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|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
|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; decrease dose with renal impairment|