eMedicine Specialties > Pediatrics: Cardiac Disease and Critical Care Medicine > Neonatology

Shock and Hypotension in the Newborn: Treatment & Medication

Author: Samir Gupta, MD, MRCP, FRCPCH, Consulting Neonatologist, University Hospital of North Tees
Coauthor(s): Sunil K Sinha, MBBS, MD, MRCP, PhD, FRCP, FRCPCH, Director of Neonatal Services, South Cleveland Hospital, UK; Steven M Donn, MD, Professor of Pediatrics, Director, Neonatal-Perinatal Medicine, Department of Pediatrics, University of Michigan Health System
Contributor Information and Disclosures

Updated: Jun 25, 2008

Treatment

Medical Care

Once shock is suspected in a newborn, appropriate supportive measures must be instituted as soon as possible. These include securing the airway and assuring its patency, providing supplemental oxygen and positive-pressure ventilation, achieving intravascular or intraosseous access, and infusing 10 mL/kg of colloid or crystalloid (to repeat the same volume if needed). Use of crystalloid or colloid solutions is appropriate, unless the source of hypovolemia is hemorrhage, in which case whole or reconstituted blood is more appropriate.

Obtain hematocrit level, electrolyte levels, blood gases and pH level, blood culture, and glucose level as soon as vascular access is obtained. At this stage, attempt to determine the type of shock (eg, hypovolemic, cardiogenic, maldistributive) because each requires a different therapeutic approach. In neonates who are hypotensively compromised, the authors encourage the early use of a bladder catheter. Hourly urine output is one of the few objective methods of evaluating hypoperfusion that leads to specific organ failure, and its accurate objective measurement can augment clinical decision making.

Hypovolemic shock is the most common cause of shock in infancy. The key to successful resuscitation is early recognition and controlled volume expansion with the appropriate fluid. The estimated blood volume of a newborn is 80-85 mL/kg of body weight. 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. Initial resuscitation with 20 mL/kg of volume expansion should replace a quarter of the blood volume. If circulatory insufficiency persists, this dose should be repeated. The Table below lists agents commonly used in the treatment of neonatal shock.

Dopamine has been found to be more effective than dobutamine and albumin in correcting blood pressure for short-term treatment, but the effect of these drugs on long-term outcome is unknown. Although adrenaline is used for cardiovascular compromise, its effect on mortality and morbidity is not yet evaluated.

Once 20 mL/kg of blood volume is replaced, a decision to provide any further volume expansion should prompt the clinician to ascertain the cause of hypotension and to evaluate circulatory status (see Imaging Studies). The information regarding central venous pressure (CVP) values in stable ventilated newborns is limited; therefore, interpretation of readings in ill neonates is problematic. Its role in the management of systemic hypotension is uncertain, but serial measurements through an appropriately placed umbilical venous or other central venous catheter may help to guide volume expansion in suspected hypovolemia.⁵

In the absence of CVP, titration against clinical parameters should be completed. Use of crystalloid or colloid solutions is appropriate unless the source of hypovolemia has been hemorrhage, in which case whole or reconstituted blood is more appropriate. If blood is needed in an emergency, type-specific or type O (Rh-negative) blood can be administered. Frequent and careful monitoring of the infant's vital signs with frequently repeated assessment and reexamination is mandatory.

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. Inotropic agents, with or without peripheral vasodilators, are warranted in most circumstances. Structural heart disease or arrhythmia often requires specific pharmacologic or surgical therapy. Excessive volume expansion may be potentially harmful.

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 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. Survival from septic shock depends on maintenance of a hyperdynamic circulatory state. In the early phase, volume expansion with agents that are likely to remain within the intravascular space is needed, whereas inotropic agents with or without peripheral vasodilators may be indicated later. In early onset neonatal sepsis, ampicillin and gentamicin are the empiric antimicrobials of choice until a specific infectious agent is identified. Cefotaxime is sometimes substituted for gentamicin, although studies have raised concerns about this practice. In the face of renal failure, serum levels of gentamicin should be closely monitored to minimize iatrogenic renal toxicity.

During and following restoration of circulation, varying degrees of organ damage may remain and should be actively sought and managed. For example, acute tubular necrosis may be a sequela of uncompensated shock. Once hemodynamic parameters have improved, consider fluid administration according to urine output and renal function as assessed by serum creatinine, electrolyte, and BUN levels.

Despite adequate volume restoration, myocardial contractility may still be compromised due to the prior poor myocardial perfusion. In this scenario, inotropic agents and intensive monitoring may need to be continued. During the process of shock, production of chemical mediators may initiate disseminated intravascular coagulopathy (DIC), which requires careful monitoring of coagulation profiles and management with fresh frozen plasma, platelets, and/or cryoprecipitate. The liver and bowel may be damaged by shock, leading to GI bleeding and increasing the risk for necrotizing enterocolitis, particularly in the premature infant. However, the extent of irreversible brain damage is probably most anxiously monitored following shock because the brain is so sensitive to hypoxic-ischemic injury once compensation fails.

In circumstances in which volume expansion and vasoactive and inotropic agents have been unsuccessful, glucocorticoids (eg, dexamethasone, hydrocortisone) have been shown to be effective. The findings that steroids rapidly up-regulate cardiovascular adrenergic receptor expression and serve as hormone replacement therapy in cases of adrenal insufficiency explain their effectiveness in stabilizing the cardiovascular status and decreasing the requirement for pressure support in the critically ill newborn with volume-resistant and pressure-resistant hypotension.

The use of milrinone in premature infants is still not established and is limited to babies with low output cardiac failure (eg, postoperative states) or in refractory hypotension (with other inotropic drugs). Its use for prevention of low SVC flow in very preterm infants was not substantiated in a randomized controlled trial.

Agents Used to Treat Neonatal Shock

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Surgical Care

Structural heart disease or arrhythmias often require specific pharmacologic or surgical therapy. The liver and bowel may be damaged by shock, leading to GI bleeding and increasing the risk for necrotizing enterocolitis, particularly in the premature infant.

Consultations

Depending on the type of shock, potential consultants include the following pediatric subspecialists: neonatologist, cardiologist, nephrologist, surgeon, infectious disease specialist, and hematologist.

Diet

Infants in shock should not be fed, and feedings should not be resumed until GI function has recovered. Initiate total parenteral nutrition as soon as possible.

Medication

Adrenergic agonists

Cardiovascular performance deteriorates and cardiac output falls if effective therapy is not administered. These agents improve the hemodynamic status by increasing myocardial contractility and heart rate, resulting in increased cardiac output. They also increase peripheral resistance by causing vasoconstriction. Increased cardiac output and increased peripheral resistance lead to increased blood pressure.

Dopamine (Intropin)

Stimulates both adrenergic and dopaminergic receptors. Hemodynamic effect is dependent on the dose. Lower doses predominantly stimulate dopaminergic receptors that, in turn, produce renal and mesenteric vasodilation. Cardiac stimulation and peripheral vasoconstriction is produced by higher doses.

Dobutamine (Dobutrex)

Produces vasodilation and increases inotropic state. At higher dosages, may cause increased heart rate, exacerbating myocardial ischemia.

Epinephrine (Adrenaline)

Elicits alpha-agonist effects that include increased peripheral vascular resistance, reversed peripheral vasodilatation, systemic hypotension, and vascular permeability. Beta-agonist effects include bronchodilatation, chronotropic cardiac activity, and positive inotropic effects.

Hydralazine (Apresoline)

Decreases systemic resistance through direct vasodilation of arterioles.

Isoproterenol (Isuprel)

Possesses beta1- and beta2-adrenergic receptor activity. Binds beta-receptors of heart, smooth muscle of bronchi, skeletal muscle, vasculature, and alimentary tract. Elicits positive inotropic and chronotropic actions.

Nitroprusside (Nitropress)

Produces vasodilation and increases inotropic activity of the heart. At higher dosages, may exacerbate myocardial ischemia by increasing heart rate.

Norepinephrine (Levophed)

For protracted hypotension following adequate fluid-volume replacement. Stimulates beta1- and alpha-adrenergic receptors, increasing cardiac muscle contractility and heart rate as well as vasoconstriction, resulting in systemic blood pressure and coronary blood flow increases. After obtaining a response, the rate of flow should be adjusted and maintained at a low-normal blood pressure, such as 80-100 mm Hg systolic, sufficient to perfuse vital organs.

Phentolamine (Regitine)

Alpha1- and alpha2-adrenergic blocking agent that blocks circulating epinephrine and norepinephrine action, reducing hypertension resulting from catecholamine effects on alpha-receptors.

Milrinone (Primacor)

Bi-pyridine positive inotrope and vasodilator with little chronotropic activity. Different in mode of action from both digitalis glycosides and catecholamines. Selectively inhibits phosphodiesterase type III (PDE III) in cardiac and smooth vascular muscle, resulting in reduced afterload, reduced preload, and increased inotropy.

Volume expanders

The use of crystalloid or colloid solutions is appropriate, unless the source of hypovolemia is hemorrhage, in which case whole or reconstituted blood is more appropriate.

Sodium chloride 0.9%

Isotonic sodium chloride solution is a low-cost alternative that is readily available.

Albumin 5% (Albumisol, Buminate)

Useful for plasma volume expansion and maintenance of cardiac output.

Lactated ringer solution with isotonic sodium chloride

Each fluid is essentially isotonic and have equivalent volume restorative properties. Although some differences between metabolic changes are observed with administration of large quantities of either fluid, for practical purposes and in most situations, differences are clinically irrelevant. Importantly, no demonstrable difference in hemodynamic effect, morbidity, or mortality with resuscitation.

Antimicrobials

In early onset neonatal sepsis, ampicillin and either gentamicin or cefotaxime are the antimicrobials of choice until a specific infectious agent is identified.

Ampicillin (Principen, Omnipen)

Bactericidal activity against susceptible organisms.

Cefotaxime (Claforan)

Third-generation cephalosporin that possesses antimicrobial effect on a predominantly gram-negative spectrum. Has a lower efficacy against gram-positive organisms.

Gentamicin (Garamycin)

Aminoglycoside antibiotic for gram-negative coverage. Used in combination with both an agent against gram-positive organisms and one that covers anaerobes.
Dosing regimens are numerous; adjust dose based on CrCl and changes in volume of distribution. May be administered IV/IM.
Follow each regimen by at least a trough level drawn on the third dose (0.5 h before dosing). Peak levels may be drawn 0.5 h after 30-min infusion. If trough level >2 mg/L, increase dosing interval.

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