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Shock and Hypotension in the Newborn Treatment & Management

  • Author: Samir Gupta, DM, MRCP, MD, FRCPCH, FRCPI; Chief Editor: Ted Rosenkrantz, MD  more...
 
Updated: Mar 27, 2014
 

Approach Considerations

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.

See the video of assisted ventilation in the newborn, below.

Assisted ventilation newborn –Intubation and meconium aspiration. Video courtesy of Therese Canares, MD, and Jonathan Valente, MD, Rhode Island Hospital, Brown University.

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.

Patent ductus arteriosus

The patent ductus arteriosus (PDA) is a significant cause of hypotension in preterm infants. Although the increase in left ventricular output (LVO) and other compensatory mechanisms may initially offset the effects of ductal shunt on systemic circulation, effective LVO is reduced over time. This can lead to organ hypoperfusion, and treatment of shock in such situations should be directed towards closing the PDA.

Surgical care

Structural heart disease and 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.

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.

Consultations

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

Transfer

Infants presenting with evidence of shock should be transferred immediately to a full-service neonatal intensive care unit with adequate support, personnel, and expertise.

Monitoring

Infants recovering from neonatal shock are at risk for multiple sequelae and should be intensively screened for neurodevelopmental abnormalities using brain imaging and brainstem audiometric evoked responses. Other tests are determined by the clinical course and complications.

Outpatient care should include neurodevelopmental follow-up testing and other studies, as indicated by the neonatal course.

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Hypovolemic Shock

Hypovolemic shock is caused by perinatal blood loss in newborn infants. 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.

If blood loss is confirmed, initial resuscitation with 20 mL/kg of volume expansion should replace a quarter of the blood volume. Blood transfusion is preferred, but in an emergency, colloids or crystalloids can be used. If circulatory insufficiency persists, this dose can be repeated.

Once 10 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. 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.[10]

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.

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Cardiogenic 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. 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.

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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 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.[6] 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.

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Organ Damage

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 blood urea nitrogen (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.

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.

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.

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Pharmacologic Therapy

The choice of drug for medical management of shock depends on the underlying cause. Table 1, below, lists agents commonly used in the treatment of neonatal shock.

Table 1. Agents Used To Treat Neonatal Shock (Open Table in a new window)

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; decrease dose with renal impairment

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.

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Contributor Information and Disclosures
Author

Samir Gupta, DM, MRCP, MD, FRCPCH, FRCPI Professor of Neonatal Medicine, Deputy Director, Research and Development, University of Durham and North Tees University Hospital, UK

Samir Gupta, DM, MRCP, MD, FRCPCH, FRCPI is a member of the following medical societies: British Medical Association, Society for Pediatric Research, European Society for Paediatric Research, Royal College of Paediatrics and Child Health, European Respiratory Society, Royal College of Physicians of Ireland

Disclosure: Nothing to disclose.

Coauthor(s)

Sunil K Sinha, MBBS, MD, MRCP, PhD, FRCP, FRCPCH Director of Neonatal Services, South Cleveland Hospital, UK

Sunil K Sinha, MBBS, MD, MRCP, PhD, FRCP, FRCPCH is a member of the following medical societies: British Medical Association, Royal College of Physicians

Disclosure: Nothing to disclose.

Chief Editor

Ted Rosenkrantz, MD Professor, Departments of Pediatrics and Obstetrics/Gynecology, Division of Neonatal-Perinatal Medicine, University of Connecticut School of Medicine

Ted Rosenkrantz, MD is a member of the following medical societies: American Academy of Pediatrics, American Pediatric Society, Eastern Society for Pediatric Research, American Medical Association, Connecticut State Medical Society, Society for Pediatric Research

Disclosure: Nothing to disclose.

Acknowledgements

David A Clark, MD Chairman, Professor, Department of Pediatrics, Albany Medical College

David A Clark, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, American Pediatric Society, Christian Medical & Dental Society, Medical Society of the State of New York, New York Academy of Sciences, and Society for Pediatric Research

Disclosure: Nothing to disclose.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Pharmacy Editor, eMedicine

Disclosure: Nothing to disclose.

References
  1. Schmaltz C. Hypotension and shock in the preterm neonate. Adv Neonatal Care. 2009 Aug. 9(4):156-62. [Medline].

  2. Al-Aweel I, Pursley DM, Rubin LP, et al. Variations in prevalence of hypotension, hypertension, and vasopressor use in NICUs. J Perinatol. 2001 Jul-Aug. 21(5):272-8. [Medline].

  3. Northern Neonatal Nursing Initiative. Systolic blood pressure in babies of less than 32 weeks gestation in the first year of life. Arch Dis Child Fetal Neonatal Ed. 1999 Jan. 80(1):F38-42. [Medline].

  4. Gupta S, Wyllie J. Correlation of Non-invasive Systolic and Mean Blood pressure (BP) Measurements with Echocardiographic Haemodynamic Assessment. Third Congress of the European Academy of Paediatric Societies (EAPS). Copenhagen, Denmark. October 23-26, 2010.

  5. Laughon M, Bose C, Allred E, et al. Factors associated with treatment for hypotension in extremely low gestational age newborns during the first postnatal week. Pediatrics. 2007 Feb. 119(2):273-80. [Medline].

  6. [Guideline] Dellinger RP, Levy MM, Carlet JM, et al. Surviving Sepsis Campaign: international guidelines for management of severe sepsis and septic shock: 2008. Intensive Care Med. 2008 Jan. 34(1):17-60. [Medline].

  7. Wahab Mohamed WA, Saeed MA. Mannose-binding lectin serum levels in neonatal sepsis and septic shock. J Matern Fetal Neonatal Med. 2011 Jun 1. [Medline].

  8. Kluckow M, Evans N. Superior vena cava flow in newborn infants: a novel marker of systemic blood flow. Arch Dis Child Fetal Neonatal Ed. 2000 May. 82(3):F182-7. [Medline].

  9. Osborn DA, Evans N, Kluckow M, et al. Low superior vena cava flow and effect of inotropes on neurodevelopment to 3 years in preterm infants. Pediatrics. 2007 Aug. 120(2):372-80. [Medline].

  10. Skinner JR, Milligan DW, Hunter S, et al. Central venous pressure in the ventilated neonate. Arch Dis Child. 1992 Apr. 67(4 Spec No):374-7. [Medline].

 
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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.
Assisted ventilation newborn –Intubation and meconium aspiration. Video courtesy of Therese Canares, MD, and Jonathan Valente, MD, Rhode Island Hospital, Brown University.
Table 1. Agents Used To Treat Neonatal Shock
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; decrease dose with renal impairment
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