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Shock and Hypotension in the Newborn Clinical Presentation

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

Physical Examination

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

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

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.

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 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.

Compensated shock

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.

Uncompensated shock

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.

Irreversible shock

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.

 
 
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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