Journal Logo

Feature

Recognition, management, and prevention of burn sepsis in pediatric patients

Comeau, Nicholas P. BSN, RN, CCRN, CPN

Author Information
doi: 10.1097/01.CCN.0000503415.36982.5f
  • Free

FU1-6
Figure

Despite the rapid development and advances in pediatric burn care and management, sepsis is still one of the leading causes of postinjury morbidity and mortality. Increased risk of infection stems from wounds, postinjury immunosuppression, and invasive equipment and therapies. Utilization of antimicrobial wound-care modalities and implementation of early excision and wound closure can reduce mortality.

This article discusses the signs and symptoms of burn sepsis in pediatric patients, the diagnostic workup, therapeutic interventions, ongoing evaluations of those interventions, and prevention of this potentially fatal infection.

Risk factors

Burn sepsis in pediatric patients can stem from a multitude of different risk factors. The most common is burn wound infection, which is broken down into five separate categories (see Burn wound infection definitions).1,2

Iatrogenic device infections, such as central venous catheter infections, are another source of burn sepsis. According to the CDC, 80,000 catheter-related bloodstream infections occur in ICUs each year. As many as 250,000 cases of bloodstream infections related to catheters occur annually.3 A central venous catheter may be the source of an infection if one is in place at any time in the 48 hours before infection.2

Ventilator-associated pneumonia (VAP) rates remain low since the utilization of surveillance and prevention strategies.4 According to Klompas and colleagues, clinical surveys suggest 5% to 15% of all ventilated patients still develop facility-acquired VAP.4 Infection from indwelling urinary catheters happens at an average rate of 3.1 to 7.5 infections per 1,000 patient days. The highest rates of infection occur in burn ICUs.5 Based on all this evidence, it is clear that invasive devices considerably contribute to the likelihood that a pediatric burn patient will develop sepsis secondary to iatrogenic device infections.

Further, pediatric burn patients run an increased risk of respiratory tract infections, which can contribute to the development of sepsis. Two main types of respiratory and pulmonary infections are exhibited in the pediatric burn population: tracheobronchitis and pneumonia. Seriously burned pediatric patients have the most profound response to injury and are at high risk for pulmonary sequelae. The American Burn Association defines serious burns as those that cover greater than 20% of a patient's total body surface area.2

Clinical criteria for pneumonia include leukocytosis or leukopenia, purulent secretions, development of a worsening cough, changes in respiratory effort (tachypnea, dyspnea), adventitious breath sounds, and worsening gas exchange. Clinical findings can be confirmed with microbiologic and radiologic findings.6

TU1
Table:
Burn wound infection definitions2

In critically ill pediatric burn patients, gastrointestinal permeability greatly increases because of poor splanchnic perfusion, in relation to burn size, and with the presence of infection. Typically, gastrointestinal bacterial translocation ensues. Permeability of the gut also increases with inadequate fluid resuscitation; splanchnic ischemia begins to form. This sets the stage for sepsis and a hypermetabolic inflammatory state.

In such cases, the patient presents with organ ischemia and peritonitis.1 Gut microflora is disrupted by the proliferation of bacteria. Tran postulates that this proliferation is caused by peristaltic stasis, starvation, and exposure to antibiotics.7 Nurses should know that burn patients do experience a suppressed immune response because of decreases in both the splenic and peripheral T-cell reproduction and dysfunction of the macrophages. This compromises the natural ability of the gut barrier system, facilitating the passage of endotoxins and other organisms across the intestinal wall. This results in systemic inflammation, organ injury, and sepsis.7

Signs and symptoms

The definitions and guidelines for systemic inflammatory response syndrome (SIRS) and the recognition and diagnosis of sepsis are well defined for the majority of disciplines.8 Burn patients are an exception. Recognition and diagnosis of sepsis in a burn patient is complicated by the body's constant state of inflammation and hypermetabolism. It is not uncommon to see tachycardia, tachypnea, leukocytosis, and pyrexia in burn patients months after initial injury without the presence of any infection.

The standard SIRS criteria is broad, making it more difficult to identify a burn patient with sepsis.7 The SIRS criteria was initially developed for adults, and therefore applicability to pediatrics is limited.2 Goldstein and colleagues devised the consensus pediatric SIRS criteria in the International Pediatric Sepsis Consensus Conference: Definition for Sepsis and Organ Dysfunction in Pediatrics.9 When comparing the utilization of the SIRS criteria in the adult population and pediatric population, the pediatric SIRS criteria requires that either temperature or leukocyte abnormality be present.9

In 2007, the American Burn Association set out the latest clinical and diagnostic guidelines to improve the recognition of sepsis in burn patients (see American Burn Association pediatric sepsis criteria).2 Nurses caring for this patient population should suspect sepsis if a patient meets three or more of the criteria, and recognize that further workup and interventions are warranted to accurately diagnose and treat impending infection.7 Ultimately, the patient's primary care provider will decide whether or not to pursue septic workup and stabilization.

Diagnostic workup

Following the recommendations of the American Heart Association and the Surviving Sepsis Campaign, diagnostic workup, rapid intervention, and stabilization should occur simultaneously.10-13 The following diagnostic tests should be performed as soon as possible:

  • complete blood cell count with differential
  • basic metabolic panel
  • procalcitonin14
  • lactate/lactic acid
  • venous or arterial blood gas
  • chest radiograph.

In addition to these lab and radiologic studies, nurses should obtain cultures from peripheral I.V. sites and central venous access and other invasive equipment such as endotracheal tubes. Obtain these cultures prior to the start of any antibiotic therapy. Although most of the pediatric burn infections and sepsis are bacterial, viral and fungal infections can also occur in severely immunocompromised patients.15

The nurse plays a pivotal role in the diagnostic process by obtaining and maintaining all necessary peripheral I.V. access as well as all lab specimens. The placement of central venous catheters and other invasive lines should be the decision of the patient's healthcare provider.

TU2
Table:
American Burn Association pediatric sepsis criteria2

Treatment

Once a patient is diagnosed with sepsis, the nurse should initiate the appropriate basic life support measures. Ensure that the patient has a patent and maintainable airway to support ventilation and oxygenation. Treat initial respiratory distress and hypoxemia with high-flow nasal cannula or nasal continuous positive airway pressure.10 If the degree of hypoxemia is so severe that intubation and mechanical ventilation is warranted, anticipate the need for additional cardiac resuscitation. The patient's diminished functional residual capacity and increased intrathoracic pressure reduce systemic venous return. The resuscitation providers can combat this by ensuring the patient has received adequate volume resuscitation.10

Establish appropriate venous access. If peripheral I.V. access is not easily obtainable, shift the focus to I.O. access. Do not delay I.V. or I.O. access for central line placement. Rapid fluid resuscitation should begin as soon as possible for patients in hypotensive shock states—within the first hour, if possible.10

Consider additional interventions within the first hour of treatment, including the correction of hypocalcemia and hyperglycemia.10,12 Baseline lab values should be collected simultaneously with the initiation of resuscitation and ultimately guide glycemic management and calcium correction.

Administer broad-spectrum antibiotics immediately following the collection of blood cultures. The goal is culture to broad-spectrum loading infusion within 60 minutes. The transition from broad-spectrum to narrow-spectrum antibiotics should occur as soon as culture results identify the specific infectious agent.12

Following initial weight-based fluid resuscitation, if therapeutic response has not been achieved, consider initiating vasoactive therapy. If additional fluid boluses are administered, assess the patient for the development of crackles, respiratory distress, or hepatomegaly.12 Should these develop, initiate inotropic support rather than continue the fluid resuscitation. Do not delay inotropic support in the absence of central venous access. Nurses should anticipate and plan to administer peripheral inotropic support until central access is obtained.10 If the patient is fluid responsive, healthcare providers should see a normalization of perfusion and hemodynamics. (See Therapeutic endpoints for initial resuscitation in pediatric septic shock.)

The specific vasoactive agent utilized is dependent on the specific shock state that the patient presents with:12

  • normotensive
  • vasodilated hypotensive
  • vasoconstricted hypotensive.

Patients suffering from burn sepsis typically demonstrate a vasodilated hypotensive shock state, or with central venous oxygen saturation (SvcO2) greater than 70% and persistent hypotension despite fluid resuscitation. Continue fluid resuscitation (20 mL/kg isotonic crystalloid boluses) and assess the patient for crackles, respiratory distress, or hepatomegaly; if these findings are present, stop the fluid resuscitation.12,16

TU3
Table:
Therapeutic endpoints for initial resuscitation in pediatric septic shock10

The vasoactive agent indicated for this state is norepinephrine. Norepinephrine increases the mean arterial pressure with little change in heart rate, which causes a decrease in stroke volume.17 Vasopressin can also help combat hypotension, and works to antagonize the mechanisms of vasodilation and works synergistically with catecholamines to stabilize BP.16 Monitor urinary and cardiac output closely for ischemia in the coronary, mesenteric, and/or cutaneous systems.17

Pediatric burn patients may also exhibit a vasoconstricted (cold) hypotensive shock state. In this shock state, the patient's ScvO2 is less than 70% with hypotension, and he or she has poor perfusion despite fluid resuscitation. In this shock state, it is important to correct anemia. Consider transfusion of packed red blood cells for hemoglobin less than 10 g/dL. Transfusion volume is dependent on the degree of anemia, and also the size of the patient.10 Further, nurses should optimize arterial oxygenation saturation. To optimize saturation, increase the FiO2 on supplemental oxygen and consider treatment with an advanced airway and mechanical ventilation. After stabilization, the hemoglobin goal is 7.0 g/dL.10

If the patient does not exhibit adventitious assessment findings of fluid volume overload, continue fluid resuscitation but ensure that reassessment occurs following every bolus. Epinephrine is the vasoactive agent of choice.12,16 Epinephrine increases heart rate and stroke volume, which causes a cumulative increase in cardiac output and cardiac oxygen consumption. Epinephrine increases blood glucose concentrations and sets the stage for persistent lactic acidosis. Patients on epinephrine can demonstrate decreased splanchnic blood flow, which can increase the production of lactic acid. Implement routine monitoring of lactic acid.17

Another option is dobutamine. However, dobutamine can exacerbate hypotension, so ensure that adequate intravascular volume is present prior to initiation. Combining dobutamine and norepinephrine allows for better splanchnic perfusion.13

In the last shock state, a normotensive shock state, the patient will demonstrate normotension but altered perfusion with ScvO2 less than 70%. As with vasoconstricted hypotensive shock state, it is important to correct anemia. Transfuse packed red blood cells for hemoglobin less than 10 g/dL. Optimize arterial oxygenation saturation by treating accompanying anemia and increase FiO2 on supplemental oxygen as well as consider treatment with an advanced airway and mechanical ventilation.10,12

Dopamine may allow for renal and splanchnic perfusion (low dose), cardiac contractility (intermediate doses), and increased systemic vascular resistance (high doses). Continue to monitor perfusion closely. If perfusion does not improve, start the patient on either a norepinephrine or epinephrine infusion.13,16,17 Norepinephrine should be administered to patients with low vascular resistance, and epinephrine should be administered to patients with normal-to-high vascular resistance.13,17

Fluid refractory and pressor-dependent states are concerning for adrenal insufficiency, so it is important to consider stress-dose hydrocortisone to combat the adrenal insufficiency. Adrenal insufficiency can be diagnosed based on cortisol level, indicated by a random cortisol level less than 18 mcg/dL. When this presents, administer hydrocortisone.13 The Surviving Sepsis Campaign asserts that hydrocortisone therapy administration be timely in fluid refractory and catecholamine-resistant shock states and with a suspected or demonstrated absolute adrenal insufficiency.10

Evaluation and ongoing nursing care

Jaco and colleagues state that pediatric patients in septic states should demonstrate normalized capillary refill of less than 2 seconds in the presence of normal equal pulses in all extremities and no difference in strength between central and peripheral assessment.18 In addition, peripheral vascular assessment should also reveal warm extremities. The patient's overall mental status should improve. Urine output should stabilize around 1 mL/kg/hr.10,18 The patient should demonstrate a smaller base deficit and decreasing lactic acid/serum lactate of less than 2 mmol/L. The improvements of the base deficit and the lactate exhibit the correction of the associated metabolic acidosis. Last, the patient's SvcO2 should be greater than 70%.

As the clinical picture improves, titrate any vasoactive agents that were begun during stabilization to avoid prolonged organ vasoconstriction.10 Maintain tight glycemic control throughout the shock state. An appropriate target is glucose levels less than 180 mg/dL.10 Consider diuretic therapy to mitigate fluid volume overload, but only after shock has resolved. More advanced modalities such as continuous renal replacement therapy or hemodialysis may be indicated should diuretic therapy fail.10

Nutritional management during septic states is complicated. Peristaltic stasis can decrease splanchnic perfusion, delaying gastric emptying. Therefore, consider total parenteral nutrition. Burn patients are also at high risk for a Curling ulcer. Curling ulcer, also known as acute ulcerative gastroduodenal disease, is caused by an alteration in the gastric mucosal function. Compromise of the mucosal barrier produces hydrogen ions, leading to the further development of gastric and duodenal ulcerations. This ulceration can lead to pain, gastrointestinal hemorrhage, and perforation.19

Regardless of nutrition modality, the patient should be prescribed an H2-receptor antagonist or proton pump inhibitor.18 According to the Surviving Sepsis Campaign, gastrointestinal bleeding occurs similarly in pediatric patients as in adults; therefore, gastrointestinal prophylaxis should be utilized with proton pump inhibitors or H2-receptor antagonists.10

Prevention

Surgical excision and closure of deep partial and/or full thickness burns is the best way to prevent sepsis in burn patients. This greatly reduces the incidence of burn wound infections such as cellulitis.15 Comprehensive wound care is also vital to prevention. Aggressive hydrotherapy to remove dead tissue and to clean all wounds can help prevent infection. Antimicrobial agents such as silver sulfadiazine can aid in infection control.19

Every facility should educate staff, patients, and visitors as part of their infection control program. Strict adherence to standard precautions and infection control surveillance is paramount. Facilities that have implemented a comprehensive infection control program geared at the prevention of sepsis, especially in burn patients, have been highly effective in reducing infection rates.1

Iatrogenic infection prevention is also important because of the risk of infections associated with ventilators, central venous lines, and urinary catheters. Strategies to prevent VAP, catheter-associated urinary tract infections (CAUTI), and central line-associated bloodstream infections (CLABSI) are pivotal in infection prevention. Utilize the CDC's infection prevention initiatives for CLABSI, VAP, and CAUTI to reduce the incidence of infection related to central lines, ventilators, and urinary catheters. Examples of initiatives include using chlorhexidine mouth swabs to prevent VAP, maintaining an unobstructed flow of urine with a closed drainage system for CAUTI, and implementing sterile dressing changes for central lines to prevent CLABSI.3-5

Conclusion

Pediatric burn patients are highly complex trauma patients and a unique challenge to sepsis prevention. Nurses must be vigilant for the signs and symptoms of infection. Providers must understand and act on lab findings in conjunction with their physical assessment of the patient.

All staff members and family involved in the care of a pediatric burn patient must achieve the highest levels of infection prevention and control. Though burn sepsis is very complicated and the diagnosis and treatment is very individualized, ongoing research will help improve the recognition, treatment, and prevention of sepsis in pediatric burn patients.

REFERENCES

1. Sheridan RL. Infections in critically ill pediatric burn patients. Semin Pediatr Infect Dis. 2000;11(1):25–34.
2. Greenhalgh DG, Saffle JR, Holmes JH 4th, et al. American Burn Association consensus conference to define sepsis and infection in burns. J Burn Care Res. 2007;28(6):776–790.
3. O'Grady NP, Alexander M, Burns LA, et al2011 guidelines for the prevention of intravascular catheter-related infections. Centers for Disease Control and Prevention. 2011. www.cdc.gov/hicpac/pdf/guidelines/bsi-guidelines-2011.pdf.
4. Klompas M, Branson R, Eichenwald EC, et al. Strategies to prevent ventilator-associated pneumonia in acute care hospitals: 2014 update. Infect Control Hosp Epidemiol. 2014;35(suppl 2):S133–S154.
5. Gould CV, Umscheid CA, Agarwal RK, et alGuideline for prevention of catheter associated urinary tract infections 2009. Centers for Disease Control and Prevention. www.cdc.gov/hicpac/pdf/CAUTI/CAUTIguideline2009final.pdf.
6. Aelami MH, Lotfi M, Zingg W. Ventilator-associated pneumonia in neonates, infants and children. Antimicrob Resist Infect Control. 2014;3:30.
7. Tran S, Chin AC. Burn sepsis in children. Clin Pediatr Emerg Med. 2014;15(2):149–157.
8. Singer M, Deutschman CS, Seymour CW, et al. The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA. 2016;315(8):801–810.
9. Goldstein B, Giroir B, Randolph A. International Consensus Conference on Pediatric Sepsis. International pediatric sepsis consensus conference: definitions for sepsis and organ dysfunction in pediatrics. Pediatr Crit Care Med. 2005;6(1):2–8.
10. Dellinger RP, Levy MM, Rhodes A, et al. Surviving Sepsis Campaign: international guidelines for management of severe sepsis and septic shock, 2012. Intensive Care Med. 2013;39(2):165–228.
11. de Caen AR, Berg MD, Chameides L, et al. Part 12: Pediatric Advanced Life Support: 2015 American Heart Association guidelines update for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation. 2015;132(18 suppl 2):S526–S542.
    12. American Heart Association. Pediatric advanced life support. In: A. H. Association, ed. 2015 Handbook of Emergency Cardiovascular Care for Healthcare Providers. Dallas, TX: American Heart Association; 2015.
    13. American Heart Association. Pediatric Advanced Life Support - Provider Manual. Dallas, TX: American Heart Association; 2011.
    14. Jin M, Khan A. Procalcitonin: uses in the clinical laboratory for the diagnosis of sepsis. Lab Med. 2010;41(3):173–177.
    15. Sheridan RL. Sepsis in pediatric burn patients. Pediatr Crit Care Med. 2005;6(3 suppl):S112–S119.
    16. Brierley J, Carcillo JA, Choong K, et al. Clinical practice parameters for hemodynamic support of pediatric and neonatal septic shock: 2007 update from the American College of Critical Care Medicine. Crit Care Med. 2009;37(2):666–688.
    17. Simmons ML, Durham SH, Carter CW. Pharmacological management of pediatric patients with sepsis. AACN Adv Crit Care. 2012;23(4):437–448.
    18. Jaco M, Owens Lane C, Dickerson P, Gordon MD. Burns. In: Slota MC, ed. Core Curriculum for Pediatric Critical Care Nursing. St. Louis, MO: Elsevier; 2006.
    19. Pietsch JB, Chung DH. Care of the child with burns. In: Hazinski MF, ed. Nursing Care of the Critically Ill Child. St. Louis, MO: Elsevier; 2013.
    Keywords:

    burn sepsis; infection prevention; pediatric burns; sepsis; systemic inflammatory response syndrome

    Wolters Kluwer Health, Inc. All rights reserved.