- Email: [email protected]
Refractory Septic Shock in a 17 Year Old Female With Fever, Neutropenia, and Severe Abdominal Pain: The First 24 Hours
Abstract: Early recognition and timely intervention are vital in decreasing mortality associated with septic shock. The following is a case study describing the initial 24-hour course of a 17 year-old female with relapsed acute lymphocytic leukemia and refractory septic shock.
Keywords: septic shock; fever; hypotension
Reprint requests and correspondence: Lauren Sorce RN, MSN, CPNP-AC/PC, FCCM, Division of Pediatric Critical Care Medicine, Ann & Robert H. Lurie Children’s Hospital of Chicago, Northwestern University Feinberg School of Medicine, 225 East Chicago Avenue, Box 246, Chicago, Illinois 60611–2605. (E-mail: [email protected]) 1522-8401 © 2014 Elsevier Inc. All rights reserved.
158
Refractory Septic Shock in a 17 Year Old Female With Fever, Neutropenia, and Severe Abdominal Pain: The First 24 Hours Laura Crisanti, RN, MSN, CPNP-AC/PC, Lisa Genualdi, RN, MSN, CPNP-AC/PC, Kalyn Mahoney, RN, MSN, CPNP-AC/PC, Sabrina Derrington, MD, Lauren Sorce, RN, MSN, CPNP-AC/PC, FCCM
T
he patient is a 17-year-old Hispanic female diagnosed with pre B cell acute lymphocytic leukemia (ALL) in 2008. Her course was complicated by relapse in 2012 and acute pancreatitis secondary to pegasparaginase.
VOL. 15, NO. 2 • REFRACTORY SEPTIC SHOCK IN A 17 YEAR OLD FEMALE WITH FEVER / CRISANTI ET AL.
REFRACTORY SEPTIC SHOCK IN A 17 YEAR OLD FEMALE WITH FEVER / CRISANTI ET AL. • VOL. 15, NO. 2 159
She presented to the emergency department (ED) with a chief complaint of sudden onset of severe abdominal pain and fever. Initial vital signs revealed a temperature of 101.5°F, heart rate 148 beats per minute (BPM), respiratory rate of 18 breaths per minute, blood pressure of 71/35 mmHg, and oxygen saturation of 99% on room air. On physical exam she was noted to be ill-appearing and moaning in pain with abdominal guarding. She had dry mucous membranes, weak peripheral pulses, prolonged capillary refill, and cool extremities. Initial laboratory studies were further concerning, with a lactate of 11.6 mEq/L, mixed venous oxygen saturation (SvO2) of 71%, BUN of 26 mg/dL, and creatinine of 1.17 mg/dL. The serum chemistry panel revealed the presence of transaminitis (ALT 118 IU/L, AST 80 IU/L, total bilirubin 3.7 mg/dL, and direct bilirubin 2.9 mg/dL). A complete blood count demonstrated depression of all cell lines, with a white blood count of 0.31 thou/uL with 15% bandemia, hemoglobin 10.2 g/dL, platelet count 15 thou/uL, and absolute neutrophil count of 255 thou/uL. Clotting studies were also abnormal with an activated partial thromboplastin time of 127.5 sec, INR 2.1, fibrinogen 66 mg/dL, and D-dimer 1.7 mg/ml FEU. Her amylase and lipase were within normal limits. Within the first hour of ED presentation, the patient received a total of 3.8 liters of crystalloid fluids, with initiation of dopamine and norepinephrine infusions; hydrocortisone was given for volume resistant septic shock. Oxygen via non-rebreather mask was applied to augment oxygen delivery. Blood cultures were obtained, and ceftazidime was administered within the first 60 minutes; a 10% dextrose bolus was also given for hypoglycemia. Because of the unremitting abdominal pain, the pediatric surgery team was consulted. An abdominal radiograph was obtained and there was no evidence of pneumatosis, thus acute surgical intervention was not recommended. Abdominal computed tomography was deferred until the patient was more stable. She was transferred to the pediatric intensive care unit (PICU) with a diagnosis of septic shock.
abdomen with intense pain in response to light palpation. Repeat lab studies were concerning for persistent lactic acidemia N 10 meq/L and continued coagulopathy. Within the first hour of PICU admission she had received an additional 600 ml of isotonic fluid, and was intubated to offload metabolic demand. Chest imaging confirmed satisfactory positioning of the endotracheal tube and opacity of the apex of the right lung, representing atelectasis versus pleural fluid (Figure 1). Both vasopressin and epinephrine infusions were added for persistent hypotension and borderline SvO2 despite dopamine and norepinephrine drips. An echocardiogram confirmed brisk systolic function on multiple pressors and absence of a pericardial effusion. Home medications of fluconazole and sulfamethoxazole-trimethoprim were continued. Continuous infusions of morphine and midazolam were started for analgesia and sedation. A nasogastric tube was placed to gravity in order to decompress the stomach. Six hours after initial ED presentation, metronidazole and vancomycin were added to the antibiotic regimen. Within 12 hours of initial presentation she was in acute oliguric kidney failure necessitating placement of a hemodialysis catheter for continuous renal replacement therapy. Dopamine, vasopressin, and norepinephrine infusions were continued to maintain adequate mean arterial blood pressures. A repeat echocardiogram was significant for moderate to severely depressed left ventricular systolic function, and a milrinone infusion was added. A central venous line was placed for additional monitoring and access. Within 24 hours of presentation, bacterial cultures from endotracheal tube aspirates and blood from the indwelling PICC line were positive for
PEDIATRIC INTENSIVE CARE UNIT COURSE Upon arrival to the PICU, 2.5 hours after presenting to the ED, she was awake and able to converse with examiners. Her PICU admission vital signs included a temperature of 100.8˚F, heart rate of 169 BPM, respiratory rate of 20, blood pressure 92/49 mmHg, and an oxygen saturation of 96% on a non-rebreather. Her physical examination was again significant for weak distal pulses, cool peripheral extremities with delayed capillary refill (3–4 seconds), and a distended
Figure 1. Post-intubation chest x-ray demonstrating an opacity in the apex of the right lung.
Guideline
0 min
Recognition of decreased mental status and inadequate perfusion
5 min
Initial Resuscitation • Administer boluses of 20 ml/kg isotonic saline or colloid up to and over 60 ml/kg until improved perfusion or unless hepatomegaly or rales develop • Correct hypocalcemia and hypoglycemia • Start antibiotics Fluid Refractory Shock • Begin inotrope, reverse warm shock by titrating norepinephrine • Obtain airway and central access if needed
15 min
60 min
Catecholamine Resistant Shock • Initiate hydrocortisone if at risk for absolute adrenal insufficiency CVP monitoring, goal to achieve normal MAP, CVP and SvO2 N 70% Warm Shock With Low Blood Pressure •Titrate norepinephrine and fluid for goal SvO2 N 70% • Consider vasopressin, terlipressin or angiotensin for persistent hypotension • Consider low dose epinephrine if SvO2 b 70% Persistent Catecholamine Resistant Shock • Evaluate for and correct pneumothorax, pericardial effusion, elevated intra-abdominal pressure • Consider additional diagnostic interventions (pulmonary artery catheter, PICCO monitor, etc.)
Case Timeline • • • • • • • • •
Admitted to ED at 1203 Ill-appearing, moaning, dry mucous membranes Tachycardia, hypotensive, febrile Peripheral IV placed PICC in situ Placed on oxygen 1207: Given 800 ml NS bolus Blood cultures drawn from the PICC line and peripherally Moved to trauma bay at 1213
• • • • • • • •
1217: 1230: 1234: 1245: 1243: 1255: 1315: 1330:
Given 2L NS Started on dopamine Stress dose hydrocortisone initiated Started on norepinephrine Given ceftazidime Given D10 bolus for hypoglycemia Given vancomycin Given metronidazole
• Admitted to PICU at 1400 • 1410: Intubated for impending respiratory failure • 1416: SvO2 71% • 1430: Given additional 600 ml NS fluid bolus • 1445: Started on vasopressin and epinephrine • 1448: SvO2 31%, lactate 11.6 • 1420: CXR without evidence of pneumothorax • 1430: Echocardiogram with brisk systolic function and no pericardial effusion • Hemodialysis catheter placed for oliguria and need for continuous renal replacement therapy within 8 hours of PICU admission
Abbreviations: PIV, peripheral intravenous line; PICC, peripherally inserted central catheter; CVP, central venous pressure; D10, 10% dextrose; MAP, mean arterial pressure; ml, milliliter; NS, normal saline; L, liter; SvO2, mixed venous oxygen saturation; CXR, chest radiograph.
VOL. 15, NO. 2 • REFRACTORY SEPTIC SHOCK IN A 17 YEAR OLD FEMALE WITH FEVER / CRISANTI ET AL.
Time
160
TABLE 1. Comparison of case presentation timeline to sepsis management guideline. Adapted from Brierley J, Carcillo JA, Choong K, et al. [1]
REFRACTORY SEPTIC SHOCK IN A 17 YEAR OLD FEMALE WITH FEVER / CRISANTI ET AL. • VOL. 15, NO. 2 161
pseudomonas aeruginosa. Tobramycin and meropenem were added to the antibiotic regimen for synergistic gram-negative coverage, while metronidazole and ceftazidime were discontinued. Her lactic acidosis persisted, prompting concern for an intra-abdominal process versus hypo-perfusion due to pseudomonal sepsis.
CASE DISCUSSION Early identification of sepsis is paramount for the timely initiation of therapeutic interventions. Appropriate therapies initiated within the initial hours of the development of sepsis positively affect survival outcomes. [1–9] Maintaining established standards as described by Brierley et al. [1] may be difficult in the busy ED setting. In Table 1, we compare published guidelines with the actual events in our case. This sort of comparison may be helpful to emergency and critical care resuscitation teams, in order to identify processes that impact optimal timing of interventions, and strategies to improve. As is evident in the table, meeting established guidelines for pediatric sepsis in the ED can be difficult even in a tertiary center. Although this patient received the appropriate therapies, she did not receive all of them according to the guideline’s established timeframe. Prompt recognition of shock during triage is critical to timely initiation of the sepsis guidelines. In this case study, the patient was initially placed in a standard ED exam room and was later moved into the trauma bay upon recognition of sepsis (Table 1). During this time, precious minutes were potentially lost that could have been dedicated to ongoing resuscitation. During patient transport, the goal is to maintain patient safety and the continuation of resuscitative interventions. However, even in the best scenario, it is difficult for the care team to physically move the patient while simultaneously providing interventions as delineated by the sepsis guidelines. Placement of the patient with presumed septic shock in the resuscitation suite clearly communicates the presence of a patient with a critical illness and the need for timely interventions. Furthermore, the trauma bay is likely to be stocked with all the necessary equipment for the resuscitation of the patient with septic shock, minimizing the need for staff to leave the patient’s bedside. In other types of resuscitations (i.e., cardiopulmonary resuscitation) common to the PICU environment the role of a timekeeper is invaluable in facilitating adherence to pediatric advanced life support (PALS) guidelines during the chaos of a code event. This experience may translate well to
resuscitation in children with septic shock. While to our knowledge this has not been specifically studied, identification of a timekeeper may improve compliance with sepsis guidelines, impact timely interventions during septic shock resuscitation, and facilitate escalation of therapies as needed while awaiting PICU admission, or interfacility transfer to a tertiary center. However, it is imperative to recognize that inherent to any key process change, whether in the ED or PICU, a shift in culture may be necessary to embrace change. One therapeutic goal for resuscitation of septic shock is normalizing elevated lactate levels. [10] This patient presented with a lactic acidemia that persisted well beyond the first 24 hours of initial resuscitative efforts. This marker of tissue perfusion is correlated with effectiveness of intervention and has been shown to be predictive of risk of mortality. One must inquire whether escalating efforts to increase oxygen delivery or decrease oxygen demand would have improved the patient’s persistent state of hypoperfusion. Potential management strategies could have included earlier intubation, exploratory laparotomy in a patient with neutropenia at high risk for septic typhlitis and necrotic bowel, or early initiation of ECMO. Intermittently taking a step back and reevaluating the situation (Where are we now? Are we meeting goals? What else should we think about?) is another common ‘best practice’ during resuscitation events in the PICU that may be helpful in managing septic shock. As in this case, lack of response to escalating therapy should prompt reevaluation for unaddressed etiologies or complicating factors. Equally concerning was this young woman’s rapid heart rate that never appeared to improve following aggressive volume administration. An electrocardiogram and an echocardiogram earlier in her course may have helped to delineate what component of her tachycardia was due to profound hypovolemia and not a manifestation of developing cardiogenic shock. Her BUN and creatinine were indeed elevated, but not considerably, and the young woman was mentating well, suggesting adequate cerebral perfusion. Given her underlying disease, a cardiomyopathy due to anthracyclines would not be unexpected and the etiology of her cardiovascular decompensation may indeed have been multifactorial. The value of a random cortisol level in a patient with multi-drug resistant hypotension and apparent fluid non-responsiveness, who likely was treated with steroids as part of her leukemia treatment course, prior to empiric treatment with hydrocortisone could be debated, if the consensus was that there wasn’t time to perform an ACTH stimulation test.
162
VOL. 15, NO. 2 • REFRACTORY SEPTIC SHOCK IN A 17 YEAR OLD FEMALE WITH FEVER / CRISANTI ET AL.
CASE FOLLOW-UP This patient survived her pseudomonal sepsis; however, three months later peripheral blood smear confirmed relapsed PreB ALL and she and her family elected palliative care. She expired one month later.
5.
REFERENCES
7..
1. 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;37:666–88. 2. Carcillo JA, Davis AL, Zaritsky A. Role of early fluid resuscitation in pediatric septic shock. JAMA 1991;266:1242–5. 3. Cruz AT, Perry AM, Williams EA, et al. Implementation of goal-directed therapy for children with suspected sepsis in the emergency department. Pediatrics 2011;127:e758–66. 4. de Oliveira CF, de Oliveira DS, Gottschald AF, et al. ACCM/ PALS haemodynamic support guidelines for paediatric septic shock: an outcomes comparison with and without monitoring
6.
8. 9. 10.
central venous oxygen saturation. Intensive Care Med 2008;34:1065–75. Han YY, Carcillo JA, Dragotta MA, et al. Early reversal of pediatric-neonatal septic shock by community physicians is associated with improved outcome. Pediatrics 2003;112:793–9. Levy MM, Dellinger RP, Townsend SR, et al. The Surviving Sepsis Campaign: results of an international guideline-based performance improvement program targeting severe sepsis. Crit Care Med 2010;38:367–74. Muszynski JA, Knatz NL, Sargel CL, et al. Timing of correct parenteral antibiotic initiation and outcomes from severe bacterial community-acquired pneumonia in children. Pediatr Infect Dis J 2011;30:295–301. Rivers E, Nguyen B, Havstad S, et al. Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med 2001;345:1368–77. Smith SH, Perner A. Higher vs. lower fluid volume for septic shock: clinical characteristics and outcome in unselected patients in a prospective, multicenter cohort. Crit Care 2012;16:R76. Dellinger RP, Levy MM, Rhodes A, et al. Surviving Sepsis Campaign: international guidelines for management of severe sepsis and septic shock: 2012. Crit Care Med 2013;41(2): 580–637.
Keywords: septic shock; fever; hypotension
Reprint requests and correspondence: Lauren Sorce RN, MSN, CPNP-AC/PC, FCCM, Division of Pediatric Critical Care Medicine, Ann & Robert H. Lurie Children’s Hospital of Chicago, Northwestern University Feinberg School of Medicine, 225 East Chicago Avenue, Box 246, Chicago, Illinois 60611–2605. (E-mail: [email protected]) 1522-8401 © 2014 Elsevier Inc. All rights reserved.
158
Refractory Septic Shock in a 17 Year Old Female With Fever, Neutropenia, and Severe Abdominal Pain: The First 24 Hours Laura Crisanti, RN, MSN, CPNP-AC/PC, Lisa Genualdi, RN, MSN, CPNP-AC/PC, Kalyn Mahoney, RN, MSN, CPNP-AC/PC, Sabrina Derrington, MD, Lauren Sorce, RN, MSN, CPNP-AC/PC, FCCM
T
he patient is a 17-year-old Hispanic female diagnosed with pre B cell acute lymphocytic leukemia (ALL) in 2008. Her course was complicated by relapse in 2012 and acute pancreatitis secondary to pegasparaginase.
VOL. 15, NO. 2 • REFRACTORY SEPTIC SHOCK IN A 17 YEAR OLD FEMALE WITH FEVER / CRISANTI ET AL.
REFRACTORY SEPTIC SHOCK IN A 17 YEAR OLD FEMALE WITH FEVER / CRISANTI ET AL. • VOL. 15, NO. 2 159
She presented to the emergency department (ED) with a chief complaint of sudden onset of severe abdominal pain and fever. Initial vital signs revealed a temperature of 101.5°F, heart rate 148 beats per minute (BPM), respiratory rate of 18 breaths per minute, blood pressure of 71/35 mmHg, and oxygen saturation of 99% on room air. On physical exam she was noted to be ill-appearing and moaning in pain with abdominal guarding. She had dry mucous membranes, weak peripheral pulses, prolonged capillary refill, and cool extremities. Initial laboratory studies were further concerning, with a lactate of 11.6 mEq/L, mixed venous oxygen saturation (SvO2) of 71%, BUN of 26 mg/dL, and creatinine of 1.17 mg/dL. The serum chemistry panel revealed the presence of transaminitis (ALT 118 IU/L, AST 80 IU/L, total bilirubin 3.7 mg/dL, and direct bilirubin 2.9 mg/dL). A complete blood count demonstrated depression of all cell lines, with a white blood count of 0.31 thou/uL with 15% bandemia, hemoglobin 10.2 g/dL, platelet count 15 thou/uL, and absolute neutrophil count of 255 thou/uL. Clotting studies were also abnormal with an activated partial thromboplastin time of 127.5 sec, INR 2.1, fibrinogen 66 mg/dL, and D-dimer 1.7 mg/ml FEU. Her amylase and lipase were within normal limits. Within the first hour of ED presentation, the patient received a total of 3.8 liters of crystalloid fluids, with initiation of dopamine and norepinephrine infusions; hydrocortisone was given for volume resistant septic shock. Oxygen via non-rebreather mask was applied to augment oxygen delivery. Blood cultures were obtained, and ceftazidime was administered within the first 60 minutes; a 10% dextrose bolus was also given for hypoglycemia. Because of the unremitting abdominal pain, the pediatric surgery team was consulted. An abdominal radiograph was obtained and there was no evidence of pneumatosis, thus acute surgical intervention was not recommended. Abdominal computed tomography was deferred until the patient was more stable. She was transferred to the pediatric intensive care unit (PICU) with a diagnosis of septic shock.
abdomen with intense pain in response to light palpation. Repeat lab studies were concerning for persistent lactic acidemia N 10 meq/L and continued coagulopathy. Within the first hour of PICU admission she had received an additional 600 ml of isotonic fluid, and was intubated to offload metabolic demand. Chest imaging confirmed satisfactory positioning of the endotracheal tube and opacity of the apex of the right lung, representing atelectasis versus pleural fluid (Figure 1). Both vasopressin and epinephrine infusions were added for persistent hypotension and borderline SvO2 despite dopamine and norepinephrine drips. An echocardiogram confirmed brisk systolic function on multiple pressors and absence of a pericardial effusion. Home medications of fluconazole and sulfamethoxazole-trimethoprim were continued. Continuous infusions of morphine and midazolam were started for analgesia and sedation. A nasogastric tube was placed to gravity in order to decompress the stomach. Six hours after initial ED presentation, metronidazole and vancomycin were added to the antibiotic regimen. Within 12 hours of initial presentation she was in acute oliguric kidney failure necessitating placement of a hemodialysis catheter for continuous renal replacement therapy. Dopamine, vasopressin, and norepinephrine infusions were continued to maintain adequate mean arterial blood pressures. A repeat echocardiogram was significant for moderate to severely depressed left ventricular systolic function, and a milrinone infusion was added. A central venous line was placed for additional monitoring and access. Within 24 hours of presentation, bacterial cultures from endotracheal tube aspirates and blood from the indwelling PICC line were positive for
PEDIATRIC INTENSIVE CARE UNIT COURSE Upon arrival to the PICU, 2.5 hours after presenting to the ED, she was awake and able to converse with examiners. Her PICU admission vital signs included a temperature of 100.8˚F, heart rate of 169 BPM, respiratory rate of 20, blood pressure 92/49 mmHg, and an oxygen saturation of 96% on a non-rebreather. Her physical examination was again significant for weak distal pulses, cool peripheral extremities with delayed capillary refill (3–4 seconds), and a distended
Figure 1. Post-intubation chest x-ray demonstrating an opacity in the apex of the right lung.
Guideline
0 min
Recognition of decreased mental status and inadequate perfusion
5 min
Initial Resuscitation • Administer boluses of 20 ml/kg isotonic saline or colloid up to and over 60 ml/kg until improved perfusion or unless hepatomegaly or rales develop • Correct hypocalcemia and hypoglycemia • Start antibiotics Fluid Refractory Shock • Begin inotrope, reverse warm shock by titrating norepinephrine • Obtain airway and central access if needed
15 min
60 min
Catecholamine Resistant Shock • Initiate hydrocortisone if at risk for absolute adrenal insufficiency CVP monitoring, goal to achieve normal MAP, CVP and SvO2 N 70% Warm Shock With Low Blood Pressure •Titrate norepinephrine and fluid for goal SvO2 N 70% • Consider vasopressin, terlipressin or angiotensin for persistent hypotension • Consider low dose epinephrine if SvO2 b 70% Persistent Catecholamine Resistant Shock • Evaluate for and correct pneumothorax, pericardial effusion, elevated intra-abdominal pressure • Consider additional diagnostic interventions (pulmonary artery catheter, PICCO monitor, etc.)
Case Timeline • • • • • • • • •
Admitted to ED at 1203 Ill-appearing, moaning, dry mucous membranes Tachycardia, hypotensive, febrile Peripheral IV placed PICC in situ Placed on oxygen 1207: Given 800 ml NS bolus Blood cultures drawn from the PICC line and peripherally Moved to trauma bay at 1213
• • • • • • • •
1217: 1230: 1234: 1245: 1243: 1255: 1315: 1330:
Given 2L NS Started on dopamine Stress dose hydrocortisone initiated Started on norepinephrine Given ceftazidime Given D10 bolus for hypoglycemia Given vancomycin Given metronidazole
• Admitted to PICU at 1400 • 1410: Intubated for impending respiratory failure • 1416: SvO2 71% • 1430: Given additional 600 ml NS fluid bolus • 1445: Started on vasopressin and epinephrine • 1448: SvO2 31%, lactate 11.6 • 1420: CXR without evidence of pneumothorax • 1430: Echocardiogram with brisk systolic function and no pericardial effusion • Hemodialysis catheter placed for oliguria and need for continuous renal replacement therapy within 8 hours of PICU admission
Abbreviations: PIV, peripheral intravenous line; PICC, peripherally inserted central catheter; CVP, central venous pressure; D10, 10% dextrose; MAP, mean arterial pressure; ml, milliliter; NS, normal saline; L, liter; SvO2, mixed venous oxygen saturation; CXR, chest radiograph.
VOL. 15, NO. 2 • REFRACTORY SEPTIC SHOCK IN A 17 YEAR OLD FEMALE WITH FEVER / CRISANTI ET AL.
Time
160
TABLE 1. Comparison of case presentation timeline to sepsis management guideline. Adapted from Brierley J, Carcillo JA, Choong K, et al. [1]
REFRACTORY SEPTIC SHOCK IN A 17 YEAR OLD FEMALE WITH FEVER / CRISANTI ET AL. • VOL. 15, NO. 2 161
pseudomonas aeruginosa. Tobramycin and meropenem were added to the antibiotic regimen for synergistic gram-negative coverage, while metronidazole and ceftazidime were discontinued. Her lactic acidosis persisted, prompting concern for an intra-abdominal process versus hypo-perfusion due to pseudomonal sepsis.
CASE DISCUSSION Early identification of sepsis is paramount for the timely initiation of therapeutic interventions. Appropriate therapies initiated within the initial hours of the development of sepsis positively affect survival outcomes. [1–9] Maintaining established standards as described by Brierley et al. [1] may be difficult in the busy ED setting. In Table 1, we compare published guidelines with the actual events in our case. This sort of comparison may be helpful to emergency and critical care resuscitation teams, in order to identify processes that impact optimal timing of interventions, and strategies to improve. As is evident in the table, meeting established guidelines for pediatric sepsis in the ED can be difficult even in a tertiary center. Although this patient received the appropriate therapies, she did not receive all of them according to the guideline’s established timeframe. Prompt recognition of shock during triage is critical to timely initiation of the sepsis guidelines. In this case study, the patient was initially placed in a standard ED exam room and was later moved into the trauma bay upon recognition of sepsis (Table 1). During this time, precious minutes were potentially lost that could have been dedicated to ongoing resuscitation. During patient transport, the goal is to maintain patient safety and the continuation of resuscitative interventions. However, even in the best scenario, it is difficult for the care team to physically move the patient while simultaneously providing interventions as delineated by the sepsis guidelines. Placement of the patient with presumed septic shock in the resuscitation suite clearly communicates the presence of a patient with a critical illness and the need for timely interventions. Furthermore, the trauma bay is likely to be stocked with all the necessary equipment for the resuscitation of the patient with septic shock, minimizing the need for staff to leave the patient’s bedside. In other types of resuscitations (i.e., cardiopulmonary resuscitation) common to the PICU environment the role of a timekeeper is invaluable in facilitating adherence to pediatric advanced life support (PALS) guidelines during the chaos of a code event. This experience may translate well to
resuscitation in children with septic shock. While to our knowledge this has not been specifically studied, identification of a timekeeper may improve compliance with sepsis guidelines, impact timely interventions during septic shock resuscitation, and facilitate escalation of therapies as needed while awaiting PICU admission, or interfacility transfer to a tertiary center. However, it is imperative to recognize that inherent to any key process change, whether in the ED or PICU, a shift in culture may be necessary to embrace change. One therapeutic goal for resuscitation of septic shock is normalizing elevated lactate levels. [10] This patient presented with a lactic acidemia that persisted well beyond the first 24 hours of initial resuscitative efforts. This marker of tissue perfusion is correlated with effectiveness of intervention and has been shown to be predictive of risk of mortality. One must inquire whether escalating efforts to increase oxygen delivery or decrease oxygen demand would have improved the patient’s persistent state of hypoperfusion. Potential management strategies could have included earlier intubation, exploratory laparotomy in a patient with neutropenia at high risk for septic typhlitis and necrotic bowel, or early initiation of ECMO. Intermittently taking a step back and reevaluating the situation (Where are we now? Are we meeting goals? What else should we think about?) is another common ‘best practice’ during resuscitation events in the PICU that may be helpful in managing septic shock. As in this case, lack of response to escalating therapy should prompt reevaluation for unaddressed etiologies or complicating factors. Equally concerning was this young woman’s rapid heart rate that never appeared to improve following aggressive volume administration. An electrocardiogram and an echocardiogram earlier in her course may have helped to delineate what component of her tachycardia was due to profound hypovolemia and not a manifestation of developing cardiogenic shock. Her BUN and creatinine were indeed elevated, but not considerably, and the young woman was mentating well, suggesting adequate cerebral perfusion. Given her underlying disease, a cardiomyopathy due to anthracyclines would not be unexpected and the etiology of her cardiovascular decompensation may indeed have been multifactorial. The value of a random cortisol level in a patient with multi-drug resistant hypotension and apparent fluid non-responsiveness, who likely was treated with steroids as part of her leukemia treatment course, prior to empiric treatment with hydrocortisone could be debated, if the consensus was that there wasn’t time to perform an ACTH stimulation test.
162
VOL. 15, NO. 2 • REFRACTORY SEPTIC SHOCK IN A 17 YEAR OLD FEMALE WITH FEVER / CRISANTI ET AL.
CASE FOLLOW-UP This patient survived her pseudomonal sepsis; however, three months later peripheral blood smear confirmed relapsed PreB ALL and she and her family elected palliative care. She expired one month later.
5.
REFERENCES
7..
1. 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;37:666–88. 2. Carcillo JA, Davis AL, Zaritsky A. Role of early fluid resuscitation in pediatric septic shock. JAMA 1991;266:1242–5. 3. Cruz AT, Perry AM, Williams EA, et al. Implementation of goal-directed therapy for children with suspected sepsis in the emergency department. Pediatrics 2011;127:e758–66. 4. de Oliveira CF, de Oliveira DS, Gottschald AF, et al. ACCM/ PALS haemodynamic support guidelines for paediatric septic shock: an outcomes comparison with and without monitoring
6.
8. 9. 10.
central venous oxygen saturation. Intensive Care Med 2008;34:1065–75. Han YY, Carcillo JA, Dragotta MA, et al. Early reversal of pediatric-neonatal septic shock by community physicians is associated with improved outcome. Pediatrics 2003;112:793–9. Levy MM, Dellinger RP, Townsend SR, et al. The Surviving Sepsis Campaign: results of an international guideline-based performance improvement program targeting severe sepsis. Crit Care Med 2010;38:367–74. Muszynski JA, Knatz NL, Sargel CL, et al. Timing of correct parenteral antibiotic initiation and outcomes from severe bacterial community-acquired pneumonia in children. Pediatr Infect Dis J 2011;30:295–301. Rivers E, Nguyen B, Havstad S, et al. Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med 2001;345:1368–77. Smith SH, Perner A. Higher vs. lower fluid volume for septic shock: clinical characteristics and outcome in unselected patients in a prospective, multicenter cohort. Crit Care 2012;16:R76. Dellinger RP, Levy MM, Rhodes A, et al. Surviving Sepsis Campaign: international guidelines for management of severe sepsis and septic shock: 2012. Crit Care Med 2013;41(2): 580–637.