Shock is a life-threatening condition that represents a state of circulatory failure, where the delivery of oxygen and nutrients to tissues and organs is insufficient to meet metabolic demands.1 this critical imbalance disrupts normal cellular function and can lead to multi-organ failure if not promptly recognized and managed. Shock can result from various causes, including hypovolemia, cardiac dysfunction, or vascular maldistribution, each requiring targeted interventions. Early recognition and intervention are vital, especially in critically ill children, as these measures can significantly improve survival rates.2 Notably, shock often coexists with other severe conditions such as myocardial dysfunction and acute lung injury, adding complexity to its management and increasing the urgency for rapid response.3,4 The prevalence of shock is notable even in developed countries, where it affects approximately 2% of all hospitalized infants, children and adults.5 The mortality rate associated with shock varies widely depending on the underlying cause, the timeliness of treatment and the available healthcare resources. In pediatric populations, shock is a significant contributor to admissions in pediatric intensive care units (PICUs), accounting for around 2% of cases globally.5,6 According to western literature and the Nelson Textbook of Pediatrics, this proportion underscores the critical need for effective diagnostic and therapeutic strategies in managing pediatric shock. On a global scale, the situation is even more dire with an estimated 10 million children dying from shock each year. Most of these deaths occur in developing countries, where children under five years of age experience the highest mortality rates.7,8 The causes of shock in young children are varied but frequently tied to preventable or treatable conditions. Leading causes include pneumonia (19%), diarrhea (18%), malaria (8%), neonatal pneumonia or sepsis (10%), preterm delivery (10%) and birth asphyxia (8%).9 These statistics highlight the significant burden of infectious and perinatal conditions in low-resource settings, where limited access to healthcare and delayed treatment exacerbate outcomes. Our study incorporates the Pediatric Logistic Organ Dysfunction 2 (PELOD-2) scoring system to predict mortality in critically ill children. The PELOD-2 score, which evaluates the severity of multiple organ dysfunction, serves as a validated tool for assessing outcomes. By correlating the PELOD-2 score with mortality risk, our research aims to enhance clinical decision-making, optimize patient care and improve survival rates in pediatric shock cases.

This prospective observational study was conducted at the Pediatrics Department of Mahatma Gandhi Medical College and Hospital, Jaipur, Rajasthan. The study duration extended from April 1, 2023, to September 30, 2024. Approval from the Institute Ethics Committee was obtained before study commencement to ensure adherence to ethical guidelines and research protocols. Written informed consent was obtained from all parents/guardians before enrollment with thorough information provided about study objectives, procedures, potential risks and benefits. The study included children aged 1 month to 18 years presenting with a clinical profile of shock. The sample size was 210 patients. Inclusion criteria encompassed all patients between 1 month to 18 years admitted with shock and having complete data for PELOD-2 score calculation. Exclusion criteria included newborns and preterm infants, parents/guardians providing negative consent for study participation and cases with participation withdrawal after initial inclusion or unknown final outcomes. Data Collection and Clinical Assessment A detailed medical history was recorded for each patient using a structured proforma to ensure consistency in data collection. Comprehensive clinical assessment included rapid cardiopulmonary evaluation focusing on airway stability, breathing patterns, work of breathing, bilateral air entry, skin color, heart rate, pulse volume, core-peripheral temperature gap, capillary refill time, liver span, blood pressure and neurological status using Glasgow Coma Scale and pupillary reactions. Laboratory Investigations Essential laboratory investigations were conducted as part of the shock workup, including arterial blood gas (ABG) analysis, complete blood count (CBC), serum electrolytes, renal function tests (RFT) and liver function tests (LFT). Based on investigation results, a standardized algorithm was followed to guide further evaluation and management. PELOD-2 Score Assessment The Pediatric Logistic Organ Dysfunction-2 (PELOD-2) score was calculated within the first 24 hours after PICU admission. The number of organ dysfunctions was determined using PELOD-2 criteria, considering five major dysfunctions: neurological, cardiovascular, respiratory, renal and hematological. PICU mortality was considered the primary outcome with additional outcomes including prolonged PICU stay (>72 hours), respiratory distress and organ dysfunction. Statistical Analysis Data analysis was performed using SPSS version 23.0. Results were presented as frequency distributions, means, standard deviations and graphical representations. Chi-square test was applied for comparison of qualitative variables, while t-test was used for quantitative variables. A p-value <0.05 was considered statistically significant. Sensitivity and specificity of PELOD-2 in predicting mortality were evaluated using receiver operating characteristic (ROC) curve analysis.

Table 1: Demographic and Patient Characteristics (N=210) Characteristic N Percentage Age Distribution 1-11 months 56 26.7% 12-23 months 18 8.6% 24-59 months 56 26.7% 60-143 months 22 10.5% ≥144 months 58 27.6% Gender Female 122 58.1% Male 88 41.9% Shock Severity Compensated 156 74.3% Decompensated 54 25.7% Etiology of Shock Septic 105 50.0% Hypovolemic 69 32.9% Cardiogenic 15 7.1% Neurogenic 11 5.2% Anaphylactic 10 4.8% Clinical Presentation Fever 121 57.6% Breathlessness/Bradypnoea 90 42.9% Vomiting 73 34.8% Diarrhea 47 22.4% Convulsions 36 17.1% Respiratory Distress 123 58.6% Interventions Invasive Ventilation 102 48.6% Organ Dysfunction No dysfunction 40 19.0% 1 organ dysfunction 35 16.7% 2 organ dysfunctions 36 17.1% 3 organ dysfunctions 47 22.4% 4 organ dysfunctions 37 17.6% 5 organ dysfunctions 15 7.1% PELOD-2 Score <8 143 68.1% ≥8 67 31.9% Outcome Discharged 155 73.8% Mortality 55 26.2% Out of 210 patients, the majority were either infants (1–11 months, 26.7%) or adolescents ≥144 months (27.6%) with a nearly equal distribution to children aged 24–59 months (26.7%). Gender distribution showed a female predominance (58.1%) compared to males (41.9%). Most patients presented with compensated shock (74.3%), while 25.7% had decompensated shock. Septic shock was the leading etiology (50%), followed by hypovolemic (32.9%) and cardiogenic (7.1%) causes with smaller proportions of neurogenic (5.2%) and anaphylactic (4.8%). Clinical features commonly included respiratory distress (58.6%) and fever (57.6%). Nearly half of the patients required invasive ventilation (48.6%). Regarding organ dysfunction, 19% had none, whereas multiple dysfunctions were frequent: 22.4% had three, 17.6% had four and 7.1% had five. A PELOD-2 score <8 was seen in 68.1%, while 31.9% had ≥8. Overall, the discharge rate was 73.8% with mortality at 26.2%. Table 2: Relationship between Shock Etiology and Severity Etiology Compensated Decompensated Total p-value Septic 84 (53.8%) 21 (38.9%) 105 0.001* Hypovolemic 63 (40.4%) 6 (11.1%) 69 Cardiogenic 5 (3.2%) 10 (18.5%) 15 Neurogenic 0 (0.0%) 11 (20.4%) 11 Anaphylactic 4 (2.6%) 6 (11.1%) 10 Total 156 54 210 *Significant (p<0.05) Significant differences were found between compensated and decompensated shock across physiological parameters (p<0.05). Patients with decompensated shock showed much poorer neurological status with 22.2% having GCS 3–4 compared to only 1.3% in compensated shock. Pupillary reaction was abnormal in nearly half (48.1%) of decompensated cases, whereas 98.7% of compensated patients had normal reactivity. Respiratory distress and invasive ventilation were markedly higher in the decompensated group (92.6% each) compared to compensated patients (46.8% and 33.3%, respectively). Table 3: Physiological Parameters and Shock Severity Parameter Compensated (n=156) Decompensated (n=54) p-value Glasgow Coma Score 3-4 2 (1.3%) 12 (22.2%) 0.001* 5-10 52 (33.3%) 37 (68.5%) ≥11 102 (65.4%) 5 (9.3%) Pupillary Reaction Both Reactive 154 (98.7%) 28 (51.9%) 0.001* Both Fixed 2 (1.3%) 26 (48.1%) Respiratory Distress 73 (46.8%) 50 (92.6%) 0.001* Invasive Ventilation 52 (33.3%) 50 (92.6%) 0.001* *Significant (p<0.05) Table 4: Comparison of clinical parameters between compensated and decompensated shock patients Parameter Compensated Shock (n=156) Decompensated Shock (n=54) P-value Arterial Blood Gas pH 7.36 ± 0.29 7.15 ± 0.23 0.001* PCO₂ (mmHg) 48.66 ± 51.27 46.06 ± 12.05 0.712 PO₂ (mmHg) 78.66 ± 12.98 48.62 ± 10.08 0.001* Lactate (mmol/L) 2.37 ± 2.32 6.80 ± 7.14 0.001* Hematological Parameters TLC (10³/μL) 11.22 ± 6.02 19.53 ± 11.57 0.001* Platelets (10³/μL) 297.65 ± 177.88 242.24 ± 264.10 0.086 Hemoglobin (g/dL) 9.45 ± 2.07 9.26 ± 2.19 0.578 Renal Function Blood Urea (mg/dL) 35.35 ± 22.79 75.06 ± 72.18 0.001* S. Creatinine (mg/dL) 0.65 ± 0.83 1.69 ± 2.15 0.001* Electrolytes S. Sodium (mmol/L) 140.68 ± 9.26 152.38 ± 27.03 0.001* S. Potassium (mmol/L) 4.26 ± 0.66 4.56 ± 1.09 0.018* S. Chloride (mmol/L) 108.77 ± 16.29 114.34 ± 14.08 0.026* Urine Output (mL/kg/hr) 1.34 ± 0.55 0.93 ± 0.21 0.024* *Statistically significant (P<0.05) Arterial blood gas analysis revealed that decompensated shock patients had significantly lower pH (7.15 vs. 7.36) and PO₂ (48.62 vs. 78.66), alongside markedly elevated lactate (6.80 vs. 2.37), all with p=0.001. Hematological parameters showed higher TLC in decompensated shock (19.53 vs. 11.22, p=0.001), though platelet counts and hemoglobin were not significantly different. Renal dysfunction was evident with elevated blood urea (75.06 vs. 35.35) and creatinine (1.69 vs. 0.65), both significant at p=0.001. Electrolyte derangements were also more pronounced with higher sodium, potassium and chloride levels in decompensated patients. Urine output was significantly reduced in decompensated shock (0.93 vs. 1.34 mL/kg/hr, p=0.024). Table 5: Relationship between Number of Organ Dysfunctions and Mortality Organ Dysfunctions Discharged Mortality Total Mortality Rate 0 40 (100%) 0 (0%) 40 0% 1 35 (100%) 0 (0%) 35 0% 2 35 (97.2%) 1 (2.8%) 36 2.8% 3 38 (80.9%) 9 (19.1%) 47 19.1% 4 7 (18.9%) 30 (81.1%) 37 81.1% 5 0 (0%) 15 (100%) 15 100% Total 155 55 210 26.2% χ²=92.405; p=0.001 Mortality increased sharply with the number of organ dysfunctions (p=0.001). Patients with no or single organ dysfunction had 100% survival, while those with two organ dysfunctions had a small mortality rate (2.8%). However, mortality rose steeply with three organ dysfunctions (19.1%), four (81.1%) and reached 100% in patients with five organ dysfunctions. This highlights the strong predictive value of multiple organ dysfunctions for poor outcomes. Table 6: PELOD-2 Score Performance in Predicting Mortality PELOD-2 Score Discharged Mortality Total <8 139 (97.2%) 4 (2.8%) 143 ≥8 16 (23.9%) 51 (76.1%) 67 Total 155 55 210 PELOD-2 scores showed high diagnostic accuracy for mortality prediction. Among patients with scores <8, 97.2% survived and only 2.8% died, whereas scores ≥8 were associated with a mortality rate of 76.1%. The score demonstrated a sensitivity of 92.7%, specificity of 89.7%, PPV of 76.1% and NPV of 97.2%. These results validate PELOD-2 as a reliable tool in predicting outcomes in pediatric shock. Outcome Analysis Based on Shock Characteristics The overall mortality rate was 26.19% (55 patients) with significant variations based on shock etiology (χ²=69.101; P=0.001). Neurogenic shock showed the highest mortality (100%), followed by cardiogenic shock (66.7%), while hypovolemic shock had the lowest mortality rate (2.9%). Septic shock, despite being the most common, contributed to 47.3% of total mortality cases. Age emerged as a significant determinant of outcome (χ²=14.178; P=0.007) with the 1-11 month group showing the highest mortality rate (30.4%), followed by the ≥144 month group (29.3%). The 12-23 month group had the most favorable outcome with only 5.6% mortality. Decompensated shock was associated with extremely high mortality (90.7%) compared to compensated shock (3.8%), demonstrating the critical importance of early recognition and intervention (χ²=156.685; P=0.001).

This comprehensive analysis of pediatric shock in a tertiary care setting provides crucial insights into the clinical presentation, management challenges and prognostic factors influencing patient outcomes. Our findings align with and extend previous research while highlighting important regional considerations in shock management. The female predominance observed in our study (58.09% females vs 41.91% males) contrasts with Wong et al. (2015)10 large-scale analysis of 5,100 pediatric shock cases, which showed a male predominance of 52.8%. This difference might reflect regional variations or referral patterns in our study population. The age distribution showing peaks in both 1-11 months (26.7%) and ≥144 months (27.6%) aligns with Schlapbach et al. (2018)11 international point-prevalence study, which reported similar age-related incidence peaks. Our etiological distribution identified septic shock as the predominant type (50%), followed by hypovolemic shock (32.85%). These findings align with Morin et al. (2016)12 analysis of 3,762 pediatric shock cases, which reported septic shock in 47.9% and hypovolemic shock in 29.8% of cases. This is consistent with Singh et al. (2006)13, who found hypovolemic shock as the most prevalent type, followed by septic and cardiogenic shock. However, our study demonstrated higher mortality rates in septic shock patients in the decompensated stage, supporting Singh et al. (2006)13 conclusion that hypovolemic shock had the best prognosis while septic shock had the worst. The analysis of physiological parameters revealed strong correlations with shock severity. The 92.6% incidence of respiratory distress in decompensated shock exceeded rates reported by Chen et al. (2017)14 study of 2,345 patients (83.7%) and Kumar et al. (2014)15 multicenter analysis of 1,983 cases (87.2%). The high rate of invasive ventilation requirement (92.6% in decompensated shock) surpassed figures from Rodriguez et al. (2021)16 international cohort study reporting 82.4% ventilation rates. This finding aligns with Ranjit S et al. (2013)17, who showed that ventilator support was essential for children with fluid- and inotrope-refractory septic shock, yet it was associated with high mortality rates. Our findings regarding pulse characteristics and neurological status align with Lee EP et al. (2017)18, who found that low systemic vascular resistance and reduced cardiac index were critical hemodynamic predictors of mortality in pediatric septic shock. The significant correlation between Glasgow Coma Score and shock severity (p=0.001) supports the importance of neurological assessment in prognostication. The laboratory parameters demonstrated clear metabolic and organ-specific changes associated with shock severity. Elevated lactate levels in decompensated shock (6.80±7.14 mmol/L vs 2.37±2.32 mmol/L; p=0.001) align with Munde A et al. (2014)19 findings that lactate clearance was a reliable marker for predicting mortality. The significant elevation in renal function tests reflects the kidney's vulnerability to hypoperfusion, consistent with Kaddourah et al. (2017)20 AWARE study findings. The relationship between organ dysfunction and mortality showed a clear progression with mortality increasing from 0% with no dysfunction to 100% with five dysfunctions. This progression closely matches Leclerc et al. (2017)21 prospective multicenter study and supports findings by Kurade A et al. (2016)6, who reported that multiorgan dysfunction syndrome was the most common complication in pediatric septic shock. Similarly, Bhatta M et al. (2021)22 and Sankar J et al. (2024)23 reported that sepsis with multiple organ failure had the highest mortality rates (50-60%). The PELOD-2 score analysis demonstrated excellent predictive value with scores ≥8 showing 92.7% sensitivity and 89.7% specificity. These values exceed those reported in Leteurtre et al. (2013)24 validation study (sensitivity 86%, specificity 82%) and align with Jeevan GJ et al. (2017)25 findings that PRISM III scores were significantly higher in non-survivors. The outcome analysis revealing highest mortality rates in neurogenic (100%) and cardiogenic shock (66.7%) aligns with recent studies by Wong et al. (2012)26 and Davis et al. (2017)27. Our septic shock mortality rate (24.8%) was higher than Fisher JD et al. (2010)28 reported 5% in developed settings, suggesting differences in healthcare access and treatment protocols. This aligns with Santschi M et al. (2013)29 findings that adherence to international sepsis resuscitation guidelines was low in developing countries. The high mortality in decompensated shock (90.7%) underscores the critical importance of early recognition and intervention. This finding supports Deshmukh CT et al. (2020)30 emphasis on early identification of systemic inflammatory response syndrome to prevent progression to septic shock.

This comprehensive analysis highlights the significant clinical, physiological and laboratory distinctions between compensated and decompensated shock in pediatric patients. Age, pupillary response, respiratory distress, pulse quality and need for invasive ventilation emerged as strong predictors of shock severity. Etiological analysis revealed septic and cardiogenic shock as the leading contributors to decompensated states and higher mortality, while hypovolemic shock was more commonly associated with better outcomes. A greater number of organ dysfunctions was directly correlated with increased mortality, further underscoring the progressive nature of multi-organ failure in shock. Neurological status, as assessed by the Glasgow Coma Score and PELOD-2 scoring system, showed strong predictive value for patient outcomes with higher scores clearly indicating worse prognosis. While certain postoperative and biochemical parameters did not significantly vary between shock types, the overall data affirms that early identification and aggressive management of decompensated shock are crucial in improving survival. Moreover, the high sensitivity and specificity of both severity classification and PELOD-2 scoring support their utility in clinical decision-making and triage. These findings reinforce the value of a multifactorial approach in the assessment and management of pediatric shock, combining bedside clinical signs with structured scoring systems for optimal patient outcomes.

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