ABSTRACT
BACKGROUND:
Crush Syndrome is a major cause of morbidity and mortality following large-scale catastrophic earthquakes. Since there are no randomized controlled studies on Crush Syndrome, knowledge on this subject is limited to expert experience. The primary objective is to analyze the epidemiological and demographic characteristics, clinical outcomes, and mortality factors of earthquake victims after the Pazarcik and Elbistan earthquakes on February 6, 2023.
METHODS:
This cross-sectional and observational retrospective study evaluated 610 earthquake victims who presented to our center between February 6 and April 30, 2023. Among these patients, 128 with Crush Syndrome were included in the study. Patient information was gathered from hospital records during their stay and from national registries upon referral. The primary outcome was to identify risk factors for mortality. Demographic and laboratory data were analyzed by acute kidney injury (AKI) stages; mortality-affecting factors were identified through regression analysis.
RESULTS:
Of the 128 Crush Syndrome patients (100 adults, 28 children), 64 were female. The AKI rate was 32.8%. Among patients with AKI, the frequency of hemodialysis requirement was 69%, and the mortality rate was 14.2%. The overall mortality rate for patients with Crush Syndrome was 4.6%, compared to 3.9% (19/482) in earthquake victims without Crush Syndrome (p=0.705). Notably, low systolic blood pressure at admission was the only factor significantly affecting mortality in Crush Syndrome patients (Hazard Ratio [HR]: 1.088, p=0.021, 95% Confidence Interval [CI]).
CONCLUSION:
Our study highlights low systolic blood pressure upon admission as a significant risk factor for increased mortality in Crush Syndrome patients. This finding may contribute to the literature by emphasizing the importance of monitoring blood pressure under rubble and administering more aggressive fluid therapy to patients with low systolic blood pressure.
Keywords: Crush Syndrome, Pazarcik, Elbistan earthquake, renal disaster
INTRODUCTION
Crush Syndrome, also known as traumatic rhabdomyolysis, occurs when all or a part of the body is subjected to significant pressure.[1] Earthquakes are the primary causes of this syndrome, although other situations, such as building collapses, being trapped under heavy objects for extended periods, or traffic accidents, can also lead to Crush Syndrome. The most important factor influencing the development of Crush Syndrome is the severity and duration of the compression. In treating Crush Syndrome, the rapid initiation of fluid replacement is considered the gold standard to prevent acute kidney injury and related mortality. Current guidelines recommend administering isotonic saline at a rate of 1 liter per hour for adults, starting as soon as possible after rescue.[2]
The rarity of large-scale disasters leading to a high number of Crush Syndrome patients and the impossibility of conducting randomized controlled studies underscores the critical importance of sharing experiences. This is crucial for developing more effective treatment algorithms. For instance, the medical records of 600 patients who required dialysis after the earthquake in Japan in 2011 and their subsequent relocation were analyzed based on knowledge gained from previous earthquakes.[3] In an effort to contribute to the development of new algorithms for treating Crush Syndrome, our study aims to identify mortality factors in Crush Syndrome patients following the dual earthquakes in Pazarcik on February 6, 2023, at 04:17, and in Elbistan at 13:24, with magnitudes of 7.7 and 7.6 on the Richter Scale, respectively. Additionally, our study seeks to determine the morbidity and mortality rates following treatment.
MATERIALS AND METHODS
Definitions: All individuals extracted from the rubble and admitted to our hospital were classified as earthquake victims. The creatinine level upon hospital admission was considered the baseline creatinine. Acute kidney injury (AKI) levels were classified according to the Acute Kidney Injury Network (AKIN) criteria. In AKIN staging, stage 1 AKI is defined by a serum creatinine increase of 0.3 mg/dL or an increase to 1.5 times the baseline value, or a decrease in urine output (oliguria <0.5 mL/kg/hour for six hours) within 48 hours. Stage 2 AKI is defined by a two to threefold increase in the creatinine value compared to the baseline, or a urine output of <0.5 mL/kg/hour over 12 hours. Stage 3 AKI criteria include a more than threefold increase in the creatinine value or a level of >4 mg/dL, or a decrease in urine output (<0.3 mL/kg/hour for 24 hours or anuria for 12 hours). Despite being a retrospective study, patient adherence to the current protocol was closely monitored from initial admission to discharge, with all findings recorded.
Patients with serum creatine kinase (CK) >1000 U/L and oliguria (less than 500 cc urine per day), exhibiting at least one of the following parameters, were diagnosed with Crush Syndrome: serum blood urine nitrogen (BUN) >40 mg/dL, serum creatinine >2.0 mg/dL, serum uric acid >8 mg/dL, serum potassium >6 mEq/L, serum phosphorus >8 mg/dL, or serum calcium <8 mg/dL.[4]
Patients and Treatment: Following the earthquake, the Emergency Command System was activated, and trauma teams were formed. All individuals rescued from the rubble and admitted to our hospital were treated as earthquake victims. The adult and pediatric nephrology clinics implemented the Standard Crush Syndrome Emergency Nephrology Protocol (CSENP). According to the CSENP, if the earthquake victim had not received fluid therapy under the rubble, an initial administration of 1000 cc 0.9% Sodium chloride (NaCl) per hour was given upon arrival at the emergency room. This was followed by a maintenance fluid therapy of 500 cc 0.9% NaCl per hour until reaching a total of 3000 cc. After administering 3000 cc, urine output was closely monitored. If urine output was present, the infusion of 100 cc of 0.9% NaCl per hour continued. In the absence of urine output, the rate was reduced to 50 cc of 0.9% NaCl per hour. Urine output was regularly monitored, and a catheter was inserted when necessary. For pediatric patients, 0.9% NaCl was initiated at a rate of 15-20 mL/kg/hour, aiming for a urine output of approximately 3-4 mL/kg/hour.
If the patient presented with anuria upon admission, urine output of less than 50 cc/hr, elevated creatinine, brown urine color, potassium level greater than 5.5 mEq/L, pH less than 7.20, HCO3 less than 15 meq/L, and lactate less than 2 mmol/ L, the team was instructed to urgently consult the Nephrology clinic. Initial hospitalization assessments included blood glucose, serum levels of sodium, potassium, calcium, phosphorus, BUN, creatinine, uric acid, CK, albumin, alanine aminotransferase (ALT), aspartate aminotransferase (AST), total and direct bilirubin, International Normalized Ratio (INR), urinalysis, C-Reactive Protein (CRP), venous blood gas, electrocardiography (ECG), and chest X-ray.
Upon arrival at the emergency department, all patients were triaged and evaluated according to the Advanced Trauma Life Support (ATLS) guidelines, version 10. Tetanus prophylaxis was administered to all patients, with Tetanus Immunoglobulin given to those with contaminated wounds. Prior to hospitalization, open wounds and fractures were debrided by irrigating with physiological saline solution; primary suturing was performed, and antibiotic therapy (Cefazolin 1 g, intravenously [IV]) was administered. All fractures were immobilized with a splint. Based on the results, patients were referred to the appropriate departments for hospitalization in either the general ward or the intensive care unit. Patients requiring emergent surgical interventions, such as fasciotomy or amputation, were immediately taken to the operating room. The Mangled Extremity Severity Score (MESS) was utilized to guide decisions regarding amputation in cases of crushed extremities. A joint decision-making process was undertaken among the departments of plastic surgery, orthopedics, and pediatric nephrology, particularly regarding the necessity and extent of amputation for crushed extremities in children. Patients referred to external centers for reconstructive surgery and physical rehabilitation therapy were contacted by phone, and information was obtained through national medical records.
The study was designed retrospectively. The Institutional Review Board of Baskent University Medical and Health Sciences waived the requirement for informed consent, as this study involved a retrospective review of existing data. The Baskent University Medical and Health Sciences Research Board approved this study (Project Number: KA23/168) and it was supported by the Baskent University Research Fund. This study adhered to the ethical principles outlined in the Declaration of Helsinki. The authors declare no conflicts of interest.
Blood Pressure Measurement
Blood pressure was measured using five calibrated Erka Switch 2.0 aneroid manual sphygmomanometers upon the patients’ admission to the emergency department. The obtained blood pressure values were recorded in the medical records. Pediatric patients were evaluated according to their percentile ranges.
Statistical Evaluation
For statistical evaluation, the Statistical Package for the Social Sciences (SPSS) 18.0 for Windows was utilized. Descriptive statistics such as minimum and maximum values, mean, and standard deviation were calculated for quantitative data; numbers and percentages were used for qualitative data. In comparing the groups, the Chi-square and Fisher’s Exact tests were applied to categorical variables; the One-Way Analysis of Variance (ANOVA) was utilized for continuous variables with a normal distribution when comparing more than two groups; the Kruskal-Wallis test was employed for variables without normal distribution. The Bonferroni test was conducted for post hoc comparisons. Logistic regression analysis was performed to assess the effect of independent variables on the dependent variable. A significance level of p<0.05 was set for the evaluations.
RESULTS
The total number of earthquake victims admitted to our hospital was 610 (287 males, 323 females). Of these, 111 were under 18 years of age (mean age: 8.64 years, min/max: 3 months/17 years), and 499 were 18 years or older (mean age: 48.8 years, min/max: 18 years/89 years). Four hundred and one patients were hospitalized, while 209 were treated as outpatients. Geographically, 543 patients were from Hatay, 19 from Kahramanmaras, 18 from Gaziantep, and 30 from other provinces.
Among the 610 patients, 128 (100 adults, 28 children) were diagnosed with Crush Syndrome, with 64 being male (min/max: 1 year/89 years). Table 1 displays the demographic data of patients with Crush Syndrome. Table 2 outlines the urine findings, vital signs, and laboratory values at first admission for patients with Crush Syndrome.
Table 1.
Demographic data of patients with Crush Syndrome
| Variables | Number of Patients (Total, n=128) |
|---|---|
| Age (years, min-max) | 35.9±21.91 (1-89) |
| Gender Distribution (M/F, n/%) | 64/64 (50%/50%) |
| Average Time Under Rubble (hours, min-max) | 29.13±27.96 (1-120) |
| Presence of Venous Line on Admission | |
| Yes (n/%) | 119 (93%) |
| No (n/%) | 9 (7%) |
| Comorbidities | 34/85 (28.6%/71.4%) |
| Hypertension | 16 (13.4%) |
| Diabetes Mellitus | 8 (6.7%) |
| Coronary Artery Disease | 8 (6.4%) |
| Chronic Kidney Disease | 16 (12.5%) |
| Other | 11 (9.2%) |
| Extremity Trauma | 109 (86.5%) |
| Abdominal Trauma | 9 (7%) |
| Thoracic Trauma | 19 (85%) |
| Erythrocyte Transfusion (n) | 34 (163 units in total) |
| Albumin Infusion (n) | 1 |
| Mannitol Infusion (n) | 18 (6,450 cc in total) |
Table 2.
Macroscopic urine and laboratory findings of Crush Syndrome
| Variables | %/Mean±SD/Median |
|---|---|
| Urine Color on Admission | |
| Yellow (n/%) | 101 (88.6%) |
| Brown (n/%) | 13 (10.2%) |
| CRP (mg/dL) | 94.21±64.21 |
| CK (U/L) | Min: 1425 - Max: 203,995, Median:16,650* |
| BUN (mg/dL) | 34.13±29.12 |
| Creatinine (mg/dL) | 1.59±1.55 |
| Sodium (mmol/L) | 135.56±5.92 |
| Potassium (mmol/L) | 4.67±1.07 |
| Calcium (mg/dL) | 8±0.99 |
| Phosphorus (mg/dL) | 3.9±1.76 |
| Albumin (g/L) | 29.1±5.42 |
| Hgb (g/dL) | 12.6±3.6 |
| Leukocyte (x109/L) | 15.61±6.05 |
| Neutrophils (x109/L) | 78.08±10.45 |
| Lymphocytes (x109/L) | 13,24±11,07 |
| Platelets (x109/L) | 236.71±84.37 |
| Uric Acid (mg/dL) | 5.73±3.62 |
| LDH (U/L) | Min: 151 – Max: 7.443, Median: 813* |
| AST (U/L) | Min: 3 – Max: 6.023, Median: 241* |
| ALT (U/L) | Min: 6 – Max: 5.206, Median: 116* |
| HCO3 (mmol/L) | 21.12±4.98 |
Abbreviations: ALT: Alanine Aminotransferase; AST: Aspartate Aminotransferase; BUN: Blood Urea Nitrogen; CK: Creatine Kinase; CRP: C-Reactive Protein; HCO3: Bicarbonate; Hgb: Hemoglobin; LDH: Lactate Dehydrogenase; N/A: Not Applicable; SD: Standard Deviation.
The median value is indicated when the standard deviation exceeds the mean value.
Table 3 compares the laboratory findings of patients without AKI and those with Crush Syndrome and stages 1, 2, and 3 AKI, including post hoc comparisons. Twenty-nine of the 42 patients who developed AKI required hemodialysis (HD). For HD access, the internal jugular vein was the preferred route for intravenous access in 96.6% of the patients, while the femoral vein was chosen in 3.4%. No severe complications occurred during any HD session.
Table 3.
Comparison of laboratory values upon admission in patients with Crush Syndrome by AKI stage
| Variables | Crush Syndrome without AKI (n=86) | Stage 1 AKI (n=11) | Stage 2 AKI (n=15) | Stage 3 AKI (n=16) | Groups | P Value | |||
|---|---|---|---|---|---|---|---|---|---|
|
| |||||||||
| Crush Syndrome without AKI | Stage 1 AKI | Stage 2 AKI | Stage 3 AKI | ||||||
| The Average Hour Under the Rubble (hour) | 27.64±28.42 | 24.25±31.96 | 44.6±32.81 | 22.55±16.35 | CS without AKI | * | * | * | 0.497 |
| Stage 1 AKI | |||||||||
| Stage 2 AKI | |||||||||
| Stage 3 AKI | |||||||||
| Age (years) | 34.60±22.27 | 43.50±25.71 | 40.73±20.28 | 32.81±18.89 | CS without AKI | * | * | * | 0.359 |
| Stage 1 AKI | |||||||||
| Stage 2 AKI | |||||||||
| Stage 3 AKI | |||||||||
| Gender (M/F) | 43/43 | 6/5 | 8/7 | 7/9 | CS without AKI | * | * | * | 0.405 |
| Stage 1 AKI | |||||||||
| Stage 2 AKI | |||||||||
| Stage 3 AKI | |||||||||
| Stage 1 AKI | |||||||||
| Stage 2 AKI | |||||||||
| Stage 3 AKI | |||||||||
| CRP Ref. range (< 2.0 mg/L) | 76.73±57.77 | 112.79±68.63 | 130.46±62.61 | 135.37±63.1 | CS without AKI | * | 0.544 | 0.012 | 0.005 |
| Stage 1 AKI | 0.544 | * | 1.000 | 1.000 | |||||
| Stage 2 AKI | 0.012 | 1.000 | * | 1.000 | |||||
| Stage 3 AKI | 0.005 | 1.000 | 1.000 | * | |||||
| CK Ref. range (30-200 U/L) | 7392.00 | 8415.00 | 59519.00 | 67450.50 | CS without AKI | * | 1.000 | 0.001 | 0.001 |
| Stage 1 AKI | 1.000 | * | 0.001 | 0.001 | |||||
| Stage 2 AKI | 0.001 | 0.001 | * | 1.000 | |||||
| Stage 3 AKI | 0.001 | 0.001 | 1.000 | * | |||||
| BUN Ref. range (8-23 mg/dL) | 17.44 | 48.21 | 50.28 | 64.27 | CS without AKI | * | 0.001 | 0.001 | 0.001 |
| Stage 1 AKI | 0.001 | * | 1.000 | 1.000 | |||||
| Stage 2 AKI | 0.001 | 1.000 | * | 1.000 | |||||
| Stage 3 AKI | 0.001 | 1.000 | 1.000 | * | |||||
| Creatinine Ref. range (0.7-1.3 mg/dL) | 0.65 | 1.68 | 2.65 | 4.21 | CS without AKI | * | 0.001 | 0.001 | 0.001 |
| Stage 1 AKI | 0.001 | * | 0.001 | 0.001 | |||||
| Stage 2 AKI | 0.001 | 0.001 | * | 0.001 | |||||
| Stage 3 AKI | 0.001 | 0.001 | 0.001 | * | |||||
| Sodium Ref. range (136–145 mmol/L) | 136.53±4.42 | 136.5±8.34 | 134±6.97 | 131.44±8.2 | CS without AKI | * | 1.000 | 0.702 | 0.009 |
| Stage 1 AKI | 1.000 | * | 1.000 | 0.179 | |||||
| Stage 2 AKI | 0.702 | 1.000 | * | 1.000 | |||||
| Stage 3 AKI | 0.009 | 0.179 | 1.000 | * | |||||
| Calcium Ref. range (8.8-10 mg/dL) | 7.7±0.81 | 8.49±0.58 | 7.31±0.59 | 6.98±1.3 | CS without AKI | * | 1.000 | 0.001 | 0.001 |
| Stage 1 AKI | 1.000 | * | 0.010 | 0.001 | |||||
| Stage 2 AKI | 0.001 | 0.010 | * | 1.000 | |||||
| Stage 3 AKI | 0.001 | 0.001 | 1.000 | * | |||||
| Phosphorus Ref. range (2.3-4.7 mg/dL) | 3.17±1.15 | 4.16±1.62 | 4.93±1.89 | 5.64±2.12 | CS without AKI | * | 0.422 | 0.001 | 0.001 |
| Stage 1 AKI | 0.422 | * | 1.000 | 0.147 | |||||
| Stage 2 AKI | 0.001 | 1.000 | * | 1.000 | |||||
| Stage 3 AKI | 0.001 | 0.147 | 1.000 | * | |||||
| Albumin Ref. range (33-46 g/L) | 31.76±5.55 | 29.56±2.26 | 25.38±3.98 | 26.23±3.54 | CS without AKI | * | 1.000 | 0.001 | 0.034 |
| Stage 1 AKI | 1.000 | * | 0.595 | 1.000 | |||||
| Stage 2 AKI | 0.001 | 0.595 | * | 1.000 | |||||
| Stage 3 AKI | 0.034 | 1.000 | 1.000 | * | |||||
| Hgb Ref. range (13.5-18 g/dL) | 12.36±3.03 | 12.54±3.09 | 14.48±3.36 | 12.12±2.5 | CS without AKI | * | 1.000 | 0.081 | 1.000 |
| Stage 1 AKI | 1.000 | * | 0.703 | 1.000 | |||||
| Stage 2 AKI | 0.081 | 0.703 | * | 0.188 | |||||
| Stage 3 AKI | 1.000 | 1.000 | 0.188 | * | |||||
| Leukocyte Ref. range (4.5-11 x109/L) | 14.38±5.3 | 16.72±6.46 | 19.16±4.98 | 18.24±8.34 | CS without AKI | * | 1.000 | 0.032 | 0.100 |
| Stage 1 AKI | 1.000 | * | 1.000 | 1.000 | |||||
| Stage 2 AKI | 0.032 | 1.000 | * | 1.000 | |||||
| Stage 3 AKI | 0.100 | 1.000 | 1.000 | * | |||||
| Neutrophils Ref. range (2-7.8 x109/L) | 76.17±11.59 | 79.96±8.15 | 84.4±5.16 | 81.03±5.14 | CS without AKI | * | 1.000 | 0.028 | 0.493 |
| Stage 1 AKI | 1.000 | * | 1.000 | 1.000 | |||||
| Stage 2 AKI | 0.028 | 1.000 | * | 1.000 | |||||
| Stage 3 AKI | 0.493 | 1.000 | 1.000 | * | |||||
| Lymphocytes Ref. range (0.9-5.06 x109/L) | 11.89 | 10.02 | 5.61 | 9.32 | CS without AKI | * | 1.000 | 0.036 | 0.363 |
| Stage 1 AKI | 1.000 | * | 1.000 | 1.000 | |||||
| Stage 2 AKI | 0.036 | 1.000 | * | 1.000 | |||||
| Stage 3 AKI | 0.363 | 1.000 | 1.000 | * | |||||
| Platelets Ref. range (150-400 x109/L) | 245.31±88.4 | 229.98±49.07 | 230.37±65.25 | 201.72±91.67 | CS without AKI | * | 1.000 | 1.000 | 0.359 |
| Stage 1 AKI | 1.000 | * | 1.000 | 1.000 | |||||
| Stage 2 AKI | 1.000 | 1.000 | * | 1.000 | |||||
| Stage 3 AKI | 0.359 | 1.000 | 1.000 | * | |||||
| Uric Acid Ref. range (3.7-7.7 mg/dL) | 4.18±2.26 | 7.69±3.7 | 8.17±3.83 | 9.11±4.36 | CS without AKI | * | 0.015 | 0.000 | 0.000 |
| Stage 1 AKI | 0.015 | * | 1.000 | 1.000 | |||||
| Stage 2 AKI | 0.001 | 1.000 | * | 1.000 | |||||
| Stage 3 AKI | 0.001 | 1.000 | 1.000 | * | |||||
| LDH Ref. range (120-246 U/L) | 569.00 | 710.00 | 1614.50 | 2153.50 | CS without AKI | * | 1.000 | 0.013 | 0.018 |
| Stage 1 AKI | 1.000 | * | 0.219 | 0.214 | |||||
| Stage 2 AKI | 0.013 | 0.219 | * | 1.000 | |||||
| Stage 3 AKI | 0.018 | 0.214 | 1.000 | * | |||||
| AST Ref. range (0-45 U/L) | 137.00 | 268.50 | 533.00 | 1166.50 | CS without AKI | * | 1.000 | 0.006 | 0.001 |
| Stage 1 AKI | 1.000 | * | 0.185 | 0.001 | |||||
| Stage 2 AKI | 0.006 | 0.185 | * | 0.009 | |||||
| Stage 3 AKI | 0.001 | 0.001 | 0.009 | * | |||||
| ALT Ref. range (0-45 U/L) | 79.00 | 145.50 | 307.00 | 541.00 | CS without AKI | * | 1.000 | 0.285 | 0.001 |
| Stage 1 AKI | 1.000 | * | 1.000 | 0.005 | |||||
| Stage 2 AKI | 0.285 | 1.000 | * | 0.118 | |||||
| Stage 3 AKI | 0.001 | 0.005 | 0.118 | * | |||||
| HCO3 Ref. range (21-26 mmol/L) | 23.59±3.62 | 21.17±5.23 | 19.71±3.53 | 17.79±7.75 | CS without AKI | * | 0.785 | 0.023 | 0.001 |
| Stage 1 AKI | 0.785 | * | 1.000 | 0.456 | |||||
| Stage 2 AKI | 0.023 | 1.000 | * | 1.000 | |||||
| Stage 3 AKI | 0.001 | 0.456 | 1.000 | * | |||||
Abbreviations: AKI: Acute Kidney Injury; ALT: Alanine Aminotransferase; AST: Aspartate Aminotransferase; BUN: Blood Urea Nitrogen; CK: Creatine Kinase; CRP: C-Reactive Protein; CS: Crush Syndrome; HCO3: Bicarbonate; Hgb: Hemoglobin; LDH: Lactate Dehydrogenase; Ref. Range: Reference Range.
In the non-survivor group, levels of CK, BUN, creatinine, potassium, AST, ALT, and the number of hemodialysis sessions were statistically higher, while serum levels of calcium and bicarbonate, platelets, and systolic blood pressure were statistically lower compared to the survivor group (Table 4). Regression analysis indicated that lower systolic blood pressure at the time of admission significantly increased mortality in patients with Crush Syndrome (p=0.021, Hazard Ratio [HR]: 1.088, 95% Confidence Interval [CI]) (Table 5).
Table 4.
Comparison of non-survivors and survivors among patients with Crush Syndrome
| Variables | Non-Survivors (n=6) | Survivors (n=122) | P |
|---|---|---|---|
| Age | 51.50±21.70 | 35.42±21.65 | 0.078 |
| Gender M/F | 5 (83.3%)/1 (16.7%) | 57 (47.5%)/63 (52.5%) | 0.112 |
| The Average Time Under the Rubble (hour) | 33.67±18.34 | 29.19±28.56 | 0.790 |
| Peripheral Venous Line on Admission | 5(83.3%) | 112(93.3%) | 0.365 |
| CRP (mg/dL) | 143.92±102.77 | 92.3±60.94 | 0.275 |
| CK (U/L) | 58616 | 15452 | 0.040 |
| BUN (mg/dL) | 46.77 | 23.53 | 0.021 |
| Creatinine (mg/dL) | 3.63 | 0.83 | 0.003 |
| Sodium (mmol/L) | 134.33±7.5 | 135.61±5.89 | 0.610 |
| Potassium (mmol/L) | 6.08±1.55 | 4.6±1.01 | 0.001 |
| Calcium (mg/dL) | 7.06±0.73 | 8.04±0.99 | 0.031 |
| Phosphorus (mg/dL) | 5.2±1.04 | 3.81±1.76 | 0.179 |
| Albumin (g/L) | 25.4±6.8 | 29.33±5.33 | 0.227 |
| Hgb (g/dL) | 10.54±2.64 | 12.71±3.07 | 0.092 |
| Leukocyte (x109/L) | 16.21±8.63 | 15.55±6 | 0.813 |
| Neutrophils (x109/L) | 81.29±7.79 | 77.88±10.6 | 0.439 |
| Lymphocytes (x109/L) | 9.25 | 10.57 | 0.673 |
| Platelets (x109/L) | 168.3±78.49 | 239.84±83.7 | 0.043 |
| Uric Acid (mg/dL) | 6.57±2.14 | 5.67±3.65 | 0.674 |
| LDH (U/L) | 908.5 | 851 | 0.852 |
| AST (U/L) | 973 | 217 | 0.006 |
| ALT (U/L) | 405 | 114 | 0.015 |
| HCO3 (mmol/L) | 16.03±8.2 | 22.42±4.58 | 0.002 |
| Systolic Blood Pressure (SBP) (mmHg) | 86.67±16.33 | 110.88±18.72 | 0.002 |
| DBP (mmHg) | 56.67±10.33 | 67.68±13.44 | 0.051 |
| Pulse (beats/min) | 96.83±22.42 | 103.75±20.75 | 0.429 |
| Respiration Rate* | |||
| (per min) | 20 | 20 | 0.059 |
| Fasciotomy | 2 (33.3%) | 22(18.3%) | 0.321 |
| Amputation | 1 | 10 | 0.352 |
| Culture Positivity on Pus or Tissue | 0 | 13 | 0.513 |
| Bacteriemia | |||
| in Other Cultures | 2 (40%) | 31 (26.5%) | 0.611 |
| AKI Stage | |||
| Stage 1 | 0 (0%) | 9 (25.7%) | 0.423 |
| Stage 2 | 2 (40%) | 13 (37.1%) | |
| Stage 3 | 3 (60%) | 13 (37.1%) | |
| Hemodialysis | |||
| (number of patients) | 4 | 25 | 0.028 |
median. Abbreviations: AKI: Acute Kidney Injury; ALT: Alanine Aminotransferase; AST: Aspartate Aminotransferase; BUN: Blood Urea Nitrogen; CK: Creatine Kinase; CRP: C-Reactive Protein; DBP: Diastolic Blood Pressure; HCO3: Bicarbonate; Hgb: Hemoglobin; LDH: Lactate Dehydrogenase; SBP: Systolic Blood Pressure.
Table 5.
Multiple regression analysis of mortality in Crush Syndrome
| Variables | B | p | Exp (B) | 95% CI for EXP (B) | |
|---|---|---|---|---|---|
|
| |||||
| Lower | Upper | ||||
| Systolic BP on Admission (mmHg) | 0.084 | 0.021 | 1.088 | 1.013 | 1.168 |
| Creatinine on Admission | |||||
| (mg/dL) | -0.026 | 0.952 | 0.974 | 0.420 | 2.258 |
| Potassium on Admission | |||||
| (mmol/L) | -0.672 | 0.348 | 0.511 | 0.126 | 2.077 |
| Calcium on Admission | |||||
| (mg/dL) | 1.317 | 0.142 | 3.734 | 0.644 | 21.663 |
| AST on Admission | |||||
| (U/L) | 0.002 | 0.329 | 1.002 | 0.998 | 1.006 |
| HCO3 on Admission | |||||
| (mmol/L) | 0.121 | 0.301 | 1.128 | 0.897 | 1.419 |
Abbreviations: AST: Aspartate Aminotransferase; BP: Blood Pressure; HCO3: Bicarbonate.
Serum CK levels measured at the first admission were significantly higher in patients who underwent fasciotomy compared to those who underwent amputation (57809.1±6039.37 U/L vs. 25754.27±18047.68 U/L, p=0.021). No significant difference was found in other parameters (for details, see Supplementary Table 1). Nine patients received hyperbaric oxygen therapy, of whom one could not survive due to septicemia (for details, see Supplementary Table 2). Six of the Crush Syndrome patients who developed AKI at different stages succumbed to various causes, such as heart failure, hyperkalemia, hypovolemic shock, disseminated intravascular coagulation (DIC), and septic shock (for details, see Supplementary Table 3).
DISCUSSION
The incidence of Crush Syndrome is reported to be 2-5% among earthquake victims and 30-50% among patients with post-traumatic rhabdomyolysis.[5] In our study, the incidence of Crush Syndrome was found to be 20.9% among all earthquake victims. Trauma-related deaths tend to be proportionally higher in earthquakes occurring during the daytime compared to deaths due to Crush Syndrome. Conversely, traumas due to crushing and Crush Syndrome are proportionally more common in earthquakes that occur at night, as people are mostly in sleeping positions. The timing (04:17 a.m.) and the extensive geography affected by the Kahramanmaras-Pazarcik earthquake, which resulted in over 50,000 deaths, may explain the higher rate of Crush Syndrome observed in our study.
The leading cause of mortality following Crush Syndrome is known to be acute kidney injury resulting from rhabdomyolysis. Current protocols advocate for the initiation of fluid replacement therapy while earthquake victims are still trapped under the rubble. In our study, the rate of intravenous fluid treatment in patients with Crush Syndrome at the time of admission was high (93%), owing to the lessons learned from the 1999 Marmara Earthquake and the prompt organization of the Renal Disaster Group by the Turkish Society of Nephrology.[6]
Biochemical abnormalities characteristic of rhabdomyolysis-related AKI include hyperkalemia, hyperphosphatemia, hypocalcemia (although hypercalcemia may be observed during recovery), elevated CK, and low fractional sodium excretion, which can pose life-threatening risks. AKI can range from mild to severe, with some cases necessitating dialysis. Our study included 11 patients with AKIN stage 1, 15 with stage 2, and 16 with stage 3. At the first admission, levels of CK, BUN, creatinine, potassium (K), AST, and ALT were statistically significantly higher, while levels of calcium, platelets, bicarbonate, and systolic blood pressure were statistically significantly lower in patients who did not survive compared to those with Crush Syndrome who did. However, regression analysis revealed no significant differences between these groups. One potential explanation is that all patients suffered from Crush Syndrome, and the number of non-survivors was relatively small.
Although hypokalemia may occur in isolated cases of Crush Syndrome, hyperkalemia represents a life-threatening condition in these patients.[6] Hyperkalemia can arise even in the absence of AKI, as injured muscle tissues may release large amounts of potassium. Upon their first admission to our hospital, potassium levels were ≥ 5.5 mmol/L in 23 patients, while 14 patients had potassium levels ranging from 2.9 to 3.5 mmol/L. Serum potassium levels did not rise in patients with Crush Syndrome who did not develop AKI or those with stage 1 AKI. However, the average potassium level in patients with stage 2 AKI was 5.1 mmol/L, and it was 6.2 mmol/L in patients with stage 3 AKI.
During earthquakes, the mortality and morbidity rates associated with Crush Syndrome are lower among children, likely due to their smaller physique, which results in less impact.[7] In our study, the incidence of Crush Syndrome in pediatric patients was 25.2% (28 out of 111), compared to 20% (100 out of 499) in adult patients, with pediatric patients experiencing fewer renal complications. The incidence of Crush Syndrome with stage 1 AKI or higher was 33% (33 out of 100) in adults, whereas it was 32.1% (9 out of 28) in the pediatric group. Hemodialysis treatment was administered to 24% (24 out of 100) of the adult Crush Syndrome patients and 17.8% (5 out of 28) in the pediatric group. At discharge, no patient in either group required hemodialysis.
The incidence of Crush Syndrome-related AKI and the need for dialysis have varied in different studies. In a report from Bam, Iran, 6.5% of 1,975 hospitalized patients required dialysis, whereas 54% needed hemodialysis in the Kobe earthquake, and 75% in the Marmara earthquake. In the Kobe earthquake, the need for hemodialysis was directly associated with increased serum CK levels, with 84% of patients having CK levels above 75,000 units/l requiring dialysis, compared to 39% with lower CK levels.[8,9,10] In our study, the high incidence of AKI (32.8%, 42 out of 128) and the frequency of hemodialysis requirement among AKI patients (69%, 29 out of 42) may reflect the earthquake’s severity and the affected victim count. Twenty-four adults and five pediatric patients underwent dialysis in our study.
For Crush Syndrome, intermittent hemodialysis is recommended over other renal replacement methods. Compared to other methods, intermittent hemodialysis is most effective in excreting potassium, one of the primary causes of mortality.[11] Dialysis is initiated for typical indications such as volume overload, hyperkalemia, severe acidosis, and uremia. Due to the high risk of fatal hyperkalemia, frequent hemodialysis (two or even three times a day) may be indicated for patients with Crush Syndrome. Intermittent dialysis was employed in our study.
In Crush Syndrome, the use of fasciotomy is highly controversial. It has been shown that in selected cases, fasciotomy significantly contributes to the recovery of extremities within the first 24 hours. However, when performed in later stages, fasciotomy significantly increases the rates of sudden early mortality and long-term morbidity. In our study, 24 (18.7%) of 128 patients with Crush Syndrome underwent fasciotomy, and 11 (8.5%) underwent amputation. One patient (4.8%, 1/24) died following fasciotomy. When comparing the demographic and laboratory data of patients who were candidates for amputation to those selected for fasciotomy, CK and ALT levels were statistically significantly higher in the fasciotomy group. This may be due to impaired circulation in patients who underwent amputation, whereas circulation continued in patients who opted for fasciotomy. In a report from Bam, Iran, 70 of 200 patients (35%) with Crush Syndrome and acute kidney injury underwent fasciotomy, with no observed increase in morbidity or mortality.[12] In our study, regression analyses showed that neither fasciotomy nor amputation was associated with increased mortality.
In hyperbaric oxygen (HBO) therapy, 100% oxygen at a pressure above atmospheric level is administered in a hyperbaric chamber.[13] Authors have reported that various injuries, including crush injuries, can be treated with HBO therapy.[14,15] In our study, nine patients received hyperbaric therapy; eight recovered after the treatment. After the second hyperbaric session, one patient, who had undergone amputation and fasciotomy on the other leg, died due to septic shock.
Our study found that low systolic blood pressure measured during hospital admission was associated with increased mortality. Although low systolic blood pressure is an expected finding in shock that could lead to increased mortality, this association has not been previously reported in relation to Crush Syndrome. Fluid resuscitation is known to be crucial for patients with Crush Syndrome. Our findings suggest that low systolic blood pressure and increased mortality may be linked to inadequate fluid resuscitation before hospital admission.
One limitation of our study was the inability to measure the pressure exerted on the extremities after the disaster. Another limitation was its execution at a single center. Additionally, the fact that a significant portion of the patients self-transported to our hospital could introduce bias into the morbidity and mortality data concerning Crush Syndrome.
CONCLUSION
Although the regression analysis showed no significant differences due to the small number of deceased patients, elevated levels of CK, BUN, creatinine, K+, AST, ALT, along with lower levels of calcium, platelets, and bicarbonate, could be considered critical factors in the mortality associated with Crush Syndrome upon admission. Our study highlighted that low systolic blood pressure on admission is a risk factor for increased mortality in Crush Syndrome. This finding may contribute to the literature by suggesting the importance of measuring blood pressure under rubble when possible and administering more aggressive fluid therapy to patients with low systolic blood pressure.
Footnotes
Ethics Committee Approval: This study was approved by the Başkent University Adana Hospital Ethics Committee (Date: 25.04.2023, Decision No: E-94603339-604.01.02-226467).
Peer-review: Externally peer-reviewed.
Authorship Contributions: Concept: E.O., O.K., P.E., O.O.K., E.A., A.T.G., I.K., C.Y., M.M., I.G.B., H.A.T.; Design: E.O., Y.Z.D., O.K., C.C., D.Y., A.F., A.T.G., H.A.T., S.C., E.D., H.İ.S., K.T., S.E., T.A., R.G., M.K.; Supervision: M.H., D.T., R.I.C., H.M., S.B., G.P., B.A., A.N., H.A.T., S.E., T.A., R.G., M.K.; Fundings: M.H.; Materials: C.C., E.A., O.K., P.E., O.O.K., B.O., A.T., H.O.G., C.E., G.B., D.Y., S.E., T.A., K.G., M.I.K.; Data collection and/or processing: C.C., E.A., S.B., L.O., N.T., P.E., O.O.K., A.A., O.K., E.A., B.O., G.P., B.A., A.N.; Analysis and/or interpretation: L.O., N.T., Y.Z.L., O.Y. A.F., T.K., C.Y., M.M., I.G.B., T.C., S.C., E.D., O.K., H.I.S., K.T.; Literature search: D.T., R.K., H.M., S.B., A.T.G., A.A., B.O., T.C., A.T., H.O.G., C.E., G.B., D.Y., S.C., E.D., O.K., H.I.S., K.T.; Writing: E.O., D.T., R.K., H.M., S.B., L.O., L.T., M.H., O.Y., A.F.; Critical review: Y.Z.D., A.A., I.K., C.Y., M.M., I.G.B., G.P., B.A., A.N., A.T., H.O.G., C.E., G.B., D.Y.
Conflict of Interest: None declared.
Financial Disclosure: The author declared that this study has received no financial support.
REFERENCES
- 1.Gibney RT, Sever MS, Vanholder RC. Disaster nephrology:crush injury and beyond. Kidney Int. 2014;85:1049–57. doi: 10.1038/ki.2013.392. [DOI] [PubMed] [Google Scholar]
- 2.Sever MS, Lameire N, Van Biesen W, Vanholder R. Disaster nephrology:a new concept for an old problem. Clin Kidney J. 2015;8:300–9. doi: 10.1093/ckj/sfv024. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 3.Kazama JJ, Narita I. Earthquake in Japan. Lancet. 2011;377:1652–3. doi: 10.1016/S0140-6736(11)60673-9. [DOI] [PubMed] [Google Scholar]
- 4.Slater MS, Mullins RJ. Rhabdomyolysis and myoglobinuric renal failure in trauma and surgical patients:a review. J Am Coll Surg. 1998;186:693–716. doi: 10.1016/s1072-7515(98)00089-1. [DOI] [PubMed] [Google Scholar]
- 5.Bartal C, Zeller L, Miskin I, Sebbag G, Karp E, Grossman A, et al. Crush syndrome:saving more lives in disasters:lessons learned from the early-response phase in Haiti. Arch Intern Med. 2011;171:694–6. doi: 10.1001/archinternmed.2011.122. [DOI] [PubMed] [Google Scholar]
- 6.Sever MS, Erek E, Vanholder R, Kantarci G, Yavuz M, Turkmen A, et al. Marmara Earthquake Study Group. Serum potassium in the crush syndrome victims of the Marmara disaster. Clin Nephrol. 2003;59:326–33. doi: 10.5414/cnp59326. [DOI] [PubMed] [Google Scholar]
- 7.Sever MS, Erek E, Vanholder R, Akoğlu E, Yavuz M, Ergin H, et al. Marmara Earthquake Study Group. The Marmara earthquake:epidemiological analysis of the victims with nephrological problems. Kidney Int. 2001;60:1114–23. doi: 10.1046/j.1523-1755.2001.0600031114.x. [DOI] [PubMed] [Google Scholar]
- 8.Hatamizadeh P, Najafi I, Vanholder R, Rashid-Farokhi F, Sanadgol H, Seyrafian S, et al. Epidemiologic aspects of the Bam earthquake in Iran:the nephrologic perspective. Am J Kidney Dis. 2006;47:428–38. doi: 10.1053/j.ajkd.2005.11.019. [DOI] [PubMed] [Google Scholar]
- 9.Oda J, Tanaka H, Yoshioka T, Iwai A, Yamamura H, Ishikawa K, et al. Analysis of 372 patients with Crush syndrome caused by the Hanshin-Awaji earthquake. J Trauma. 1997;42:470–5. doi: 10.1097/00005373-199703000-00015. discussion 475–6. [DOI] [PubMed] [Google Scholar]
- 10.Sever MS, Erek E, Vanholder R, Koc M, Yavuz M, Ergin H, et al. Marmara Earthquake Study Group. Treatment modalities and outcome of the renal victims of the Marmara earthquake. Nephron. 2002;92:64–71. doi: 10.1159/000064487. [DOI] [PubMed] [Google Scholar]
- 11.Zager RA. Studies of mechanisms and protective maneuvers in myoglobinuric acute renal injury. Lab Invest. 1989;60:619–29. [PubMed] [Google Scholar]
- 12.Safari S, Najafi I, Hosseini M, Sanadgol H, Sharifi A, Alavi Moghadam M, et al. Outcomes of fasciotomy in patients with crush-induced acute kidney injury after Bam earthquake. Iran J Kidney Dis. 2011;5:25–8. [PubMed] [Google Scholar]
- 13.Mendy HO, Maximillian CO, Djony ET, Stianila WS, Ekanova RNS, Deanette MRA, et al. Hyperbaric oxygen therapy in the healing process of foot ulcers in diabetic type 2 patients marked by interleukin 6, vascular endothelial growth factor, and PEDIS score:a randomized controlled trial study. Int J Surg Open. 2020;27:154e61. [Google Scholar]
- 14.Saunders PJ. Hyperbaric oxygen therapy in the management of carbon monoxide poisoning, osteoradionecrosis, burns, skin grafts, and crush injury. Int J Technol Assess Health Care. 2003;19:521e5. doi: 10.1017/s026646230300045x. [DOI] [PubMed] [Google Scholar]
- 15.Shah J. Hyperbaric oxygen therapy. J. Am. Col. Certif. Wound Spec. 2010;2:9e13. doi: 10.1016/j.jcws.2010.04.001. [DOI] [PMC free article] [PubMed] [Google Scholar]