Early and Intensive Fluid Replacement Prevents Acute Renal Failure in the Crush Cases Associated with Spontaneous Collapse of an Apartment in Konya

Abstract

Background. Crush syndrome developing as a result of earthquake and other natural disasters has been investigated from many angles to date. Data are scarce, however, on cases associated with the spontaneous crash of buildings. This study presents the results on seven rhabdomyolysis patients treated in our clinics out of nine casualties who were rescued from the rubble of Zümrüt apartment after the building collapsed suddenly and spontaneously. Methods. As a result of the sudden, spontaneous collapse of the 10-floor Zümrüt apartment in Konya at 20:15 hours on February 2, 2004, 92 out of a total of 121 persons who were inside the building lost their lives, and 29 casualties were rescued from the rubble. Nine hospitalized patients had crush syndrome, and a prophylactic mannitol-bicarbonate cocktail was started in all at admission. Results. The time they remained entrapped under the rubble was 11.1 ± 7.3 (5–24 hours) on average. The highest CPK level of the patients was 79049 ± 75374 u/L (17478–223600 u/L), observed on the median day 1.7 ± 1.1 (days 1–4) following the incident. ARF developed in only two cases (28.6%) owing to the prophylactic mannitol-bicarbonate cocktail administered to prevent ARF, and because of hyperpotassemia, hemodialysis (HD) treatment was administered to these patients. One patient required two sessions of HD, and another required four. In both patients who received HD treatment, the level of potassium was in excess of 7 mEq/L. A total of eight fasciotomies were performed on five (71.4%) of the seven patients with crush syndrome. Five of the fasciotomies (62.5%) were performed on two of our patients who required HD treatment. None of our patients with crush syndrome developed permanent kidney damage, and no mortality occurred. Conclusion. It was deduced that rapid fluid therapy accompanied by the prophylactic administration of mannitol-bicarbonate are largely effective in preventing the development of ARF in cases with crush syndrome resulting from disasters.

Keywords:

• crush syndrome
• fluid treatment
• spontane collapse of building
• acute renal failure

INTRODUCTION

Clinical crush syndrome can develop secondary to traumatic events caused by accidents and earthquake, as well as non-traumatic events. Crush syndrome developing as a result of earthquake and other natural disasters has been investigated from many angles to date. Data are scarce, however, on cases associated with spontaneous crash of buildings.[1–3]

Damage occurs in myocytes with the compression of muscles, and the intracellular structures are released into the systemic circulation. This is called rhabdomyolysis.[1] Myoglobin, which is one of the intracellular structures released, is filtrated through the glomeruli and reaches the tubules to cause renal failure due to obstruction.[2] Similarly, protons, phosphate, potassium, and nucleoids released from damaged muscular tissues play an important role in crush pathophysiology. Finally, the loss of fluids in the injured plays a significant role in determining the extent of renal damage.[3]

This study presents the results on seven rhabdomyolysis patients treated in our clinics out of nine casualties who were rescued from the rubble of Zümrüt apartment after the building collapsed suddenly and spontaneously.

PATIENTS AND METHODS

As a result of the sudden, spontaneous collapse of the 10-floor Zümrüt apartment in Konya at 20:15 hours on February 2, 2004, 92 out of a total of 121 persons who were inside the building lost their lives, and 29 casualties were rescued from the rubble. Minor injuries were treated as outpatient cases, while nine persons who were seriously injured were hospitalized. All of the hospitalized patients had a crush syndrome, and a prophylactic mannitol-bicarbonate cocktail was started in all patients at admission.

The general information on the inhabitants of Zümrüt apartment was obtained from Konya Provincial Health Directorate's data. Whereas seven of the hospitalized patients were followed-up and treated at nephrology clinics of Selçuk University Meram Faculty of Medicine and Başkent University Training and Research Hospitals, two patients who were placed in the care of other centers were excluded from the study as their data were not accessible.

The patients' creatinine (Cr), potassium (K), calcium (Ca), phosphorus, uric acid, creatine phosphokinase (CPK), myoglobin, albumin, SGOT-SGPT, LDH, hemoglobin (Hb), leukocyte, thrombocyte, and urine myoglobin values were recorded at the time of admission and on a daily basis throughout their monitoring.

The patients were diagnosed with crush syndrome in light of their clinical and laboratory results. IV fluids were administered to the patients while monitoring their urinary volume and central venous pressure (CVP). A cocktail of mannitol-bicarbonate was started for all patients with crush syndrome as prophylaxis to the development of ARF. The solution was prepared by mixing 40 mEq NaHCO3 and 50 ml of 20% mannitol into 1000 ml of 0.45% NaCl and 5% dextrose. The patients' urinary output, CVB, blood gases, and urinary pH were monitored while 4–8 liters of this solution was administered daily. Because active urinary output (urine flow rate ≥20 mL/hour) could not be ensured initially in one patient, mannitol treatment was withheld during this stage. The amount of NaHCO3 administered was adjusted to ascertain a urinary pH of ≥6.5, without subjecting the patients to risk of alkalosis. This treatment was continued until the color of urine returned to normal. Based on the serum bicarbonate level, the amount of bicarbonate in the cocktail was reduced as of the second day. Potassium supplementation was provided to the patients who required it. In addition, prophylactic cephazolin sodium antibiotherapy was started to protect patients with open wounds from sepsis.

The values were presented as ± standard deviation in statistical analysis.

RESULTS

The patients who had developed crush syndrome (5 M, 4 F) had an age average of 23.6 ± 11.7 (6–42). The time they remained entrapped under the rubble was 11.1 ± 7.3 (5–24 hours) on average. Two of the nine cases with crush syndrome had been rescued during the first 24 hours. Two patients who were placed in the care of other centers, on the other hand, had been extricated on days 6 and 7, respectively. Half of the cases who had been rescued alive from the rubble were from the first and eighth floors.

The average blood pressure of the patients at the time of hospitalization was 85.7 ± 11.4 (75–106) mm Hg, and their mean body temperature, 36.4 ± 0.4°C (35.8–37.1°C). Table 1 presents some characteristics and laboratory results at the time of admission of the patients who were treated at nephrology clinics of Selçuk University Meram Faculty of Medicine and Başkent University Training and Research Hospitals.

Table 1 Some characteristics and laboratory results at the patients' time of admission

			Laboratory results at the time of admission
Patients number	Age (year)	Time under the rubble (hours)	Htc (%)	Platelets (/mm^3)	WBC (/mm^3)	Calcium (mg/dL)	Phosphorus (mg/dL)	Potassium (mEq/L)	Urea (mg/dL)	Creatinine (mg/dL)	Uric acid (mg/dL)	CPK (u/L)	AST (u/L)	ALT (u/L)
1	22	5	43.6	285000	10300	9.5		4.4	20	0.7	3.9	31810	555	163
2	18	24	47.5	354000	35300	6.8	3.6	7.5	63	20		173440	642	163
3	17	6	59.2	267000	29400	9.4	8	6.9	34	1.4	19	85880	470	120
4	42	7	36.8	444000	20900	10.2	3	4.8	29	1	2.8	64740	432	173
5	6	9	43.4	489000	31200	10.0	6.1	7.1	34	0.8	3.6	13980	132	60
6	25	8	43.5	380000	24400	9.3		4.6	41	0.9	2	11478	76	64
7	35	19	41.4	266000	7400	8.7	3.4	5.3	20	0.6	3.8	17300	280	93

The highest CPK level of the patients was 79049 ± 75374 u/L (17478–223600 u/L), observed on the median day 1.7 ± 1.1 (days 1–4) following the incident. The initial and highest laboratory values of the patients are presented in Table 2.

Table 2 The initial and highest laboratory values of the patients (n = 7)

Parameters	Initial levels	Highest levels
Urea (mg/dL)	34.4 ± 14.7	44.1 ± 31.2
Creatinine (mg/dL)	1.06 ± 0.5	1.3 ± 0.7
Uric acid (mg/dL)	5.9 ± 6.5	6.3 ± 6
Potassium (meq/L)	5.8 ± 1.3	5.8 ± 1.3
Phosphorus (mg/dL)	4.8 ± 2.1	5.3 ± 2.1
Calcium (mg/dL)	9.1 ± 1.1	9.8 ± 0.5
Serum albumin (g/dL)	3.4 ± 0.7	4 ± 0.4
CPK (u/L)	56946.9 ± 58574.5	79049 ± 75374
AST (u/L)	369.6 ± 213.4	967 ± 1009.2
ALT (u/L)	119.4 ± 48.2	283 ± 194.4
LDH (u/L)	3660.4 ± 4196.7	4819.7 ± 6984.6
Hct (g/dL)	45.1 ± 7.0	45.1 ± 7.0
WBC (/mm^3)	22700 ± 10566.3	25857.1 ± 9886.2
PLT (/mm^3)	355000 ± 88570.1	432250 ± 87682

Within the first 24 hours of their hospitalization, an average of 5580 ± 3300 ml of fluid treatment was administered to the patients. Oligouria developed in only one patient (<400 mL/day urine), which improved in two days.

ARF developed in only two cases (28.6%) owing to the prophylactic mannitol-bicarbonate cocktail administered to prevent ARF, and because of hyperpotassemia, hemodialysis (HD) treatment was administered to these patients. One patient required two, and another four, sessions of HD. In both patients who received HD treatment, the level of potassium was in excess of 7 mEq/L, and the CPK level was over 100,000 u/L. While sepsis developed in one of the cases, disseminated intravascular coagulation (DIC) occurred in the other, and ARF improved.

A total of 122 units of blood and plasma transfusion (total blood = 48 U, FFP = 74 U) and 80 units of human albumin infusion was administered to six (85.7%) of the seven patients we monitored and treated. The per patient average quantity of blood and plasma transfused was 17.4 ± 25.7 U (4–69), and of human albumin infusion, 13.3 ± 17.1 U (2–46). One of the patients who received HD was given 69 units of blood and plasma and 46 pieces of human albumin, and the other, 35 units of blood and plasma and six pieces of human albumin transfusion. The reason for this fluid replacement was due to excessive loss of blood and plasma from the fasciotomy incisions.

A total of eight fasciotomies were performed on five (71.4%) of the seven patients with crush syndrome. Six of the fasciotomies were done on the lower extremities, and two were performed on the upper extremities. Five of the fasciotomies (62.5%) were performed on two of our patients who required HD treatment. Rib fractures developed (ribs 6–8) in one patient, and orthopedic surgery was performed on two patients for arm and leg fractures.

None of our patients with crush syndrome developed permanent kidney damage, and no mortality occurred. Muscular enzymes returned completely to normal after an average monitoring period of one week (5–10 days). In the ensuing phase the fasciotomies were closed.

DISCUSSION

Crush syndrome, which develops as a result of rhabdomyolysis, is an important cause of ARF. The serum creatine phosphokinase levels of trauma victims can help differentiate patients with crush syndrome and identify the extent of damage.[[4] The highest serum creatine phosphokinase levels were observed in the two patients who developed sepsis and DIC and received HD treatment.

Sever et al. reported that the magnitude of traumatized extremities in dialysis patients treated after the Marmara earthquake caused a meaningful increase in the need for dialysis, in terms of both the number of cases requiring dialysis and the number of sessions necessary for treatment.[[5] Tattersal et al. concluded that extensive trauma to the extremities is a determinant of nephrological problems.[[6] Similarly, in our study, fasciotomies were performed on a total of five extremities of the two patients we treated with HD.

A critical problem for survivors of disasters is the management of acute muscle compartment syndrome (AMCS), a devastating edema of crushed muscle that creates an emergency with major muscular, circulatory, and renal involvement. Muscle crush syndrome thus results in gross edema that may, in extreme cases, incarcerate the entire extracellular fluid, leading to hypovolemic shock within hours of injury. A description of ANCS usually includes the “six Ps”: pain, pressure, paresthesia, paresis or paralysis, pallor, and pulselessness. Laboratory diagnosis is made by intramuscular manometry; increases in manometrically documented intracompartmental pressure more than 30–40 mmHg established the diagnosis of AMCS. The diagnosis of AMCS is solidly based on clinical signs supported by increased compartmental pressure.[[7] In our study, a total of eight fasciotomies were performed on five (71.4%) of the seven patients with crush syndrome. However, the indications for fasciotomy were made only clinical signs by our surgeries and intramuscular manometry was not used for diagnosis of AMCS.

In our study, a total of 122 units of blood and plasma transfusion (total blood = 48 U, FFP = 74 U) and 80 units of human albumin infusion was administered to six (85.7%) of the seven patients we monitored and treated. The reason for this fluid replacement was due to excessive loss of blood and plasma from the fasciotomy incisions, because Better et al.[[7] reported that fasciotomy following crush injury may lead to profuse bleeding.

Until the early 1980s, fasciotomy was regularly and universally used to manage AMCS. However, the disappointing outcome of fasciotomy for AMCS complicating muscle crush injury from at least four countries (Turkey, Japan, Iran, and Taiwan) dictates a conservative approach.[[7] Better et al. reported a conservative approach that mannitol is a powerful tool to prevent myoglobinuric acute renal failure, as well as for ameliorating AMCS in casualties.[[8]

In a retrospective analysis, Ward reported that the highest serum creatine phosphokinase levels emerged during the first 24 hours in nearly 90% of patients.[[9] In our study, the highest CPK levels were observed on the median 1.7 ± 1.1 days (1–4) following the collapse of the building.

Sever has reported that general mortality occurs at a rate of 15.2% in crush syndrome patients with ARF complication. Sever also has reported that mortality is meaningfully higher among cases with thoracic and abdominal trauma, while the incidence of trauma to the extremities, the head, the pelvis, and the vertebrae and fractures in various localizations is not statistically different for patients who expired and survivors.[[10] None of our patients who developed crush syndrome had major thoracic or abdominal trauma. In addition, not only did permanent renal failure not develop in any patient, but no mortality occurred.

To date, cases that developed crush syndrome following sudden, spontaneous collapse of a building have been reported from Israel in 1984 by Ron et al. These investigators reported that seven cases (ages 18–41) were extricated from the rubble between 1 and 28 hours, all of whom had serious rhabdomyolysis and extensive crush injuries. They treated all of these patients by starting alkaline-solute diuresis immediately following their extraction from the remains. None of the patients developed either azotemia or renal failure, and this success was associated with immediate administration of treatment.[[3]

Volume replacement is the most important step in the prevention of ARF. Early and intensive post-traumatic volume replacement can prevent both hypovolemic shock and related development of ARF.[[3,], [11,], [12]

Energetic fluid replacement was administered to seven of the eight patients with detected crushing damage in the very early stage following the collapse of a building in Israel, and none developed ARF. On the other hand, another patient who did not receive adequate fluid because of a logistical error developed serious ARF and required long-term dialysis.[[3] A similar observation was made following the Marmara earthquake, in an analysis involving 20 children. ARF was not detected in any of the eight patients who received fluid therapy, while it occurred in seven (58%) of the 12 children who were not given fluids.[[11] In the other study that was reported in our country, isotonic saline and mannitol-alkaline fluid resuscitation were applied to 14 of 16 crush cases at admission after the Bingöl earthquake in 2003. They noted that duration between rescue and initiation of fluids was significantly longer in dialyzed patients as compared with non-dialyzed ones. Permenant renal failure did not develop in any patients using early and intensive fluid resuscitation with mannitol-alkaline diuresis.[[12] Likewise, in our study, as a result of the prophylactic administration of mannitol-bicarbonate cocktail, ARF developed in only two cases (28.6%), and these patients were provided HD treatment because of hyperpotassemia. Permanent renal failure did not develop in any of our patients with crush syndrome, nor did any of the cases result in a mortality.

In conclusion, it was deduced that rapid fluid therapy accompanied by prophylactic administration of mannitol-bicarbonate are largely effective in preventing the development of ARF in cases with crush syndrome resulting from disasters.