Article

Management of 7 earthquake crush syndrome victims with long-term continuous renal replacement therapy

hospital admission. Further research will need to deter- mine whether these data represent the true prevalence of analgesic allergies.

Table 2 Number of individual analgesic mentions

Drug

Allergies reported (n) a

Codeine

105

Morphine

69

Hydrocodone

57

Oxycodone

50

Hydromorphone

16

Fentanyl

3

Ibuprofen

50

Ketorolac

13

Naproxen

13

NSAID (unspecified)

28

a Because of 74 patients with multiple allergies, the total number of allergies reported (404) exceeds the number of analgesic allergic patients (283).

Sean H. Rhyee MD, MPH Department of Emergency Medicine University of Massachusetts Medical School

Worcester, MA, USA E-mail address: [email protected]

Lisa Bienia-Kenton MD

Department of Emergency Medicine

Harrington Hospital Southbridge, MA, USA

an adult ED population. In the study group, 10.2% of patients had a recorded allergy to an opioid or NSAID analgesic. Compared with nonallergic patients, analgesic allergic patients were older and more likely to be women. These patients were also more likely to be admitted to the hospital. The study’s findings differ from prior reports, where the total prevalence of drug allergy in ED patients is 8% to 10% [2,3]. Analgesics comprised a small minority of cases in those studies. Even in a selected adult population of 9067 patients presenting to an allergy clinic, the rate of NSAID allergy was approximately 3% with 1 case reporting past reactions to tramadol [4]. The most likely explanation is accuracy of reported allergy information. High inaccuracy of drug allergy data has been previously reported in ED

settings [5,6].

The finding of a disproportionate number of female patients reporting analgesic allergy is consistent with prior reports [4,7]. The significance of the higher age found in analgesic allergic patients is uncertain, as age has not been found to be a consistent contributor to drug allergy risk [7]. Similarly, the relationship between higher admission rates and analgesic allergy is unclear and has not been addressed in prior studies.

In regard to this study’s limitations, the study group was predominantly white; a similar review in a facility serving a larger ethnic minority population could yield differing results. In addition, the study’s design cannot verify the accuracy of recorded drug allergy information. Patient records did not include documentation on the nature of a reported analgesic allergy. Hence, it was not possible to determine whether patients had a history of true hypersen- sitivity reactions or other Adverse drug effects. In addition, study data did not include Presenting complaints or final diagnoses, limiting analysis of the relationships between allergy status and age and disposition.

In summary, the prevalence of self-reported analgesic allergies in this single-center study was higher than reported in prior studies. Patients reporting allergies differed from nonallergic patients in regard to age, sex, and rate of

Amanda Collins DO Department of Emergency Medicine St Elizabeth Health Center Youngstown, OH, USA

http://dx.doi.org/10.1016/j.ajem.2012.10.016

References

  1. Nawar EW, Niska RW, Xu J. National hospital ambulatory medical care survey: 2005 emergency department summary. Advance Data from Vital and Health Statistics. No. 386. Hyattsville, MD: National Center for Health Statistics; 2007.
  2. Wyatt JP. Patients’ knowledge about their drug allergies. J Accid Emerg

Med 1996;13:114-5.

  1. Reisfeld S, Goldberg A, Confino-Cohen R. Management of patients with known drug hypersensitivity in an emergency department in Israel. Int Arch Allergy Immunol 2011;155:361-6.
  2. Palma-Carlos AG, Medina M, Palma-Carlos ML. Prevalence of drug allergy in an out-patient population. Eur Ann Allergy Clin Immunol 2006;38(5):142-5.
  3. Raja AS, Lindsell CJ, Bernstein JA, et al. The use of penicillin skin testing to assess the prevalence of penicillin allergy in an emergency department setting. Ann Emerg Med 2009;54(1):72-7.
  4. Porter SC, Manzi SF, Volpe D. Getting the data right: information accuracy in pediatric emergency medicine. Qual Saf Health Care 2006; 15:296-301.
  5. Gomes ER, Demoly P. Epidemiology of hypersensitivity drug reactions. Curr Opin Allergy Clin Immunol 2005;5:309-16.

Management of 7 earthquake Crush syndrome victims with long-term Continuous renal replacement therapy

To the Editor,

On May 12, 2008, a catastrophic earthquake measuring 8.1 on the Richter scale struck the Wenchuan region of Sichuan province, China, causing approximately 70000 deaths and even more injuries. From May 12 to 20, 2008, 7 seriously injured patients with crush syndrome were admitted to the Chengdu Military General Hospital, including 5 males and 2 females, with a mean age of 37.9 +- 8.4 years. These patients

Patient 1

Patient 2

Patient 3

Patient 4

Patient 5

Patient 6

Patient 7

Sex

Female

Male

Male

Female

Male

Male

Male

Age

46

41

41

25

27

40

45

Trapped time (h)

78

20

9

14

22

12

4

Length before admission (h)

143

24

24

27

42

28

37

Systolic pressure (mm Hg)

130

105

96

90

98

120

105

Diastolic pressure (mm Hg)

90

75

52

60

68

52

75

Urine volume (mL/24 h)

400

100

30

100

300

200

0

White blood cells (x109)

18.8

18.4

17.3

15.6

18.2

23

20.4

Haemoglobin (g/L)

113

143

174

111

151

143

98

Platelets (x109)

114

52

94

40

181

94

73

Blood urea nitrogen (mmol/L)

35.31

23.36

22.01

20.7

14.1

20.4

24.9

Serum creatinine (umol/L)

389

463.2

481.7

473.6

331

527

495.2

Creatine kinase (U/L)

13848.5

5899.29

29338.3

16738.2

18245.6

20466.3

664

Myohemoglobin

3755.9

818.1

N4000

4000

4000

N4000

179.7

Potassium (mmol/L)

5.27

5.52

8.64

4.18

6.1

6.86

4.65

Sodium (mmol/L)

135.3

118.8

130.9

134.9

122

124.3

135.4

Calcium (mmol/L)

1.73

2.03

1.64

1.2

1.62

1.54

2.2

PaO2 (mmHg)

62

72

28

68

103

87

50

PaCO2 (mm Hg)

38

34

43

40

33

24

35

CO2CP (mmol/L)

15.5

14.4

14.9

17.8

22.9

10.3

15.9

Abbreviations: PaO2, partial pressure of oxygen; PaCO2, partial pressure of carbon dioxide; CO2CP, carbon dioxide combining power.

had been buried under a collapsed building for an extended period (22.7 +- 25.1 hours). Hypotension, oliguria, or anuria was found in all of the patients. They had elevated levels of white blood cells, blood urea nitrogen, serum creatinine, and myohemoglobin (Table 1). Serious electrolyte disturbances were also observed, including hyperkalemia, hyponatremia, hypocalcemia, and acidosis (Table 1). The 7 patients had Acute kidney injury and injuries to several other organs, including fractures, Acute respiratory distress syndrome , congestive heart failure, stress ulcer, and cerebro- vascular accident (Table 2).

Table 1 Clinical details of the 7 patients at admission

Continuous veno-venous hemofiltration (CVVH) was carried out in the 7 patients. Continuous veno-venous hemofiltration was performed using the Baxter Acuraquis

Table 2 Other complications

system (Chicago, IL, USA). A Baxter Renafto HF1200 hemofilter was used. Blood ftow was set at 180 to 250 mL/ min. Nonheparin or minidose-heparin (2 mg/h) antic- oagulation was adopted. To ensure the efficiency of the membranes, the hemofilter was replaced every 24 hours or if the filter clotted prematurely. The dose of replacement ftuid was 25 to 60 mL/kg per hour with predilution. The net ftuid removal was set according to the central venous pressure level. The average duration of CVVH was 476.0 +-

234.9 hours (range, 160-790 hours). The urine volume of 2 patients increased to more than 400 mL per 24 hours within 2 days after beginning CVVH, 1 patient’s urine volume increased on the seventh day after beginning CVVH, and the other 3 patients’ urine volume increased between 2 and

Patient 1

Patient 2

Patient 3

Patient 4

Patient 5

Patient 6

Patient 7

Sepsis

?

?

ARDS

?

Congestive heart failure

?

?

Shock

?

?

?

?

Stress ulcer

?

?

?

Intestinal perforation

?

Cerebrovascular accident

?

pulmonary infection

?

?

?

?

?

Pneumothorax

?

Fracture

?

?

?

Hepatic lesion

?

?

?

Breathing machine

?

?

?

?

employment

Patient 1

Patient 2

Patient 3

Patient 4

Patient 5

Patient 6

Patient 7

Fasciotomy

?

?

?

?

?

?

Amputation

?

?

?

?

Duration of CRRT (d)

31

16

12

31

43

27

11

Interval between admission and

1

1

1

4

1

2

1

beginning CRRT (d)

Daily CRRT duration (h)

20.0

17.4

23.0

19.5

18.4

22.3

14.5

Length until urine volume increased

2

1

Sustained oliguria

16

27

15

7

to N400 mL/24 h (d)

Prognosis

Recover

Recover

Dead

Recover

Recover

Dead

Recover

4 weeks after beginning CVVH. Meanwhile, broad- spectrum antibiotics, nutritional supportive treatment, and surgical intervention were implemented (Table 3). In the end, 5 patients survived, and 2 patients died (1 patient died on the 12th day after admission due to multiple organ failure, the other died on the 27th day after admission due to extensive cerebral infarction with cerebral haemorrhage). The 5 surviving patients were still alive and had normal renal function 3 years after the earthquake.

Table 3 Treatment and prognosis of the 7 patients

Acute renal failure related to crush syndrome is always accompanied by injury to several organs [1]. In the present report, complications included fracture in 3 patients (lower limb fracture in 2 patients and costal fracture in 1 patient.), ARDS in 3 patients, congestive heart failure in 3 patients, stress ulcer in 2 patients, and extensive cerebral infarction with cerebral haemorrhage in 1 patient.

In patients with crush-induced acute renal failure, all types of renal replacement therapy, intermittent hemodial- ysis (IHD), Continuous renal replacement therapy , and Peritoneal dialysis (PD) are valid therapeutic options [2]. During the Marmara earthquake, IHD was the most frequently used form of dialysis and was applied in 462 patients, whereas only 34 and 8 patients were treated with CRRT and peritoneal dialysis, respectively [2]. In comparison with IHD, CRRT is advocated as being more likely to promote hemodynamic stability and less likely to cause abrupt changes in plasma biochemistry [3]. It can remove myoglobin, whereas IHD cannot because of the large molecular weight (17 kDa) of myoglobin [4]. Continuous renal replacement therapy can remove cyto- kines and inftammatory media. Therefore, CRRT is now the leading form of renal replacement therapy for AKI in intensive care units worldwide [5]. As the 7 patients in the present report were critically injured, CVVH was carried out soon after admission.

Although multiple clinical trials, including the study of Ronco et al [6], suggested an improvement in survival with higher doses of CRRT, according to the RENAL study, the dialysis dose should be prescribed to the target efftuent volume, not less than 25 mL/kg per hour [6-8]. However, the dialysis dose delivered is not routinely measured, and acute renal replacement therapy is frequently interrupted for

various reasons [9]. A dose of 45 to 60 mL/kg per hour was delivered in the first 3 days, and in the later course of the hospital stay, the dose was adjusted according to the patient’s severity of illness, renal capacity, and metabolic and volume status.

The average duration of CRRT was 476.0 +- 234.9 hours, with the shortest being 160 hours and the longest being 790 hours, which was much longer than that of other patients with AKI [9,10]. Because the duration of CRRT was long, considerable metabolic waste was cleared; however, at the same time, a large amount of nutrients was lost. Therefore, adequate nutritional support was given, and large amounts of Erythrocyte suspension, blood plasma, and thrombocyte were provided. Anemia and hypoalbuminemia were corrected gradually. In addition, although minidose-heparin continuous anticoagulation was adopted in some cases, long-term CRRT did not result in serious wound bleeding. Long-term CRRT successfully preserved injured extremities in 2 patients through removing cytokines and inftammatory media. Long- term CRRT was a source of vitality to the patients.

Yue Cheng PhD Tao Wang MD Fan Zhang MD Yinghua Lu MD Yu Zheng MD

Guangming Zhang MD Dongyang Guo MD Department of Nephrology

Chengdu Military General Hospital Chengdu 600083, People’s Republic of China E-mail address: [email protected]

http://dx.doi.org/10.1016/j.ajem.2012.10.035

References

  1. Kantarci C, Vanholder R, Tuglular S, et al. Acute renal failure due to crush syndrome during Marmara earthquake. Am J Kidney Dis 2002; 40:682-9.
  2. Sever MS, Erek E, Vanholder R, et al. Renal replacement therapies in the aftermath of the catastrophic Marmara earthquake. Kidney Int 2002;62:2264-71.
  3. Bagshaw SM, Berthiaume LR, Delaney A, et al. Continuous versus intermittent renal replacement therapy for critically ill patients with acute kidney injury: a meta-analysis. Crit Care Med 2008;36:610-7.
  4. Amyot SL, Leblanc M, Thibeault Y, et al. Myoglobin clearance and removal during continuous Venovenous hemofiltration. Intensive Care Med 1999;25:1169-72.
  5. Chertow GM, Burdick E, Honour M, et al. Acute kidney injury, mortality, length of stay, and costs in hospitalized patients. J Am Soc Nephrol 2005;16:3365-70.
  6. Ronco C, Bellomo R, Homel P, et al. Effects of different doses in continuous veno-venous haemofiltration on outcomes of acute renal failure: a prospective randomised trial. Lancet 2000;356:26-30.
  7. Bellomo R, Cass A, Cole L, et al. Intensity of continuous renal replacement therapy in critically ill patients. N Eng J Med 2009;361: 1627-38.
  8. Palevsky P, Zhang JH, O’Connor TZ. renal support in critically ill patients with acute kidney injury. N Engl J Med 2008;359:1961-2.
  9. Beitland S, Sunde K, Moen H, et al. Variability in uremic control during continuous venovenous hemodiafiltration in trauma patients. Crit Care Res Pract 2012;2012:869237.
  10. Vesconi S, Cruz DN, Fumagalli R, et al. Delivered dose of renal replacement therapy and mortality in critically ill patients with acute kidney injury. Crit Care 2009;13:57.

Yunos et al [8] performed a prospective study of high quality in critically ill patients comparing chloride-rich solutions to “modern” balanced infusion solutions. The authors found a significant improvement in the rate of acute kidney injury and use of renal replacement period by use of chloride reduced balanced infusion solution.

What makes this study so interesting and important for a broad audience of medical care providers is that it is the first large, high-quality trial showing that the choice of infusion solution made by the physician is not secondary or negligible. Infusion solutions, including isotonic mainte- nance solutions such as isotonic saline or lactated Ringer‘s, are medications with indications and contraindications. This, together with recent, high-quality evidence on the adverse effects and nonsuperiority in terms of volume effect of colloids, makes me feel or hope that we are in the midst of a Copernican revolution in ftuid therapy. May it not take centuries for these new implications to arrive in the minds of physicians [9,10].

Are we in the midst of a Copernican revolution in infusion therapy?

To the Editor,

It is now 180 years ago that Dr Thomas Latta first performed an infusion of saline intravenously during an epidemic of cholera in 1832. After failed attempts by him to administer ftuids rectally, the new procedure proved to be successful. Intravenous ftuid therapy was born and a revolution in medicine began. In the ending 19th century, Alexis Hartmann added lactate as a buffer substance to the before by Sidney Ringer invented infusion solution to treat metabolic acidosis in children resulting in the first balanced infusion solution.

Given the constitution of plasma water, it is obvious that isotonic saline with its 154 mmol/L of sodium and 154 mmol/L of chloride and its osmolality of 308 mmol/L is far from being physiologic. Still, the use of it as standard infusion solution for ftuid replacement in almost all clinical settings is widely spread [1,2]. Visiting hospitalized patients with an intravenous line, one will almost certainly see the ubiquitous isotonic saline bottle hanging above the patients head. This practice was justified until today by the relative safety and the low costs of the infusion solution. However, during the 80s of the last century, studies were performed showing that the infusion of isotonic saline and the concurrent development of hyperchloremic metabolic aci- dosis lead to Renal vasoconstriction with a consequent decline in glomerular filtration rate [3-5]. Furthermore, a decrease in blood pressure due to a decreased plasma renin activity was observed [6,7]. However, these were no clinical studies, and an adverse effect of isotonic saline infusion on a hard clinical end point has never been shown until now.

Gregor Lindner MD Aristomenis K. Exadaktylos MD Department of Emergency Medicine Inselspital, University Hospital Bern Freiburgstrasse, 3010 Bern, Switzerland

E-mail address: [email protected] http://dx.doi.org/10.1016/j.ajem.2012.10.037

References

  1. McIntyre LA, Hebert PC, Fergusson D, Cook DJ, Aziz A. A survey of Canadian intensivists’ resuscitation practices in early septic shock. Crit Care 2007;11(4):R74.
  2. Finfer S, Liu B, Taylor C, Bellomo R, Billot L, Cook D, et al. Resuscitation fluid use in critically ill adults: an international cross- sectional study in 391 intensive care units. Crit Care 2007;14(5):R185.
  3. Wilcox CS. Regulation of renal blood flow by plasma chloride. J Clin Invest 1983;71(3):726-35.
  4. Quilley CP, Lin YS, McGiff JC. Chloride anion concentration as a determinant of renal vascular responsiveness to vasoconstrictor agents. Br J Pharmacol 1993;108(1):106-10.
  5. Bullivant EM, Wilcox CS, Welch WJ. Intrarenal vasoconstriction during hyperchloremia: role of thromboxane. Am J Physiol 1989; 256(1 Pt 2):F152-7.
  6. Wilcox CS, Peart WS. Release of renin and Angiotensin II into plasma and lymph during hyperchloremia. Am J Physiol 1987;253(4 Pt 2): F734-41.
  7. Kotchen TA, Luke RG, Ott CE, Galla JH, Whitescarver S. Effect of chloride on renin and blood pressure responses to sodium chloride. Ann Intern Med 1983;98(5 Pt 2):817-22.
  8. Yunos NM, Bellomo R, Hegarty C, Story D, Ho L, Bailey M. Association between a chloride-liberal vs chloride-restrictive intrave- nous fluid administration strategy and kidney injury in critically ill adults. JAMA 2012;308(15):1566-72.
  9. Myburgh JA, Finfer S, Bellomo R, Billot L, Cass A, Gattas D, et al. hydroxyethyl starch or saline for fluid resuscitation in intensive care. N Engl J Med 2012;367(20):1901-11.
  10. Perner A, Haase N, Guttormsen AB, Tenhunen J, Klemenzson G, Aneman A, et al. Hydroxyethyl starch 130/0.42 versus Ringer’s acetate in severe sepsis. N Engl J Med 2012;367(2):124-34.

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