0
Correspondence |

Hyperchloremic Metabolic Acidosis Following Resuscitation of Shock FREE TO VIEW

Cristina Gheorghe, MD; Ramona Dadu, MD; Cristina Blot, MD; Fidel Barrantes, MD; Rodrigo Vazquez, MD; Florentina Berianu, MD; Yan Feng, MD; Irwin Feintzig, MD; Yaw Amoateng-Adjepong, MD, PhD; Constantine A. Manthous, MD, FCCP
Author and Funding Information

From Bridgeport Hospital and Yale University School of Medicine.

Correspondence to: Constantine A. Manthous, MD, FCCP, Bridgeport Hospital, 267 Grant St, Bridgeport, CT 06610; e-mail: pcmant@bpthosp.org


Financial/nonfinancial disclosures: The authors have reported to CHEST that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (http://www.chestpubs.org/site/misc/reprints.xhtml).


© 2010 American College of Chest Physicians


Chest. 2010;138(6):1521-1522. doi:10.1378/chest.10-1458
Text Size: A A A
Published online

To the Editor:

Successful resuscitation of patients with shock often requires infusion of large volumes of crystalloid. Although “dilution acidosis” has been described in animal models1 and in human anecdotes, systematic examination of this phenomenon was only recently reported in children with shock.2 After receiving Institutional Review Board approval, we examined the medical records of adults admitted with a primary diagnosis of shock to Bridgeport Hospital during 19 months. Ninety-eight patients required > 1 L of normal saline (NS) administered in ≤ 1 h. Of these, 59 had sufficient data to enable computation of acid-base status, and 17 (28.8%) developed hyperchloremic metabolic acidosis (HMA) in the first 24 h. All arterial blood gases were analyzed for acid-base status by a blinded senior nephrology fellow using a nomogram-based, acid-base calculator (http://www.medcalc.com/acidbase.html). Anion gap (AG) acidosis was defined as metabolic acidosis with AG > 12 mEq/L after correction for serum albumin. When metabolic acidosis was present with AG ≤ 12 mEq/L, patients were categorized as having HMA. When AG was > 12 mEq/L, the “delta-delta” (ie, measured AG sufficient to explain the drop in bicarbonate from 24 mEq/L) was computed to ascertain whether HMA coexisted with the AG acidosis. There was no significant difference in the presence of chronic kidney disease or diabetes in patients with or without HMA. A total of 94.1% of patients had septic shock. Overall, the amount of NS administered in the 24 h ranged from 3 to 11.8 L for the HMA group compared with 0.3 to 17.2 L for the non-HMA group (median 6 vs 3 L, P = .002) (Table 1). Patients with HMA received fluids at a higher rate (276.2 vs 183.5 mL/h, P = .002). An infused volume of ≥ 4 L NS predicted HMA with a sensitivity of 82% and a specificity of 64%. In multiple logistic regression models, HMA at 24 h was highly associated with infused NS ≥ 4 L (OR, 13.9; 95% CI, 2.3-85.2). Age, diuretic use, chronic kidney disease, lactic acidosis, and bicarbonate infusion were not associated with HMA.

Table Graphic Jump Location
Table 1 —Acid-Base Data of Patients Who Developed vs Those Who Did Not Develop Hyperchloremic Metabolic Acidosis During the First 24 h of Resuscitation

AG = anion gap; HCO3 = bicarbonate; HMA = hyperchloremic metabolic acidosis.

HMA has been described in dog models and in human anecdotes since 1900. Stewart and Rourke3 described the effects of large-volume resuscitation, and Winters et al4 proposed that HMA may be caused by dilution of bicarbonate. HMA has long been appreciated after resuscitation of patients with diabetic ketoacidosis5,6 and was recently reported in children with meningococcal septic shock.2 Ketoacidosis differs somewhat in that urinary ketone excretion contributes (with dilution) to the development of HMA.6

In conclusion, this limited retrospective study suggests that HMA is common during resuscitation of patients with a primary diagnosis of shock, and that HMA is associated with volume of infused saline. The limitations of this retrospective, medical records review preclude precise estimates of frequency and risk of this phenomenon, but the findings suggest hypotheses for a prospective study.

Garella S, Tzamaloukas AH, Chazan JA. Effect of isotonic volume expansion on extracellular bicarbonate stores in normal dogs. Am J Physiol. 1973;2253:628-636. [PubMed]
 
O’Dell E, Tibby SM, Durward A, Murdoch IA. Hyperchloremia is the dominant cause of metabolic acidosis in the postresuscitation phase of pediatric meningococcal sepsis. Crit Care Med. 2007;3510:2390-2394. [CrossRef] [PubMed]
 
Stewart JD, Rourke GM. The effects of large intravenous infusions on body fluid. J Clin Invest. 1942;212:197-205. [CrossRef] [PubMed]
 
Winters RW, Scaglione PR, Nahas GG, Verosky M. The mechanism of acidosis produced by hyperosmotic infusions. J Clin Invest. 1964;43:647-658. [CrossRef] [PubMed]
 
Morgan TJ. The meaning of acid-base abnormalities in the intensive care unit: part III—effects of fluid administration. Crit Care. 2005;92:204-211. [CrossRef] [PubMed]
 
Oh MS, Carroll HJ, Goldstein DA, Fein IA. Hyperchloremic acidosis during the recovery phase of diabetic ketosis. Ann Intern Med. 1978;896:925-927. [PubMed]
 

Figures

Tables

Table Graphic Jump Location
Table 1 —Acid-Base Data of Patients Who Developed vs Those Who Did Not Develop Hyperchloremic Metabolic Acidosis During the First 24 h of Resuscitation

AG = anion gap; HCO3 = bicarbonate; HMA = hyperchloremic metabolic acidosis.

References

Garella S, Tzamaloukas AH, Chazan JA. Effect of isotonic volume expansion on extracellular bicarbonate stores in normal dogs. Am J Physiol. 1973;2253:628-636. [PubMed]
 
O’Dell E, Tibby SM, Durward A, Murdoch IA. Hyperchloremia is the dominant cause of metabolic acidosis in the postresuscitation phase of pediatric meningococcal sepsis. Crit Care Med. 2007;3510:2390-2394. [CrossRef] [PubMed]
 
Stewart JD, Rourke GM. The effects of large intravenous infusions on body fluid. J Clin Invest. 1942;212:197-205. [CrossRef] [PubMed]
 
Winters RW, Scaglione PR, Nahas GG, Verosky M. The mechanism of acidosis produced by hyperosmotic infusions. J Clin Invest. 1964;43:647-658. [CrossRef] [PubMed]
 
Morgan TJ. The meaning of acid-base abnormalities in the intensive care unit: part III—effects of fluid administration. Crit Care. 2005;92:204-211. [CrossRef] [PubMed]
 
Oh MS, Carroll HJ, Goldstein DA, Fein IA. Hyperchloremic acidosis during the recovery phase of diabetic ketosis. Ann Intern Med. 1978;896:925-927. [PubMed]
 
NOTE:
Citing articles are presented as examples only. In non-demo SCM6 implementation, integration with CrossRef’s "Cited By" API will populate this tab (http://www.crossref.org/citedby.html).

Some tools below are only available to our subscribers or users with an online account.

Related Content

Customize your page view by dragging & repositioning the boxes below.

  • CHEST Journal
    Print ISSN: 0012-3692
    Online ISSN: 1931-3543