Case Report

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American Journal of Emergency Medicine

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Survival after prolonged resuscitation from cardiac arrest due to diabetic ketoacidosis using Extracorporeal life support

Abstract

Management of cardiac arrest due to severe Diabetic ketoacidosis using bicarbonate therapy and Extracorporeal life support remains controversial. We report a case of a 24-year-old man with insulin-dependent Type 1 diabetes mellitus who survived without any neurologic complications after prolonged ECLS (includ- ing fluid resuscitation and insulin but no aggressive bicarbonate) for cardiac arrest due to severe DKA. In post-DKA cardiac arrest, insulin and fluid resuscitation is the mainstay of treatment, but ECLS should be considered when prolonged cardiac arrest is expected.

Unexpected cardiac arrest in severe diabetic ketoacidosis (DKA) may occur more frequently than previously recognized [1]. Management of such cases using bicarbonate therapy and extra- corporeal life support (ECLS) remains controversial. Chen et al [1] reported the importance of unmitigated cardiopulmonary resusci- tation (CPR) and aggressive bicarbonate therapy, whereas other reports have shown the efficacy of bicarbonate therapy in children with DKA [2,3]. However, bicarbonates for this situation have not been adequately evaluated.

Although ECLS has short- and long-term Survival benefits over conventional CPR for patients with in-hospital cardiac arrest of Cardiac origin, management of cardiac arrest due to severe DKA remains unclear [4].

We successfully treated a patient with cardiac arrest due to severe DKA using prolonged ECLS, fluid resuscitation, and insulin therapy without aggressive bicarbonate administration.

A 24-year-old man with insulin-dependent type 1 diabetes mellitus was brought to our hospital with disturbance of conscious- ness; he was found lying naked in his room in a weak condition. A few days before admission, he caught a common cold, experience appetite loss, and stopped taking insulin injections.

On presentation, his Glasgow Coma Scale score was 6/15, and vital signs were as follows: body temperature, 30.1?C; blood pressure, 118/ 72 mm Hg; heart rate, 60 per minute; and respiratory rate, 18 per minute. Oxygen saturation was 100% while breathing 10 L/min of oxygen through a nonrebreathing mask. His pupils were 5.0 mm, equal in size, and round. Other findings were unremarkable.

Arterial blood gas analysis during Oxygen administration showed a pH of 6.781, PCO2 of 52.5 mm Hg, PO2 of 294.3 mm Hg, HCO₃ of 7.6 mmol/L, and oxygen saturation of 100%.

Laboratory data revealed the following: blood glucose, 1743 mg/dL; blood urea nitrogen, 104.1 mg/dL; creatinine, 5.8 mg/dL; sodium, 130.7 mEq/L; potassium, 7.5 mEq/L; ketone bodies (+++). Electrocardiog- raphy showed an escaped rhythm; chest radiography was normal.

Severe DKA with accidental hypothermia was diagnosed, and treatment with warm fluids and Intravenous insulin was immediately initiated followed by endotracheal intubation and active External rewarming with forced air.

The patient suddenly became unresponsive 38 minutes after admission; electrocardiography revealed asystole, for which exter- nal cardiac massage was immediately initiated followed by epinephrine injections.

After inserting a 16.5F cannula into the left femoral artery and a

19.5F cannula into the right femoral vein toward the right atrium, ECLS was initiated with 3.5 L/min.

During resuscitation, 3.5-L normal saline, 13-mg epinephrine, and 100-U rapid-acting insulin were administered. Defibrillation for ventricular fibrillation and return of spontaneous circulation (ROSC) was performed thrice. Final ROSC was obtained after 103 minutes of resuscitation without bicarbonate administration; he was admitted to the critical care unit for postresuscitative care and additional DKA treatment. Arterial blood gas analysis 10 minutes before final ROSC showed a pH of 6.838, PaCO2 of 33.1 mm Hg, and HCO₃ of 5.6 mmol/L. After 24 hours of therapeutic hypothermia, Neurologic recovery was evident, and the patient was extubated on day 3. He was shifted to the general ward and discharged on days 10 and 32, respectively,

with no neurologic complications.

Our case emphasizes that clinicians should consider the in- dications for bicarbonate therapy and ECLS during resuscitation from cardiac arrest due to DKA.

Because severe acidosis inhibits myocardial contractility and reduces responsiveness to catecholamines, aggressive bicarbonate therapy probably shortened the resuscitation period in this case (N 100 minutes with ECLS), but no evidence exists for improved hemodynamic stability following bicarbonate therapy in patients with DKA [5]. Perceived benefits from acute reversal of severe acidemia are only based on animal and experimental studies [6]. buffer therapy during CPR can exacerbate intracellular acidosis because it generates free carbon dioxide diffusion across cellular membranes [7]. Bicarbonates used during CPR may also cause hypernatemia and hyperosmolality in an already compromised brain, with increased hemoglobin-oxygen affinity and impaired Tissue oxygenation [7]. Because cerebral edema followed by coma is a devastating DKA complication with a 24% mortality rate [8,9], worsening of tissue hypoxia is a major concern in post-DKA cardiac arrest. Kamarzaman et al [10] reported survival with post-DKA cardiac arrest after administering only 30 mL of 8.4% sodium bicarbonate despite an initial arterial blood gas pH of 6.27. Aggressive bicarbonate therapy is, therefore, unwarranted even in post-DKA cardiac arrest.

Cardiac arrest due to severe DKA including our case showed severe acidosis with hypothermia, requiring a longer CPR duration [10].

0735-6757/$ - see front matter (C) 2013

Therefore, ECLS may be useful when rewarming hypothermic patients with cardiac arrest [11,12].

Because previous cardiac arrest patients developed tension pneu- mothorax due to chest compression during prolonged resuscitation for severe DKA [10], ECLS represents a rational and innovative alternative. Although insulin and fluid resuscitation remain the mainstay of treatment, ECLS should be considered when prolonged cardiac arrest is expected. Further studies are required to evaluate bicarbonate therapy and ECLS use during resuscitation from cardiac arrest due to

severe DKA.

Toru Hifumi MD Nobuaki Kiriu MD Hiroshi Kato MD Junichi Inoue MD Yuichi Koido MD

Department of Critical Care Medicine and Trauma National Hospital Organization Disaster Medical Center E-mail address: [email protected]

http://dx.doi.org/10.1016/j.ajem.2012.12.041

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