Case Report

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American Journal of Emergency Medicine

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Fatal hyperkalemia after vasodilator therapy for nonocclusive mesenteric ischemia?

Abstract

Adverse outcomes during vasodilator therapy for nonocclusive mesenteric ischemia have not been documented, although vasodila- tors are strongly recommended for its treatment. This case highlights a 76-year-old woman who developed fatal hyperkalemia immediately after vasodilator therapy for nonocclusive mesenteric ischemia. She developed septic shock, and an urgent laparotomy was conducted, in conjunction with high doses of norepinephrine and vasopressin, for suspected Acute mesenteric ischemia and peritonitis. After resection of the gangrenous bowel, the patient was diagnosed with nonocclu- sive mesenteric ischemia; in view of the viability of the remaining bowel, vasopressin was stopped, and milrinone infusion was simultaneously started; Severe hyperkalemia developed thereafter. The most probable explanation for the hyperkalemia is that vasodilator therapy promoted rapid reperfusion of the remaining ischemic bowel, especially because she had been treated with vasoconstrictive drugs. This pathophysiology is similar to that seen during reperfusion from traumatic Crush injuries. Therefore, emer- gency physicians must be aware of the potential risk of vasodilator therapy in these cases and take a pre-emptive approach, including early initiation of renal replacement therapy and treatment of the underlying disorders.

Mesenteric vasospasms or vasoconstrictions play an important role in the development of nonocclusive mesenteric ischemia. Accordingly, vasodilators are strongly recommended for its treatment [1]. However, adverse outcomes during vasodilator therapy for nonocclusive mesenteric ischemia have not been documented. Herein, we describe a case of fatal hyperkalemia immediately after vasodilator therapy for nonocclusive mesenteric ischemia.

A 76-year-old woman was admitted to our emergency department with a 2-day history of severe abdominal pain and dehydration. Upon admission, her blood pressure was labile with sinus tachycardia. Her abdomen was distended, but no tenderness or mass was noted. Initial laboratory tests showed metabolic acidosis (pH 7.15) and hemocon- centration: elevated hematocrit (49.1%), blood urea nitrogen (23.7 mmol/L), and creatinine (197 umol/L). Other laboratory tests, including potassium (4.4 mmol/L) and creatine kinase, were unre- markable. After infusion of 2 L of 0.9% saline, the metabolic acidosis improved, and urine output was restored.

However, within 8 hours of admission, she became septic with hypotension and pyrexia (39.6?C); laboratory values at that time were leukocyte count of 1800 cells/mm³, platelet count of 87000 cells/ mm³, amylase of 2173 IU/L, creatine kinase of 3028 IU/L, kidney

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function was preserved (creatinine, 150 umol/L), and myoglobinuria was not detected. Contrast-enhanced computed tomography showed extensive intestinal ischemia or necrosis, with no evidence of stenosis or obstruction. An Exploratory laparotomy, under general anesthesia, demonstrated multiple gangrenous patches, involving half of the Small intestine. The major mesenteric vessels were pulsating, and there was no evidence of thrombus or visible occlusion. The patient’s blood pressure and urinary output (6-9 mL/kg per hour) were maintained, despite using high doses of norepinephrine (N 0.3 ug/kg per minute) and vasopressin (0.05 IU/kg per hour).

Based on the surgical findings during the laparotomy, the patient was diagnosed with nonocclusive mesenteric ischemia. Therefore, to restore adequate mesenteric blood flow to the remaining bowel, we stopped vasopressin infusion and simultaneously added milrinone (0.05 ug/kg per minute); noradrenalin infusion was continued. At that time, her potassium level was slightly elevated (4.77 mmol/L), despite adequate urine output and no signs of myoglobinuria. Glucose insulin treatment and intravenous sodium bicarbonate were promptly initiated to prevent progressive hyperkalemia. Within approximately

60 minutes from the start of vasodilator therapy, however, the patient’s serum potassium level sharply increased to 7.18 mmol/L (Figure), leading to repeated ventricular fibrillation, treated by cardioversion. Because of the refractory hyperkalemia, acute contin- uous hemodiafiltration was instituted, which elicited a decrease in serum potassium. A subtotal small intestinal resection and hemi- colectomy with colostomy were completed, but the patient died 21 days after surgery owing to multiple-organ failure.

There are several possible mechanisms for the hyperkalemia described in the present case. However, insufficient renal elimination, massive blood transfusion, hemolysis, and rhabdomyolysis can be ruled out by clinical findings. In addition, the surgical procedure performed was highly unlikely to account for the potassium increase. On the other hand, vasodilator-induced restoration of local Blood supply to an extensively ischemic bowel can lead to a rapid washout of ischemic metabolites, resulting in sudden hyperkalemia. This unusual pathophysiology may be similar to that seen during reperfusion from traumatic crush injuries [2]. In addition, several reports [3-5], supporting this explanation, have demonstrated Rapid increases in serum potassium levels after revascularization, including surgery and catheter-based intervention, for acute mesenteric ischemia. An experimental study [4] demonstrated that severe hyperkalemia occurred 10 to 280 minutes after reperfusion of a mesenteric artery. The time course for the development of hyperka- lemia in that study was consistent with that observed in the present case. Given these considerations, the most probable explanation for hyperkalemia in the present case is that administration of milrinone, termination of vasopressin infusion, or both induced rapid

0735-6757/(C) 2014

Fig. Changes in serum potassium levels during surgery. A sharp increase in serum potassium is seen soon after the initiation of vasodilatory therapy. The horizontal bars superimposed on the chart represent each treatment period. Abbreviation: CHDF, continuous hemodiafiltration.

reperfusion of the remaining, nonoccluded, ischemic bowel, which had been severely affected by potent vasoconstrictors.

Because nonocclusive mesenteric ischemia is characterized by progressive mesenteric ischemia, leading to infarction and, eventual- ly, septic shock [6], the frequently delayed diagnosis of nonocclusive mesenteric ischemia may lead to a higher requirement for vasoactive drugs, including norepinephrine and vasopressin; both of these drugs are recommended for resuscitation of septic shock [6]. In contrast, these drugs may cause potent mesenteric vasoconstriction, linked to worsening of nonocclusive mesenteric ischemia; low-dose norepi- nephrine might possibly help maintain mesenteric perfusion [7]. Therefore, once nonocclusive mesenteric ischemia has been diag- nosed, these drugs should be discontinued or decreased, if possible. In addition, vasodilators should be administered and continued during and after surgical treatment of nonocclusive mesenteric ischemia [8- 12], although the aforementioned pathophysiology must be kept in mind and a high index of suspicion maintained for the development of reperfusion hyperkalemia.

In conclusion, this case highlights the life-threatening metabolic sequelae of reperfusion during nonocclusive mesenteric ischemia treatment. Emergency physicians must be aware of the potential risk of vasodilator therapy in a patient with nonocclusive mesenteric ischemia, especially if potent vasoconstrictors have been adminis- tered for a period owing to delayed diagnosis, and should consider pre-emptive initiation of renal replacement therapy.

Keiko Miyashita, MD Rie Yasumura, MD

Haruyuki Yamazaki, MD, PhD

Misa Kajitani, MD Yuka Osaki, MD

Yoshiro Kobayashi, MD, PhD

Department of Anesthesia National Hospital Organization Tokyo Medical Center

Tokyo 1528902, Japan E-mail addresses: [email protected]

http://dx.doi.org/10.1016/j.ajem.2014.01.038

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