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CASE REPORT
Year : 2017  |  Volume : 16  |  Issue : 1  |  Page : 81-83

Potassium chloride infusion as the cause of altered bio distribution of 18F-Fluorodeoxyglucose on whole-body positron emission tomography-computed tomography scan


Department of Nuclear Medicine and PET-CT, P.D. Hinduja National Hospital and MRC, Mumbai, Maharashtra, India

Date of Web Publication12-Jan-2017

Correspondence Address:
Shimpi Madhuri Mahajan
Department of Nuclear Medicine and PET-T, P.D. Hinduja National Hospital and MRC, V S Marg, Mahim. (W), Mumbai - 400 016, Maharashtra
India
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DOI: 10.4103/1450-1147.181158

PMID: 28217028

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   Abstract 

18F-fluorodeoxyglucose (18F-FDG) positron emission tomography-computed tomography is a standard diagnostic imaging tool in many types of cancer. Its physiological in vivo distribution includes the brain, liver, heart, kidneys, and urinary tract at 1 h after tracer injection. Skeletal muscle is known to show variable amounts of 18F-FDG uptake because it has a relatively high-glucose metabolism. We report a case of a 20-year-old patient with gross 18F-FDG uptake involving multiple muscle groups and its likely correlation to potassium chloride infusion before 18F-FDG injection.

Keywords: Potassium chloride and insulin, potassium chloride and muscles, potassium chloride infusion and 18F-fluorodeoxyglucose positron emission tomography-computed tomography scan


How to cite this article:
Mahajan SM, Natasha S, Sudeshna M, Pereira M. Potassium chloride infusion as the cause of altered bio distribution of 18F-Fluorodeoxyglucose on whole-body positron emission tomography-computed tomography scan. World J Nucl Med 2017;16:81-3

How to cite this URL:
Mahajan SM, Natasha S, Sudeshna M, Pereira M. Potassium chloride infusion as the cause of altered bio distribution of 18F-Fluorodeoxyglucose on whole-body positron emission tomography-computed tomography scan. World J Nucl Med [serial online] 2017 [cited 2020 Sep 23];16:81-3. Available from: http://www.wjnm.org/text.asp?2017/16/1/81/181158


   Introduction Top


18 F-fluorodeoxyglucose ( 18 F-FDG) is the radiotracer most commonly used for positron emission tomography-computed tomography (PET-CT) imaging. 18 F-FDG molecule acts like glucose during initial enzymatic reactions within cells, but the altered structure prevents further metabolism, and it accumulates in most tissues at a rate proportional to glycolysis. [1] Malignant cells have increased glucose transporter 4 (GLUT4) proteins on their cell surface as well as enhanced rates of glycolysis which facilitates their detection utilizing 18 F-FDG PET-CT imaging. Unfortunately, 18 F-FDG is not a cancer-specific agent, and its uptake has also been described in a number of inflammatory lesions. There are many potential pitfalls and artifacts associated with 18 F-FDG PET-CT imaging hence it is important to know these pitfalls and recognize the important areas of normal uptake of 18 F-FDG or absence of uptake that may or may not be of significance. This is necessary so that patients can be optimally prepared for their scans and accurate interpretation can be made.


   Case Report Top


We present a case of a 20-year-old boy with a history of kidney transplantation for medical renal disease 6 months ago, who presented with generalized weakness, weight loss, fever, and loose motions and was referred for an 18 F-FDG PET-CT scan. His K + was 2.8 mEq/l (N: 3.3-4.8), Na + was 124 mEq/l (N: 135-147), Cl-was 114 mEq/l (N: 101-111), serum creatinine: 3.4 mg% (N: 0.7-1.31), Hb: 9.8 g/dl (N: 13-18), RBC:3.16 million cells/ulit (N: 4.5-6.5), and ultrasonography revealed increased echogenicity of transplanted kidney.

Because of frequent episodes of loose motions, he had developed hypokalemia for which he required potassium chloride (KCl) infusion (10 cc KCl in 0.9% NS at a rate of 100 ml/h) which was continued till the time of 18 F-FDG injection. The whole-body PET-CT scan demonstrated altered physiological distribution of 18 F-FDG with markedly increased uptake in almost all major muscle groups, including those of the neck, thorax, abdomen, pelvis, and the extremities [Figure 1] and reduced uptake in organs that physiologically show much better uptake for example, liver. There were no obvious morphologic changes in these muscles on CT scan. Hence, the study was not interpretable. The patient's medication at the time of 18 F-FDG PET-CT scan included KCl infusion and steroids (Deflazacort). There was no history of incomplete fasting, hyperglycemia, insulin administration, or excess muscle activity before imaging. The whole-body 18 F-FDG PET-CT scan was repeated after stopping KCl infusion 12 h before 18 F-FDG injection. It showed normal biological distribution of 18 F-FDG [Figure 2] with abnormal increased diffuse heterogonous uptake in enlarged pancreas with adjacent stranding [Figure 3] raising possibility of pancreatitis, and there was a minimal uptake in muscles. Pancreatitis was subsequently confirmed by serum amylase and lipase levels which were raised (220 u/l and 513 u/l, respectively).
Figure 1: 18F-fluorodeoxyglucose whole-body positron emission tomography-computed tomography scan maximum intensity projection (after potassium chloride infusion): Altered physiological distribution of 18F-fluorodeoxyglucose with markedly increased uptake in almost all major muscle groups, including those of the neck, thorax, abdomen, and pelvis

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Figure 2: 18F-fluorodeoxyglucose whole-body positron emission tomography-computed tomography scan maximum intensity projection (12 h after stopping potassium chloride infusion): Normal biological distribution with minimal uptake in muscles

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Figure 3: 18F-fluorodeoxyglucose whole-body positron emission tomography-computed tomography scan axial views of pancreas: Abnormal increased diffuse heterogonous uptake in enlarged pancreas with adjacent stranding

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   Discussion Top


18 F-FDG PET-CT scan has been growing as a standard diagnostic tool in patients with oncological and nononcological conditions such as pyrexia of unknown origin. This imaging modality takes advantage of the overconsumption of glucose by tumor and inflammatory cells. [2],[3] A detailed knowledge of these conditions as well as normal physiological uptake at various sites is therefore important to avoid a mistaken diagnosis or missing a diagnosis. 18 F-FDG activity in muscle is frequently encountered on 18 F-FDG PET-CT scans. Normal muscles accumulate little 18 F-FDG, but muscles exercised just before or around the time of 18 F-FDG injection can exhibit intense 18 F-FDG uptake which is usually localized. Diffuse whole body muscle uptake can be caused by administration of insulin in hyperglycemic patients, recent food intake, and strenuous exercise that involves many muscle groups.

Elevated concentration of glucose in blood stimulates the release of insulin, and insulin acts on cells throughout the body to stimulate uptake, utilization, and storage of glucose. Insulin mediates the entry of glucose as well as 18 F-FDG into muscle, adipose tissue, and several other tissues and it also stimulates the liver to store glucose in the form of glycogen. Insulin increases blood flow and glucose extraction in skeletal muscles by stimulating glucose transport and phosphorylation via translocation of the insulin-sensitive GLUT4 [4] and an increase in hexokinase II activity [5] resulting in increased 18 F-FDG uptake in muscles. Insulin also increases the permeability of many cells to potassium, magnesium, and phosphate ions. Insulin causes potassium to shift into the cells thereby decreasing the extracellular K + level.

The effect of potassium ion on insulin release is clinically important. When there is more free K + concentration in blood, it causes closure of the ATP-sensitive K + channel (KATP channel). This event ends up depolarizing the plasma membrane and opening the voltage-sensitive Ca 2+ channels, which in turn increases the intracellular concentration of calcium and causes the exocytosis of insulin granules into the bloodstream (Macdonald et al., 2005).

In this patient, the typical distribution of 18 F-FDG uptake and information from correlative CT scan leaves little doubt that the F18 FDG uptake corresponds to the muscular uptake. Furthermore, the patient was so ill that he had not undergone any strenuous physical activity before scanning. He also had no history of shivering, convulsions, or insulin administration around the time of examination. However, the patient had received KCl infusion for hypokalemia just before the scan.


   Conclusion Top


Although the intensity and extent of 18 F-FDG muscular uptake, in this case, are spectacular, the actual cause remains speculative. However, the overall evidence seems to be in favor of KCl infusion causing a metabolic disturbance, which in turn increases the 18 F-FDG metabolism in all muscle groups. Such a mechanism would explain the global nature of the skeletal muscle uptake demonstrated in this patient as compared to the normal physiological distribution of 18 F-FDG seen on the scan repeated a day later after stopping KCl infusion 12 h before the scan. To the best of our knowledge, this appears to be the only case report with not much data available in literature regarding possible effects of KCl infusion on biodistribution of 18 F-FDG. Hence, more observation would be needed to support this for inclusion during patient preparation.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
   References Top

1.
Lindholm P, Minn H, Leskinen-Kallio S, Bergman J, Ruotsalainen U, Joensuu H. Influence of the blood glucose concentration on 18 F-FDG uptake in cancer: A PET study. J Nucl Med 1993;34:1-6.  Back to cited text no. 1
    
2.
Utriainen T, Malmström R, Mäkimattila S, Yki-Järvinen H. Methodological aspects, dose-response characteristics and causes of interindividual variation in insulin stimulation of limb blood flow in normal subjects. Diabetologia 1995;38:555-64.  Back to cited text no. 2
    
3.
Laakso M, Edelman SV, Brechtel G, Baron AD. Decreased effect of insulin to stimulate skeletal muscle blood flow in obese man. A novel mechanism for insulin resistance. J Clin Invest 1990;85:1844-52.  Back to cited text no. 3
    
4.
Gumà A, Zierath JR, Wallberg-Henriksson H, Klip A. Insulin induces translocation of GLUT-4 glucose transporters in human skeletal muscle. Am J Physiol 1995;268 (4 Pt 1):E613-22.  Back to cited text no. 4
    
5.
Postic C, Leturque A, Rencurel F, Printz RL, Forest C, Granner DK, et al. The effects of hyperinsulinemia and hyperglycemia on GLUT4 and hexokinase II mRNA and protein in rat skeletal muscle and adipose tissue. Diabetes 1993;42:922-9.  Back to cited text no. 5
    


    Figures

  [Figure 1], [Figure 2], [Figure 3]



 

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