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Recurrent syncope in an 84-year-old man
C Jiang, W Tang, X Hou, H Li
Department of Internal Medicine and Geriatrics, Beijing Friendship Hospital, Capital Medical University, Beijing, China
Correspondence Address:
Prof. H Li
Department of Internal Medicine and Geriatrics, Beijing Friendship Hospital, Capital Medical University, Beijing
China
Abstract
An 84-year-old man with hypertension and type 2 diabetes presented with recurrent transient loss of consciousness within 2 hours after dinner at home. Physical examination, electrocardiogram, and laboratory studies were unremarkable except hypotension. Blood pressures were measured in different postures and within 2 hours after meal, but neither orthostatic hypotension nor postprandial hypotension was detected. Further, history taking revealed that the patient was tube-fed with a fluid food pump with an inappropriate rapid infusion rate of 1500 mL per minute at home. He was eventually diagnosed as having syncope due to postprandial hypotension, which was caused by the inappropriate way of tube feeding. The family was educated about appropriate way of tube-feeding and the patient did not develop any episode of syncope during a two-year follow-up. This case highlights the importance of careful history taking in the diagnostic evaluation of syncope and the increased risk of syncope due to postprandial hypotension in the elderly.
How to cite this article:
Jiang C, Tang W, Hou X, Li H. Recurrent syncope in an 84-year-old man.J Postgrad Med 2023;69:111-113
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How to cite this URL:
Jiang C, Tang W, Hou X, Li H. Recurrent syncope in an 84-year-old man. J Postgrad Med [serial online] 2023 [cited 2023 Sep 25 ];69:111-113
Available from: https://www.jpgmonline.com/text.asp?2023/69/2/111/370402 |
Full Text
Introduction
Syncope is a common and potentially dangerous phenomenon in the elderly and the cause is often difficult or even impossible to determine, despite expensive, highly technological medical evaluations.[1],[2] The initial diagnostic evaluation of syncope consists of careful history taking concerning present and previous attacks, as well as eyewitness accounts, physical examination including supine and standing blood pressure (BP) measurements, and electrocardiogram (ECG). Based on these findings, additional examinations may be performed when needed. By using a detailed clinical history, physicians can differentiate syncope from other forms of transient loss of consciousness (LOC) in approximately 60% of cases.[3] This case highlights the importance of careful history taking in the diagnostic evaluation of syncope.
Case Report
An 84-year-old man with hypertension and diabetes presented to the emergency department with sudden LOC at home. He had started nasogastric tube feeding since he was hospitalized for aspiration pneumonia three months earlier, and the attack occurred in the evening he was discharged home. He was tube-fed with 500mL of liquid mixed meal, followed by metoprolol 12.5 mg at a 30-minute interval without change of positions, and was found unconscious in chair with sweating and salivation 10 minutes later. He had no past medical history of syncope. The BP was measured as 70/40 mm Hg 20 minutes later, with heart rate (HR) of 78 bpm and capillary glucose of 8.1 mmol/L. He recovered spontaneously on the way to hospital and recalled feeling of dizziness but no chest pain or palpitation prior to the LOC.
On arrival, his physical examination, ECG, and laboratory studies were unremarkable except for BP of 50/30 mm Hg and slightly elevated serum levels of creatinine and urea nitrogen. He was treated with fluid support combined with intravenous dopamine infusion and was admitted for further evaluation. Dynamic BP monitoring showed BP ranging from 110/52 to 158/86 mm Hg, and ambulatory ECG monitoring showed sinus rhythm without supraventricular or ventricular tachycardia or conduction disturbance. Echocardiography, electroencephalography, and cranial computed tomography revealed no notable abnormalities. When he improved two days later, BP was measured in supine, sitting, and standing positions, as well as at 10-minute interval within 2 hours of dinner [Figure 1], but neither orthostatic hypotension nor postprandial hypotension (PPH) was supported. He was discharged without definite diagnosis.{Figure 1}
Surprisingly, he experienced another very similar episode of transient LOC in the evening he was discharged home except that it occurred 80 minutes after dinner in supine position.
Through further history taking, we found that the family used a fluid food pump for tube-feeding at home with an inappropriate infusion rate of 1500 mL/min [Video]. He was eventually diagnosed as syncope due to PPH, which was caused by a surprisingly inappropriate way of tube feeding.
The family was educated about danger associated with meal-induced hypotension, particularly under high infusion rate of tube-feeding. Metoprolol was also stopped in consideration of its effect on both sympathetic nerve activity and BP. The patient was discharged again. During a two-year follow-up, the patient's BP maintained between 112/56 to 158/86 mm Hg, with HR of 66 to 84 bpm, and he experienced no syncope any more.
Discussion
PPH is an important clinical problem which has received inappropriately little attention.[4] It was first reported in 1977, in a 65-year-old man with Parkinson's disease who experienced severe dizziness and visual disturbance following an oral glucose load, when his systolic BP fell from 200 to 105 mm Hg within 10 minutes.[5] Traditionally, PPH is defined as a reduction in systolic BP of ≥20 mm Hg, or a decrease to ≤90 mm Hg when the preprandial BP is ≥100 mm Hg, within 2 hours of a meal.[6] This definition is empirical and is derived from that of orthostatic hypertension.[7] However, there is a lack of standardization pertaining to the methodological issues of PPH test, such as the nutrient composition of the meal, the timing of meal ingestion, the posture of the body during the evaluation, the technique used to measure BP, the duration of BP monitoring, the use of medications, especially antihypertensives, etc.[4] Therefore, PPH could not be completely excluded even if PPH test is negative, as shown in this case, in consideration of many interfering factors. PPH is common in the elderly and is associated with increases in the risk of syncope, falls, angina pectoris, and stroke, as well as mortality.[8]
The pathophysiology of PPH is not fully understood. In the broadest sense, it is indicative of inadequate cardiovascular compensation for meal-induced splanchnic blood pooling.[9] Current evidences suggest that multiple etiologic factors are involved in PPH [Figure 2]. A blunted sympathetic response and impaired baroreflex activity to hypotension is believed to be responsible for the compensatory failure that underlies PPH.[9]{Figure 2}
Management of PPH can be “nonpharmacologic” or “pharmacologic”.[10] The former includes giving more frequent, smaller meals, lowering carbohydrate content of the meals, water drinking immediately before the meals, slowing gastric emptying, postprandial exercise, and possibly serving food colder than room temperature.[4]
In conclusion, several important points are raised by this case. First, in the initial diagnostic evaluation of patients with LOC, careful history taking is very important. As Sir William Osler had pointed out: If you listen carefully to the patient, they will tell you the diagnosis. Second, PPH is a common phenomenon in the elderly and inappropriate feeding way may lead to potentially dangerous consequence. Physicians should be alert for PPH as a cause of syncope, falls, angina, or stoke in older patients. Third, PPH could not be completely excluded even if PPH test is negative, for many factors pertaining to the methodological issues of PPH test may influence the result. Finally, PPH is potentially treatable. Nonpharmacologic management, for example, reducing meal size, slowing the infusion rate of tube feeding, etc., may be effective in preventing PPH in the elderly.
Declaration of patient consent
The authors certify that appropriate patient consent was obtained.
Acknowledgments
We thank Dr. Yi Liu for drawing the figure of the pathophysiology of postprandial hypotension.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
References
| 1 | Brignole M, Moya A, de Lange FJ, Deharo JC, Elliott PM, Fanciulli A, et al. 2018 ESC Guidelines for the diagnosis and management of syncope. Eur Heart J 2018;39:1883-948. |
| 2 | Shen WK, Sheldon RS, Benditt DG, Cohen MI, Forman DE, Goldberger ZD, et al. 2017 ACC/AHA/HRS Guideline for the Evaluation and Management of Patients With Syncope: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. Circulation 2017;136:e60-122. |
| 3 | van Dijk N, Boer KR, Colman N, Bakker A, Stam J, van Grieken JJ, et al. High diagnostic yield and accuracy of history, physical examination, and ECG in patients with transient loss of consciousness in FAST: The Fainting Assessment study. J Cardiovasc Electrophysiol 2008;19:48-55. |
| 4 | Trahair LG, Horowitz M, Jones KL. Postprandial hypotension: A systematic review. J Am Med Dir Assoc 2014;15:394-409. |
| 5 | Seyer-Hansen K. Postprandial hypotension. Br Med J 1977;2:1262. |
| 6 | Jansen RW, Lipsitz LA. Postprandial hypotension: Epidemiology, pathophysiology, and clinical management. Ann Intern Med 1995;122:286-95. |
| 7 | Freeman R, Wieling W, Axelrod FB, Benditt DG, Benarroch E, Biaggioni I, et al. Consensus statement on the definition of orthostatic hypotension, neurally mediated syncope and the postural tachycardia syndrome. Clin Auton Res 2011;21:69-72. |
| 8 | Fisher AA, Davis MW, Srikusalanukul W, Budge MM. Postprandial hypotension predicts all-cause mortality in older, low-level care residents. J Am Geriatr Soc 2005;53:1313-20. |
| 9 | Luciano GL, Brennan MJ, Rothberg MB. Postprandial hypotension. Am J Med 2010;123:281.e1-6. |
| 10 | Shibao CA, Biaggioni I. Management of orthostatic hypotension, postprandial hypotension, and supine hypertension. Semin Neurol 2020;40:515-22. |
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