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CASE REPORT
Year : 2023  |  Volume : 17  |  Issue : 1  |  Page : 80-82

Severe bradycardia and hypotension induced by autonomic neuropathy in a diabetic patient during general anesthesia – A case report


Department of Anesthesiology and Pain Medicine, College of Medicine, Yeungnam University, Daegu, Republic of Korea

Correspondence Address:
Hyuckgoo Kim
Department of Anesthesiology and Pain Medicine, College of Medicine, Yeungnam University, Hyeonchung-ro, 170, Nam-gu, Daegu, 705-703
Republic of Korea
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/sja.sja_502_22

Rights and Permissions
Date of Submission08-Jul-2022
Date of Decision09-Jul-2022
Date of Acceptance09-Jul-2022
Date of Web Publication02-Jan-2023
 

  Abstract 


Cardiovascular autonomic neuropathy (CAN) is characterized by dysregulation of sympathetic and parasympathetic nervous systems that causes cardiovascular and respiratory disorders. The number of diabetic patients undergoing surgery is increasing in line with the prevalence of DM. Anesthesiologists should pay attention to diabetic patients with CAN because it is related to serious cardiovascular morbidity and mortality. We report an 80-year-old male who underwent cervical laminoplasty. He had severe bradycardia and hypotension from induction to the suspension of surgery. His blood pressure dropped to 70/40 mmHg and his heart rate to 20 bpm. Ephedrine, phenylephedrine, and atropine administration had minimal effect, but after epinephrine administrations, his heart rate and blood pressure increased to 70 bpm and 170/90 mmHg. The operation was discontinued because of the patient's unstable, fluctuating vital signs. The results of autonomic nervous system function examination indicated postganglionic cholinergic sympathetic dysfunction, sympathetic adrenergic dysfunction, and parasympathetic cholinergic dysfunction.

Keywords: Autonomic neuropathy, diabetes mellitus, general anesthesia


How to cite this article:
Lee N, Kim K, Kim H. Severe bradycardia and hypotension induced by autonomic neuropathy in a diabetic patient during general anesthesia – A case report. Saudi J Anaesth 2023;17:80-2

How to cite this URL:
Lee N, Kim K, Kim H. Severe bradycardia and hypotension induced by autonomic neuropathy in a diabetic patient during general anesthesia – A case report. Saudi J Anaesth [serial online] 2023 [cited 2023 Feb 1];17:80-2. Available from: https://www.saudija.org/text.asp?2023/17/1/80/364862




  Introduction Top


Autonomic neuropathy occurs secondary to diabetes mellitus and is present in about 20% of diabetic patients.[1] Cardiovascular autonomic neuropathy (CAN) is characterized by dysregulation of the autonomic nervous system which causes cardiovascular and respiratory disorders. CAN results in fluctuating blood pressure and heart rate during general anesthesia.[2] Therefore, diabetic patients who have CAN experience more cardiovascular events, such as bradycardia, hypotension, and cardiovascular collapse during anesthesia.[3] However, it is difficult to evaluate preoperative autonomic dysfunction in diabetic patients. Here, we report a diabetic patient who experienced severe bradycardia and hypotension during general anesthesia with unknown causes.


  Case Top


An 80-year-old male (height 167 cm, weight 60 kg) was scheduled for cervical laminoplasty. He had been diagnosed with diabetes ten years earlier and had been taking anti-diabetic drugs. On preoperative examination, his blood pressure (BP), heart rate (HR), and temperature were 126/62 mmHg, 51 bpm, and 37.2°C, respectively. Echocardiography showed a normal-sized chamber with hyperdynamic left ventricular systolic function, and no evidence of valvular dysfunction, and chest radiography showed no active lung disease. His serum glucose was controlled at 130 to 180, and laboratory examinations returned no abnormal results.

In the operating room, the patient's BP, HR, and pulse oximetry initially were 121/80 mmHg, 60 bpm, and 99%, respectively. General anesthesia was induced with 40 mg of propofol, 50 mg of rocuronium, and continuous intravenous remifentanil. Anesthesia was maintained with sevoflurane in air and oxygen and intravenous infusion of remifentanil at about 0.05 mcg/kg/min. Several minutes after intubation, BP and HR dropped to 70/40 mmHg and 40 bpm. Ephedrine 8 mg was administered intravenously, but BP did not increase. Phenylephedrine (100 mcg, i.v.) administration resulted in a BP increase to 120/60 mmHg, and then, he was positioned prone for surgery. However, unstable vital signs reappeared before incision, and HR dropped to 30/min. After the incision, his HR dropped to 20/min and BP to 60/30 mmHg. Administration of atropine (0.5 mg, i.v.) had no effect, but after two epinephrine (10 mcg) administrations, HR and BP increased to 70 bpm and 170/90 mmHg. Echocardiography revealed premature atrial complex and QT prolongation.

We decided to discontinue the operation because of fluctuating vital signs with severe bradycardia and hypotension. The patient emerged successfully, and his vital signs were stable in the post-anesthetic care unit. On the day following surgery, an autonomic nervous system function examination, including QSART (Quantitative Sudomotor Axon Reflex Test), HRdb (heart rate response to deep breathing), Valsalva maneuver, and head-up tilt test was performed. The result was reduced response in QSART. The average difference between the patient's inspiratory and expiratory heart rates was low at 3.99 in HRdb. In the Valsalva maneuver, late phases 2 and 4 were not observed, blood pressure recovery was delayed, and Valsalva ratio response was also reduced. Head-up tilt testing revealed orthostatic hypotension. Based on an analysis of the results, he had postganglionic cholinergic sympathetic dysfunction, sympathetic adrenergic dysfunction, and parasympathetic cholinergic dysfunction, which indicates severe autonomic failure.


  Discussion Top


The prevalence of Diabetic Mellitus (DM) is rapidly increasing. Thus, ever-increasing numbers of DM patients undergo surgery, and unfortunately, these patients have cardiovascular morbidity and mortality rates which are 2-3 times higher during surgery owing to cardiovascular system instability caused by atherosclerotic changes or diabetes-induced neuropathy.[1] In particular, uncontrolled blood glucose influences microcirculation by causing nitric oxide loss and free radical accumulation in Schwann cells leading to neuronal apoptosis and axonal degeneration. These neural cell injuries also occur in the cardiovascular autonomic nervous system,[4] and autonomic system damage disrupts cardiac autonomic regulation. Cardiovascular autonomic neuropathy (CAN) is related to elevated risks of arrhythmia, myocardial dysfunction, and major cardiovascular events.[4] However, in diabetic patients, CAN is easily overlooked, and in the absence of no clinical symptoms or signs in diabetic patients, CAN is not evaluated before surgery.

Our patient had severe bradycardia and hypotension from induction to the suspension of surgery. Initially, we considered the cause was a hypovolemic state, but pulse pressure variation (PPV) was unremarkable and fluid loading was also ineffective. There were no surgical manipulations that could cause cardiogenic reflexes. We decided to conduct an autonomic nervous system examination. The early clinical manifestations of CAN are dizziness, heart palpitations, and visual impairment,[5],[6] but these early symptoms are ambiguous and, thus, difficult to diagnose.

The important earliest clinical indicator of CAN is a decrease in heart rate variability (HRV).[6],[7],[8] HRdb evaluates parasympathetic cholinergic vagal function. The test involves measuring heart rate while the patient takes 8 deep breaths and then calculating the average difference between heart rates during inspiration and expiration. Healthy individuals have a high HRV, and this fluctuates during breathing.[8] Our patient exhibited reduced responses to HRV and HRdb testing, indicating reduced parasympathetic function. Its later clinical manifestations are resting tachycardia, fixed heart rate, exercise intolerance, and orthostatic hypotension.[2],[6] A fixed heart rate during exercise and exercise intolerance indicate severe CAN and complete cardiac denervation.[2],[8] In addition, orthostatic hypotension is caused by efferent sympathetic vasomotor denervation and reduced vasoconstriction.[8] Atropine prolongs parasympathetic dysfunction, but in the described case, bradycardia did not respond to atropine administration, which we attribute to a reduction in parasympathetic effect by autonomic neuropathy. Therefore, direct sympathetic agonists such as isoproterenol and epinephrine or a temporary pacemaker may be useful when severe bradycardia occurs in patients.[9],[10]

CAN did not adequately compensate for hemodynamic changes, which related to the suppression of adrenergic vasoconstrictive responses and baroreceptor sensitivity by general anesthesia. Our patient showed cardiovascular instability after administration of anesthetic and, in particular, no increase in blood pressure despite sympathetic stimulation by tracheal intubation. In addition, our patient developed severe hypotension after prone positioning, which we attribute to decreased venous return due to this positional change and impairment of sympathetic compensative activation.

In conclusion, the number of diabetic patients undergoing surgery is increasing in line with the prevalence of DM. However, cardiovascular autonomic dysfunction assessment is overlooked in diabetic patients. Anesthesiologists should pay more attention to diabetic patients with CAN, which is identified by non-invasive, sensitive, specific, and standardized autonomic function tests. Attentive preoperative examinations ensure an appropriate response from anesthesiologists' to severe hemodynamic instability during general anesthesia.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given his consent for his images and other clinical information to be reported in the journal. The patient understands that his name and initials will not be published, and due efforts will be made to conceal his identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Vinik AI, Nevoret ML, Casellini C, Parson H. Diabetic autonomic neuropathy. Diabetes Care 2003;26:1553-79.  Back to cited text no. 1
    
2.
Vinik AI, Ziegler D. Diabetic cardiovascular autonomic neuropathy. Circulation 2007;115:387-97.  Back to cited text no. 2
    
3.
Burgos LG, Ebert TJ, Asiddao C, Turner LA, Pattison CZ, Wang-Cheng R, et al. Increased intraoperative cardiovascular morbidity in diabetics with autonomic neuropathy. Anesthesiology 1989;70:591-7.  Back to cited text no. 3
    
4.
Agashe S, Petak S. Cardiac autonomic neuropathy in diabetes mellitus. Methodist Debakey Cardiovasc J 2018;14:251-6.  Back to cited text no. 4
    
5.
Rolim LC, de Souza JS, Dib SA. Tests for early diagnosis of cardiovascular autonomic neuropathy: Critical analysis and relevance. Front Endocrinol (Lausanne) 2013;4:173.doi: 10.3389/fendo. 2013.00173.  Back to cited text no. 5
    
6.
Vinik AI, Casellini C, Parson HK, Colberg SR, Nevoret ML. Cardiac autonomic neuropathy in diabetes: A predictor of cardiometabolic events. Front Neurosci 2018;12:591.doi: 10.3389/fnins. 2018.00591.  Back to cited text no. 6
    
7.
Ziegler D. Diabetic cardiovascular autonomic neuropathy: Prognosis, diagnosis and treatment. Diabetes Metab Rev 1994;10:339-83.  Back to cited text no. 7
    
8.
Pop-Busui R. Cardiac autonomic neuropathy in diabetes: A clinical perspective. Diabetes Care 2010;33:434-41.  Back to cited text no. 8
    
9.
Parlow JL, van Vlymen JM, Odell MJ. The duration of impairment of autonomic control after anticholinergic drug administration in humans. Anesth Analg 1997;84:155-9.  Back to cited text no. 9
    
10.
Lankhorst S, Keet SW, Bulte CS, Boer C. The impact of autonomic dysfunction on peri-operative cardiovascular complications. Anaesthesia 2015;70:336-43.  Back to cited text no. 10
    




 

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