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 Table of Contents  
CASE REPORT
Year : 2020  |  Volume : 22  |  Issue : 1  |  Page : 81-83

Postoperative relative adrenal insufficiency in elderly


1 Department of Anaesthesiology, INHS Jeevanti, Vasco-da-Gama, Goa, India
2 Department of Gyane and Obstetrics, INHS Jeevanti, Vasco-da-Gama, Goa, India

Date of Submission26-Apr-2019
Date of Decision27-Jul-2019
Date of Acceptance07-Aug-2019
Date of Web Publication03-Mar-2020

Correspondence Address:
Surg Lt Cdr Abdul Nasser
Department of Anaesthesiology, INHS Jeevanti, Vasco-da-Gama - 403 802, Goa
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jmms.jmms_29_19

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  Abstract 


Corticosteroid hormones play a significant role in the control of vascular smooth muscle tone by their permissive effects in potentiating vasoactive responses to vasoconstrictors. Inadequate cortisol response in stress conditions such as the perioperative period, despite normal serum cortisol concentrations is defined as relative adrenal insufficiency. We report a patient who underwent vaginal hysterectomy and developed hypotension postoperatively. There was no improvement on fluid administration and vasopressor infusion. The patient clinically improved with administration of hydrocortisone.

Keywords: Adrenal insufficiency, hypotension, postoperative


How to cite this article:
Nasser A, Taralkar T. Postoperative relative adrenal insufficiency in elderly. J Mar Med Soc 2020;22:81-3

How to cite this URL:
Nasser A, Taralkar T. Postoperative relative adrenal insufficiency in elderly. J Mar Med Soc [serial online] 2020 [cited 2020 Oct 20];22:81-3. Available from: https://www.marinemedicalsociety.in/text.asp?2020/22/1/81/279875




  Introduction Top


Corticosteroid hormones control the tone of vascular smooth muscle by permitting vasoactive responses to vasoconstrictors such as catecholamines, angiotensin II, and vasopressin, through glucocorticoid receptors.[1],[2] An increased glucocorticoid response will cause an increase in arterial contraction and vascular resistance. Cortisol, the principal glucocorticoid, is also an important regulator of carbohydrate, protein, lipid, and nucleic acid metabolism. Aldosterone, under the control of renin–angiotensin system, regulates sodium and potassium balance and also the intravascular volume.

Adrenal insufficiency has been reported during illnesses, usually due to adrenal hemorrhage or inadequate response from prior steroid administration. There are several reports suggesting lower than expected cortisol levels during critical illness without previous suppressive therapy or anatomical disruption. Inadequate cortisol response in stress conditions such as the perioperative period, despite normal serum cortisol concentrations, is defined as relative adrenal insufficiency.[3],[4],[5],[6] We report a patient who underwent vaginal hysterectomy and developed hypotension postoperatively. The patient clinically improved with the administration of hydrocortisone.


  Case Report Top


A 70-year-old female diagnosed with the second-degree uterovaginal prolapse was planned to undergo vaginal hysterectomy with pelvic floor repair. She was diagnosed with primary hypertension 10 years ago, for which she was receiving medication in the form of tablets amlodipine 5 mg and sustained release indapamide 1.5 mg, once daily. She was also a known case of hypothyroidism, for which she was taking 75 μg of tablet thyroxin since she had undergone thyroidectomy 10 years ago under general anesthesia. Her preoperative levels were within the normal limits. The patient confirmed that her surgery and anesthesia experience were uneventful.

Her systemic examination during the preoperative anesthetic evaluation revealed no abnormality, and her vital parameters were within the normal limits. Her metabolic equivalents were above 5. Airway examination revealed that she was edentulous and Mallampati score was Class 2. She had normal blood chemistry and complete blood count. Ultrasound of the abdomen revealed a low-lying uterus. The electrocardiogram showed a normal sinus rhythm, and her chest X-ray was also normal. A recent two-dimensional echocardiography report revealed normal-sized cardiac chambers, 60% ejection fraction, and Grade I left ventricular diastolic dysfunction. She was advised to take her antihypertensive medications on the morning of surgery. Written informed consent was obtained for the insertion of epidural catheter and for providing general anesthesia.

On the day of surgery, an 18-G intravenous (IV) cannula was secured, and monitoring was established according to the American Society of Anesthesiologists' standards. Epidural catheter was inserted at L2-3 space under local anesthesia using an 18-G Tuohy needle with the patient in the sitting position. The catheter was inserted 6 cm into the epidural space. The patient was induced with propofol at 2 mg/kg and fentanyl at 1 μg/kg; trachea was intubated with a 7.5-mm cuffed endotracheal tube after the administration of vecuronium at 0.1 mg/kg and was treated with mechanical ventilation with a mixture of N2O and oxygen at 2:1 ratio. Anesthesia was maintained with isoflurane and intermittent boluses of vecuronium. A 5 ml bolus dose of 0.1% bupivacaine was given before skin incision, and epidural infusion at 5 ml/h of 0.0625% bupivacaine with 1 μg/ml of fentanyl was started 1 h after the bolus dose.

The patient's blood pressure (BP) and pulse rate before induction was 130/76 mmHg and 80 bpm, respectively. The changes in systolic, diastolic, and mean arterial BP levels and pulse rate changes over the course of anesthesia are demonstrated in [Figure 1]. The surgery lasted for 3 h, with intraoperative blood loss of 300 ml, urine output of 120 ml, and she was given 1000 ml of Ringer's Lactate intraoperatively. Reversal of neuromuscular blockade was achieved with neostigmine and glycopyrrolate, after recording a train-of-four count of 4.
Figure 1: Intraoperative vital monitoring

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Postoperatively, the epidural infusion was continued. In evening time, the patient recorded low BP readings of below 90/60 mmHg and heart rate (HR) of 58 bpm. The epidural infusion was stopped, and a bolus of 250 ml normal saline was given over 10 min and hourly thereafter. BP and pulse rate readings were recorded every 15 min, and hourly urine output was measured. After 2 h, the BP recorded was 86/46 mmHg, HR continued to be <60 bpm, and urine output was 75–100 ml/h. At this time, hemoglobin (Hb) was ordered to rule out bleeding from the operative site, and serial abdominal girth measurements were done. Hb was 10.0 mg/dl. Random blood sugar was 142 mg/dl. Clinically, she had no complaints, with no respiratory distress or abdominal pain. Her chest was clear, with no signs of fluid overload or heart failure, and her abdomen was soft on palpation. Ultrasound sonography of the abdomen showed no evidence of free fluid in the pelvis. Electrocardiography showed a normal sinus rhythm.

At this point, it was decided to start noradrenaline infusion at a rate of 2 μg/min. The BP did not increase even after ½ h of infusion. The patient was then given 100 mg hydrocortisone iv over 5 min. After 30 min, her BP recorded 110/70 mmHg and HR of 66/min. Noradrenaline infusion was tapered off. The patient received 100 mg hydrocortisone iv every 8 h for 24 h, every 12 h for next 48 h, and every 24 h for the subsequent 48 h. Cortisol level was not measured during her stay. Postoperative Na+ level was 131 mEq/L and K+ level was 3.6 mEq/L. The patient showed no deterioration once hydrocortisone was initiated and was discharged subsequently.


  Discussion Top


Corticosteroid hormones, through their action on the glucocorticoid receptors, control the tone of vascular smooth muscle by permitting the vasoactive responses to vasoconstrictors. An increased glucocorticoid response will cause an increase in arterial contraction and vascular resistance. Surgery, anesthesia, and critical illness are potent stimulators of hypothalamic–pituitary–adrenal axis, resulting in elevated adrenocorticotropic hormone (ACTH) and cortisol levels.[7] Acute adrenal insufficiency rarely occurs, but it can be life-threatening. Various factors can influence the response of the adrenal gland in the perioperative period, such as age of the patient, severity and duration of surgical procedure, type of anesthetic used, mode of anesthesia delivered, patient comorbidities, and intake of drugs such as steroids.

Effect of surgical procedure

A good correlation is seen to exist between the severity and duration of the operation and the response of the adrenal gland. From baseline values of around 400 nmol/l, the levels can increase to a maximum of >1500 nmol/l within 4–6 h.[8] Under perioperative conditions, the adrenal glands secrete 116–185 mg of cortisol daily and under extreme stress, they may secrete 200–500 mg/day.[9] The mean maximal cortisol concentration varies between a major surgical procedure such as hysterectomy and minor surgical procedure such as herniorrhaphy. In a study of 20 patients during major and minor surgery, the mean maximal concentration of cortisol in plasma was 47 μg/dL (range, 22–75 μg/dL) and 28 μg/dL (range, 10–44 μg/dL), respectively. Values remained higher than 26 μg/dL for 72 h postoperatively during major surgery.

Effect of type of anesthesia

Perioperative stress is related to the extent of trauma and the depth of anesthesia. Deep general or regional anesthesia delays the usual intraoperative glucocorticoid surge to the postoperative period. Opioids and benzodiazepines are recognized to suppress hypothalamic and pituitary hormone secretion and while etomidate interferes with steroid synthesis, clonidine inhibits stress responses mediated by the sympathetic nervous system.[10] Widespread epidural analgesia prevents endocrine and metabolic responses to surgery, more in the pelvis and on the lower limbs than in upper abdominal or thoracic surgery.[11] Establishing epidural blockade from segments T4 to S5, before the start of surgery, prevents increase in cortisol and glucose concentrations in response to hysterectomy. This is affected by blocking the afferent inputs to the central nervous system and hypothalamic–pituitary axis and efferent autonomic pathways to the liver and adrenal medulla.[12] The adrenocortical and glycemic responses to surgery are thus abolished. Neural blockade of any lesser degree will not abolish these changes completely. Fentanyl and epidural analgesic infusion given to our patient, both may have contributed to inadequate adrenal response to the surgical and anesthetic stress postoperatively.

Effect of age

Production of androgens by the adrenal gland progressively decreases with age, but plasma cortisol and corticosteroid-binding globulin levels remain unaffected. This finding suggests that a normal fraction of free cortisol is present in older patients. The ability to metabolize and excrete glucocorticoids is progressively impaired in older patients. The quantity of 17-hydroxycorticosteroids excreted is reduced by half by the seventh decade, which reflects the reduced renal function that occurs with aging in normal individuals. Further reductions in cortisol clearance may reflect impaired hepatic metabolism of circulating cortisol. The rate of secretion of cortisol is 30% slower in the elderly, which may be interpreted as an appropriate compensatory mechanism for maintaining a normal cortisol level in the presence of decreased hepatic and renal clearance.[9]

Effect of antihypertensive medications

Antihypertensive drugs which target the renin–angiotensin–aldosterone system reduce the secretion of ACTH and aldosterone.[13] The dihydropyridine class of calcium-channel blockers block the L-type channel, thereby decreasing the free Ca2+ levels, with a concomitant decrease in aldosterone production.[14] Intake of these drugs perioperatively is likely to be a cause of postoperative hypotension.

In our patient, all the common causes of postoperative hypotension, including postoperative bleeding, sepsis, and cardiac pathology, were ruled out before suspecting adrenal insufficiency. Adrenal crisis is the development of catecholamine-resistant hypotension in patients without a prior diagnosis of adrenal insufficiency. Cortisol plays a role in the improvement of impaired vasomotor tone in the vascular system, enhances the sensitivity of catecholamine receptors, and regulates body fluid levels.[15] The improvement noticed in our patient after giving the first dose of hydrocortisone led us to believe that she was indeed suffering from a relative adrenal insufficiency. Cortisol blood levels, particularly the circadian alterations, are not well-documented in a patient under stress 24 h a day. Hence, it is prudent to suspect adrenocortical insufficiency in a hypotensive patient nonresponsive to fluid replacement and vasopressor agents.

Declaration of patient consent

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

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Yang S, Zhang L. Glucocorticoids and vascular reactivity. Curr Vasc Pharmacol 2004;2:1-2.  Back to cited text no. 1
    
2.
Sapolsky RM, Romero LM, Munck AU. How do glucocorticoids influence stress responses? Integrating permissive, suppressive, stimulatory, and preparative actions. Endocr Rev 2000;21:55-89.  Back to cited text no. 2
    
3.
Mackenzie JS, Burrows L, Burchard KW. Transient hypoadrenalism during surgical critical illness. Arch Surg 1998;133:199-204.  Back to cited text no. 3
    
4.
Latina A, Terzolo M, Pia A, Reimondo G, Castellano E, Pellegrino M, et al. Acute primary adrenal insufficiency after hip replacement in a patient with acute intermittent porphyria. Case Rep Endocrinol 2018;2018:2353172.  Back to cited text no. 4
    
5.
Doǧu B, Öksüz H, Şenoǧlu N, Yavuz C, Gişi G. Postoperative sudden hypotension due to relative adrenal insufficiency. Turk J Anaesthesiol Reanim 2014;42:283-7.  Back to cited text no. 5
    
6.
Naka N, Takenaka S, Nanno K, Moriguchi Y, Chun BM, Sonoda S, et al. Acute adrenal crisis after orthopedic surgery for pathologic fracture. World J Surg Oncol 2007;5:27.  Back to cited text no. 6
    
7.
Jung C, Inder WJ. Management of adrenal insufficiency during the stress of medical illness and surgery. Med J Aust 2008;188:409-13.  Back to cited text no. 7
    
8.
Nicholson G, Burrin JM, Hall GM. Peri-operative steroid supplementation. Anaesthesia 1998;53:1091-104.  Back to cited text no. 8
    
9.
Fleisher LA, Mythen M. Anesthetic implications of concurrent diseases. Miller's Anesthesia. 8th ed.., Ch. 39. Philadelphia: Elsevier; 2015. p. 1156-225.  Back to cited text no. 9
    
10.
Desborough JP. The stress response to trauma and surgery. Br J Anaesth 2000;85:109-17.  Back to cited text no. 10
    
11.
Singh M. Stress response and anaesthesia. Altering the peri and post-operative management. Indian J. Anaesth 2003;47:427-34.  Back to cited text no. 11
    
12.
Engquist A, Brandt MR, Fernandes A, Kehlet H. The blocking effect of epidural analgesia on the adrenocortical and hyperglycemic responses to surgery. Acta Anaesthesiol Scand 1977;21:330-5.  Back to cited text no. 12
    
13.
Jackson RE, Bellamy MC. Antihypertensive drugs. BJA Educ 2015;15:280-5.  Back to cited text no. 13
    
14.
Ikeda K, Isaka T, Fujioka K, Manome Y, Tojo K. Suppression of aldosterone synthesis and secretion by Ca (2+) channel antagonists. Int J Endocrinol 2012;2012:519467.  Back to cited text no. 14
    
15.
Mavroudis PD, Corbett SA, Calvano SE, Androulakis IP. Circadian characteristics of permissive and suppressive effects of cortisol and their role in homeostasis and the acute inflammatory response. Math Biosci 2015;260:54-64.  Back to cited text no. 15
    


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