Anesthesia & Clinical Research
Open Access

Resistant Hypertension and Rare Variant of Primary Aldosteronism: An Incidental Finding in Pediatric Patient Undergoing Opthalmic Procedure

Balbir Kumar^1*, Brajesh Kumar Ratre¹ and Alka Yadav^{2 *}Correspondence: Balbir Kumar, Department of Onco-Anaesthesia, All India Institute of Medical Sciences, New Delhi, India, Tel: 7006582855, Email:

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Introduction

Hypertension in pediatric patient is exceedingly important issue because it lead to poor outcomes and is defined as blood pressure greater than or equal to 95^th percentile or greater on minimum three separate occasions for age height and gender. It can be primary or secondary. However secondary etiology is more common children [1]. Persistent elevation of BP above the goal inspite of concurrent use of three to four antihypertensive of different classes at maximally tolerated doses including diuretic is called as resistant hypertension. Resistant hypertension in children is on rise in frequency and having significant long term and short term health consequences. Common causes of resistant hypertension include primary aldosteronism, sleep apnea, diabetes, chronic kidney disease, cones syndrome. Since primary aldosteronism is common and treatable cause of hypertension, so its diagnosis is imperative. We report a case in which unexpected refractory hypertension was diagnosed during general anaesthesia in 9 year girl posted for congenital ptosis surgery and later on further investigation found to be rare variant of primary aldosteronism.

Case Report

A 9 year old girl (18 kg) was admitted to the hospital for bilateral frontalis sling surgery for congenital ptosis under general anaesthesia. She had slight delay in mile stone and IQ was low. History of recurrent respiratory tract infection, failure to thrive and palpitation. Child was diagnosed as small ventricular septal defect which was advised to manage conservatively. On cardiac examination, PR-10⁶/min, on auscultation she had in a grade IV pansystolic murmur on left sternal border and palpable thrill was present. No history suggestive of pulmonary hypertension, congestive heart failure [2].

Preoperative blood investigations (CBC, KFT, LFT) and chest x-ray was with normal limits, ECG shows left ventricular hypertrophy and 2 D Echocardiography showed small outlet VSD, 13.5 mmHg (Left to pressure on gradient Right) with mild AR, no pulmonary hypertension, no left ventricular outlet obstruction, obstruction, ejection under fraction 60% (Figure 1).

Figure 1: ECG of the child undergoing surgery.

Patient taken inside operation room, standard ASA monitors were attached five lead ECG, NIBP, SPO₂ and 22G IV cannula was secured. Baseline parameters were pulse rate: 110 min, spo₂ 99% on room air. She was induced with inj. Fentanyl 2 mcg/kg, inj propofol 2 mg/kg, in the mean while first reading of blood pressure was noticed as 180/100 mmHg, blood pressure cuff size was changed and again blood pressure was noticed in a 164/102 mmHg. Bag and mask ventilation was done, inj atracurium 0.5 mg/kg was given and airway was secured with AMBU LMA 2.0 and maintained with oxygen and air with isoflurane. Intraoperatively blood pressure was a 130/84 mm/Hg to 140/90 mmHg. Adequate analgesia was given with inj paracetamol 270 mg, inj ketorolac 9 mg, and inj fentanyl. After completion of surgery patient was extubated successfully with adequate reversal with neostigmine and glycopyrrolate. After extubation blood pressure was 160/100 mmHg. There was no requirement of antihypertensive during intraoperative period. Procedure lasted for 30 minutes [3].

After surgery, patient was shifted to Post Anaesthesia Care Unit (PACU) for continuous haemodynamic monitoring with oxygen via face mask. After 15 minutes after shifting to PACU patient’s BP reading was 200/110 mmHg, pulse rate 72/min, regular, good volume no radio femoral delay, respiratory rate 20/min, spo 99%. Patient was immediately shifted to those in paediatric cardiologist. Patient was advised tab amlodipine 2.5 mg stat and inj nitroglycerin 1 mcg/kg/min while monitoring BP every ten mintues. Target was 25% reduction in BP over 24 hour, according to BP inj. nitroglycerin can be increased up to 4 mcg/kg/min. USG KUB, urine pulse routine and microscopy, urinary VMA to be done [4]. After 24 hour inj nitroglycerin, BP was controlled as 140-150/90-100 mmHg and inj nitroglycerin was stopped and patient was put on tab prazocin 0.3 mg/kg/ day, tab hydrochlorthiazide 0.6 mg/kg/day and a tab amlodipine 0.4 mg/kg/day. CECT of abdomen was normal. No adrenal mass lesion was seen. Thyroid profile and parathyroid hormone was with in normal limits. Aldosterone levels were detected high, rest hormonal profile cortisol levels with in normal limits. Urine routine and urinary VMA levels were with in normal limits. After 6 days of post-surgical day, patient was discharged on three anti hypertensives with provisional diagnosis of primary aldosteronism.

Discussion

Hypertension in children is classified into two stages. Stage 1 hypertension is the designation for BP levels that range from 95^th percentile to 99^th percentile plus 5 mm hg. Stage 2 with hypertension is the designation for BP levels that are above 99^th percentile plus 5 mmHg [5]. Our patient has who has in a stage 2 hypertension and her BP was not controlled evening three drugs so she has refractory hypertension. Base line blood pressure was not measured in this case before induction of anaesthesia because child was anxious and BP measurement tends to delayed until patient loses consciousness. Difficulty to recognize hypertension was encountered, as after induction BP was controlled with isoflurane, fentanyl and depth of anaesthesia. The preoperative blood Investigation and postop hormonal profile (except aldosterone which was high), USG, KUB CECT was normal. The provisional diagnosis of primary aldosteronism was made [6]. There are five well known subtypes of primary aldosteronism namely Aldosterone-Producing Adenoma (APA), Bilateral Adrenal Hyperplasia (BAH), Unilateral Adrenal Hyperplasia (UAH), Glucocorticoid-Remediable Aldosteronism (GRA) and rarely adrenocortical carcinoma. However sixth one, which may involve normal adrenal gland without any tumor or hyperplasia of adrenal gland is potential subtype. This case probably falls in this subtype of primary aldosteronism.

Conclusion

Undiagnosed hypertension is common in Pediatric patients, so we should be extra vigilant while examining these patients before any surgical procedure to avoid undesirable consequences. Moreover the possibility of primary aldosteronism must be seriously consideration in children diagnosed with essential hypertension after excluding other causes of essential hypertension as it has curable potential.

References

1. National high blood pressure education program working group on high blood pressure in children and adolescents. The fourth report on the diagnosis, evaluation, and treatment of high blood pressure in children and adolescents. Pediatrics. 2004;114(2):555-576.

   [Pubmed]

2. Calhoun DA, Jones D, Textor S, Goff DC, Murphy TP, Toto RD, et al. Resistant hypertension: Diagnosis, evaluation, and treatment: A scientific statement from the American heart association professional education committee of the council for high blood pressure research. Hypertension. 2008;51(6):1403-1419.

   [Crossref][Google Scholar][Pubmed]

3. Garg JP, Elliott WJ, Folker A, Izhar M, Black HR. Resistant hypertension revisited: A comparison of two university-based cohorts. Am J Hypertens. 2005;18(5):619-626.

   [Crossref][Google Scholar][Pubmed]

4. Hajizadeh N, Assadi F. Resistant hypertension: Current status, future challenges. Int J Prevent Med. 2014;5(Suppl 1):S21.

   [Google Scholar][Pubmed]

5. Nishimoto K, Tomlins SA, Kuick R, Cani AK, Giordano TJ, Hovelson DH, et al. Aldosterone-stimulating somatic gene mutations are common in normal adrenal glands. Proceed Nat Acad Sci. 2015;112(33):E4591-E4599.

   [Crossref][Google Scholar][Pubmed]

6. Nishimoto K, Nakagawa K, Li D, Kosaka T, Oya M, Mikami S, et al. Adrenocortical zonation in humans under normal and pathological conditions. J Clin Endocrinol Metab. 2010;95(5):2296-2305.

   [Crossref][Google Scholar][Pubmed]