|Year : 2022 | Volume
| Issue : 2 | Page : 143-145
Vasoplegic syndrome in urology: Report of an unusual case
Anil K Nallabothula, Manoj Bojja, Vaibhao M Nasare, Ashish K Singh
Department of Urology, Sri Venkateswara Institute of Medical Sciences [SVIMS], Tirupati, Andhra Pradesh, India
|Date of Submission||31-Dec-2021|
|Date of Decision||01-Jan-2022|
|Date of Acceptance||10-Jan-2022|
|Date of Web Publication||3-Aug-2022|
Dr. Vaibhao M Nasare
Department of Urology, SVIMS, Tirupati - 517 507, Andhra Pradesh
Source of Support: None, Conflict of Interest: None
Vasoplegic syndrome is often characterized by low systemic vascular resistance with clinical features of reduced blood pressure and normal or high cardiac output. Causes of vasoplegia are diverse and mostly include sepsis, cardiac surgery, non-cardiac surgery, burns, trauma, and pancreatitis. We report a case of Vasoplegic syndrome that encountered during left adrenalectomy operated for left pheochromocytoma. Postoperative hypotension is common and well documented in pheochromocytoma and it responds well to regular inotropes and volume replacement. The purpose of presenting this article is to highlight the possibility of rare resistant hypotension in this case and the invaluable role of drugs like vasopressin and methylene blue in such scenario. Hence, vasoplegia may be encountered even in urology case and we should keep high level of suspicion.
Keywords: Methylene blue, vasoplegia, vasopressin
|How to cite this article:|
Nallabothula AK, Bojja M, Nasare VM, Singh AK. Vasoplegic syndrome in urology: Report of an unusual case. J NTR Univ Health Sci 2022;11:143-5
| Introduction|| |
Vasoplegic syndrome (VS) is characterized by low systemic vascular resistance (SVR) with clinical features of reduced blood pressure (BP) and normal or high cardiac output (CO). It is mostly encountered in cardiac surgery but can also occur in non-cardiac surgery., Causes of vasoplegia are diverse and includes sepsis, cardiac surgery, non-cardiac surgery, burns, trauma, and pancreatitis. Diverse set of intrinsic vasodilatory pathway and associated hyporesponsiveness to vasopressor contribute to VS. Available treatment modalities includes fluid resucitation, catecholaminergic vasoconstrictors, vasopressin, and methylene blue. To the best of our knowledge, VS is not yet reported in urological surgery in the available literature.
| Case History|| |
A fourty-two-year-old male patient evaluated for left loin pain and diagnosed as left adrenal pheochromocytoma around 6 × 5 cm [Figure 1] with metanephrines 16.9 ng/ml and nor-metanephrines 4210 ng/ml. Endocrinology opinion was sought and was kept preoperatively on alpha-blocker (Tab.Prazosin 2.5 mg TID) and planned for left adrenalectomy.
|Figure 1: Computed tomography coronal images showing left adrenal mass measuring 6 × 5 cm|
Click here to view
Before anesthesia induction, BP was 130/80 mmHg, heart rate (HR) was 88 beats/min, sinus rhythm and peripheral oxygen saturation (SpO2) was 100%. Immediately after intubation, BP was 130/70 mmHg and HR was 82/min.
Around 70 min after start of surgery, due to intraoperative blood loss (around 300–400 ml), mean arterial pressure (MAP) falls around 49 to 55 mmHg. Inotropic support in the form of Inj. Noradrenaline 0.38 microgram/kg/min and Inj. Adrenaline 0.03 microgram/kg/min were started to recover MAP. Two units each of packed red blood cells (RBC) and fresh frozen plasma (FFP) were transfused immediately along with 1 L of fluids to cover blood loss. In spite of aggressive fluid resucitation and inotropic support, MAP remained below 60 mmHg. Intraoperative urine output was around 400 ml. Patient was observed for skin rash and urticaria. After completion of surgery, patient was shifted to recovery room and kept on mechanical ventilator while receiving Inj. Noradrenaline 0.46 microgram/kg/min and Inj. Adrenaline 0.11 microgam/kg/min.
On arrival in recovery room, patient was conscious with BP 76/54 mmHg and HR of 90/min and SpO2 99%. One unit each of packed RBC, FFP, and platelets were transfused postoperatively. Complete blood profile, Sr. Electrolyte, Sr. Lactate, Sr. creatinine, and ABG were sent. E.C.G was normal. To rule out cardiogenic shock, 2D-Echo was done and showed no abnormality. Ultrasound abdomen was done suggestive of minimal free fluid in abdomen. Intravenous fluid administered 2 ml/kg/h along with systemic antibiotic coverage. Post-tranfusion hemoglobin was 9.6 gm/dl, TLC was 15,500 cells/cumm, PCV was 23.7%, Sr. Lactate was 18.1 mmol/L, Na+ 132 meq/L, K+ 3.5 meq/L, Sr.creat 1.34 mg/dl, platelet count was 2.4 Lakhs/cumm, pH 7.3, pCO2 32.7 mmHg, and HCO3 16.2 mmol/L. Acidosis correction was done with sodium bicarbonate intravenous infusion. Inj.Noradrenaline and Adrenaline were slowly escaltated to 0.76 microgram/kg/min and 0.17 microgram/kg/min, respectively, as there was no improvement in MAP.
At 12 hours post-operatively, patient was conscious, on mechanical ventilator, BP was 82/60 mmHg, HR 94/min, SpO2 100%, drain output 200 ml sero-haemorrhagic, and urine output was 100 ml. Although MAP remains above 60 mmHg, it was still lower than expected. Hence, we suspected VS and started Inj.Vasopressin 40u @3ml/h. Our next plan was to administer Inj. Methylene blue, however with Inj. Vasopressin administration only MAP rose from 67 mmHG to 85 mmHg [Graph 1]. BP was 110/72 mmHg with HR 90/min. Inj. Noradrenaline and Inj. Adrenaline were tapered first, followed by Inj.Vasopressin as systolic BP remained above 110 mmHg and finally all inotropes were stopped. Patient was discharged on postoperative day 9 without any complications.
| Discussion|| |
Vasoplegia is an ill-defined clinical state often characterized by CO of >2.5 L/min/m2, SVR index of <1600 dynes-sec/cm/m2 and associated with severe hypotension despite volume resucitation and use of vasoconstictors. We carried out various investigations to identify the cause of patient's hypotension. Cardiac evaluation (2D-Echo, E.C.G) was normal. Patient was not having any signs of urticaria and he received ample amount of volume resuscitation with fluid and blood transfusion and hence cardiogenic, anaphylactic, and hypovolemic shock have been ruled out. We strongly suspected VS as patient's MAP was not improving in spite of high dose of catecholamines.
Vascular tone is determined by contractile activity of vascular smooth muscle cell (VSMC) that is regulated by rise in cytosolic Ca++ concentration. VS mediated by diverse set of extrinsic and intrinsic set of pathways. Vasoplegia is a response to pathogen associated molecular patterns (PAMPS), damage associated molecular patterns (DAMPS), and other mechanism that leads to vasodilation, greater vessel capacitance, and increased capillary permeability resulting in shock. Most common cause of PAMPS is sepsis. DAMPS include polytrauma or burns. Other causes include anaphylaxis, neurogenic, or drug associated mechanism. Nitric oxide (NO) is a critical intrinsic regulator of vascular tone.
In human, alpha adrenergic receptors play an important role in BP regulation. Alpha1 receptors are located postsynaptic in VSMC and on activation increase smooth muscle tone and hence MAP. Prazosin inhibits postsynaptic alpha1 receptors leading to catecholamine resistance.
Goal of treatment for VS is to increase MAP without increasing HR and myocardial O2 demand. First line drugs include catecholamine vasoconstrictor like dopamine, epineprine, norepinephrine, or phenylephrine that stimulate alpha adrenergic receptors.
Norepinephrine is a very potent, reliable vasopressor that increases MAP without increasing myocardial oxygen demand and HR. It maintains ventricular arterial coupling via Beta1 adrenergic receptor stimulation.
Vasopressin is second line agent in treatment of VS. It stimulates all vasopressin receptor subtypes (V1a, V1b, and V2). V2 receptor stimulation leads to adverse effect like fluid accumulation, microvascular thrombosis, and vasodilation. V1 receptor stimulation increases intracellular calcium via G protein coupled receptors and phospholipase C resulting in VSMC contraction.
Methylene blue may effectively treat severe VS. It inhibits excessive production and activity of both NO and cGMP by competitively binding to guanylate cyclase. NO plays an important role in vasodilation.
Our patient developed VS most probably due to preoperative administration of alpha blockers (prazosin). Intraoperative blood loss was a triggering event. Postoperative hypotension is common and well documented in pheochromocytoma and it responds well to regular inotropes and volume replacement. In our case, it responded poorly even to initial high doses of catecholamine vasopressors. However, with administration of vasopressin, MAP increased significantly. The purpose of presenting this article is to highlight the possibility of rare resistant hypotension in this case and the invaluable role of drugs like vasopressin and methylene blue in such scenario. Hence, vasoplegia may be encountered even in urology case and we should keep high level of suspicion.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Gomes WJ, Carvalho AC, Palma JH, Gonçalves I Jr, Buffolo E. Vasoplegic syndrome: A new dilemma. J Thorac Cardiovasc Surg 1994;107:942-3.
Levy B, Fritz C, Tahon E, Jacquot A, Auchet T, Kimmoun A. Vasoplegia treatments: The past, the present, and the future. Crit Care 2018;22:52.
Kimmoun A, Ducrocq N, Levy B. Mechanisms of vascular hypores ponsiveness in septic shock. CurrVascPharmacol2013;11:139-49.
Liu H, Yu L, Yang L, Green MS. Vasoplegic syndrome: An update on perioperative considerations. J Clin Anesth 2017;40:63-71.
Lambden S, Creagh-Brown BC, Hunt J, Summers C, Forni LG. Definitions and pathophysiology of vasoplegic shock. Crit Care 2018;22:174.