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Table of Contents
CASE REPORT
Year : 2021  |  Volume : 5  |  Issue : 2  |  Page : 125-127

Tourniquet complications in an upper extremity orthopedic surgery patients


Department of Anesthesiology and Intensive Care, Faculty of Medicine, Udayana University, Denpasar, Bali, Indonesia

Date of Submission16-Oct-2020
Date of Decision08-Jan-2021
Date of Acceptance11-Jan-2021
Date of Web Publication16-Apr-2021

Correspondence Address:
Dr. Christopher Ryalino
Department of Anesthesiology and Intensive Care, Faculty of Medicine, Udayana University, Jl. PB Sudirman, Denpasar 80232, Bali
Indonesia
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/bjoa.bjoa_227_20

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  Abstract 


An arterial tourniquet is a pneumatic device consisting of an inflated cuff connected to a supply of compressed gas. The most common use for these tourniquets is in surgical procedures on the extremities, where the tourniquet is very useful in optimizing the operating conditions by creating a bloodless surgical field. However, the exsanguination process followed by ischemia will result in physiological problems with local and systemic consequences. The patient in the case to be discussed is a 54-year-old woman with a diagnosis of implant loosening et causa nonunion left Montegia fracture who was scheduled for implant revision surgery. From these cases, it is possible that the patient experienced tourniquet-induced hypertension, which is one of the systemic complications that can arise due to the use of the tourniquet. It is said that tourniquet-induced hypertension is often difficult to control and is resistant so it is difficult to lower it. Emerging hypertension may not present a significant problem in young, noncomorbid patients, but in these patients with comorbid of hypertensive heart disease (HHD), elevated blood pressure can be very detrimental. Preoperative ketamine, clonidine, or lidocaine has been used to prevent tourniquet pain, which can lead to increased arterial pressure that is difficult to control. The anesthetist is also obliged to monitor the duration and pressure applied by the tourniquet so that it is not excessive so that detrimental complications can be prevented.

Keywords: Anesthesia, complications, tourniquet, tourniquet-induced hypertension, tourniquet pain


How to cite this article:
Agung Senapathi TG, Jobul IC, Pramana Suarjaya I P, Pradhana AP, Ryalino C. Tourniquet complications in an upper extremity orthopedic surgery patients. Bali J Anaesthesiol 2021;5:125-7

How to cite this URL:
Agung Senapathi TG, Jobul IC, Pramana Suarjaya I P, Pradhana AP, Ryalino C. Tourniquet complications in an upper extremity orthopedic surgery patients. Bali J Anaesthesiol [serial online] 2021 [cited 2021 Jun 23];5:125-7. Available from: https://www.bjoaonline.com/text.asp?2021/5/2/125/313887




  Introduction Top


A tourniquet is a device used to control blood flow to or from an extremity. The most common use for these tourniquets is in surgical procedures on the extremities, where the tourniquet is used in optimizing the operating conditions by creating a bloodless surgical field.[1] The exsanguination process followed by ischemia will result in physiological problems with local and systemic consequences that anesthetists should be aware of. Complications in young healthy controls are extremely rare, but the risk of tourniquet-related injury is increased in the elderly and is accompanied by comorbidities such as peripheral vascular disease.


  Case Report Top


A 54-year-old female patient came with a planned procedure revision of the left elbow implant. The patient was diagnosed with implant loosening et causa nonunion left monteggia fracture post-ORIF PS. Patients have fractured her left elbow and having ORIF PS surgery in 2016. The patient has a known history of hypertension since 2016, taking captopril but irregularly. The patient with a body mass index of 29.1 kg/m2, pain scale with numeric rating scale 2/10 when at rest. Laboratory tests were within normal limits, chest X-ray showed cardiomegaly with aortic elongation. Electrocardiogram in normal sinus rhythm and normal axis.

Anesthesia is performed using general anesthesia techniques and intubation with an endotracheal tube. Premedication was given with midazolam 2 mg intravenously, induction with propofol 150 mg, analgesic with fentanyl 150 mcg and muscle relaxant for atracurium 40 mg. The patient was intubated using ETT No. 7. Maintenance anesthesia is carried out with continuous propofol doses of 50–150 mcg/kg/min, sevoflurane gas from 0.6% to 0.8 vol%, and intermittent fentanyl and atracurium bolus.

Before induction, the patient's blood pressure ranges from 110 to 130/80–85 mmHg, pulse between 60 and 70x/min. Thirty minute after induction, a tourniquet was attached to the upper extremity of the patient under pressure of 244 mmHg. After that, the blood pressure increased quite drastically in the range 160–200/90–110 mmHg, with a pulse in the range of 70–80x/min. Continuous propofol increased to 200 mcg/kg/minute and adding intravenous (IV) fentanyl as an analgesic. Because the blood pressure was still quite high, clonidine given 75 mcg IV bolus, followed by clonidine drip 1–2 mcg/kg/h. After re-evaluation, blood pressure did not change significantly (still high). Clonidine has been increased to a dose of 4 mcg/kg/h, but blood pressure remains in the range of 170–180/100–110 mmHg. Deflation of the tourniquet is carried out after 2 h, and after deflation, the blood pressure returns to the range 80–100/50–60 mmHg.

The surgery was carried out with a total duration of 3 h, the use of a total tourniquet for 2 h. The patient was extubated, then monitored in the recovery room, before being returned to the ward with opioid postoperative analgesic. During the recovery room, blood pressure ranges from 130 to 140/80–85 mmHg, which is the same with patient's basal daily blood pressure.


  Discussion Top


Several systemic effects occur with inflation and deflation of the tourniquet in the upper limbs.

Cardiovascular effect

After exsanguination of the extremities and tourniquet inflation, there is an increase in systemic vascular resistance and an effective increase in circulating blood volume. This results in an increase in central venous pressure and in most cases accompanying increase in systolic arterial pressure, both of which are usually transient. Large increases in circulating blood volume can lead to large and sustained increases in central venous pressure and circulating volume overload. Heart failure and cardiac arrest have been reported following the insertion of bilateral tourniquets. After a temporary increase in arterial systolic pressure, there is usually a second gradual increase in arterial pressure. This is thought to be accompanied by tourniquet pain and appears after tourniquet inflation.[1],[2]

In tourniquet deflation, postischemic reactive hyperemia may occur, leading to a transient increase in limb blood volume compared to baseline. Simultaneously, metabolites from the ischemic limb are released into the systemic circulation. When combined with redistribution of blood flow, this often results in a drop in central venous and systolic pressure, which is transient but can be dramatic.[2]

Respiratory effect

The tourniquet deflation is followed immediately by an increase in end-tidal CO2 (etCO2) which usually peaks within 1 min. The increase in etCO2 occurs for reasons: mixed venous PCO2 is increased (after the release of hypercapnic blood from the distal ischemic area of the tourniquet into the systemic circulation).[2]

Central nervous system effect

The increase in PaCO2 that accompanies the tourniquet's deflation will lead to an increase in cerebral blood flow. Media cerebral artery blood flow velocity measurements showed an increase of up to 50%. In patients with head injuries, increased cerebral blood flow can lead to increased intracranial pressure and exacerbate secondary brain injury.[2],[3]

Temperature and metabolic effect

Arterial tourniquets inflation is associated with a gradual increase in core body temperature caused by reduced heat transfer and heat loss from an ischemic limb. The magnitude of this increase is only 0.5°C after 2 h of inflation.[2] Tourniquet deflation after 1–2 h of ischemia is associated with small increases in plasma concentrations of potassium and lactate. The peak increases of 0.3 and 2 mmol/l, respectively, occurred 3 min after deflation. Lactate and carbon dioxide return to the systemic circulation causing a decrease in arterial Ph.[2],[3]

The patient in the above case was a 54-year-old woman with a diagnosis of Implant loosening et causa nonunion left Monteggia fracture postORIF PS with implant revision surgery. From the above cases, it is possible that the patient experienced a tourniquet-induced hypertension, which is a systemic complication that can arise due to tourniquet use. It is said that tourniquet-induced hypertension is often difficult to control and is resistant so it is difficult to lower it. Emerging hypertension may not present a significant problem in young, noncomorbid patients, but in these patients with comorbid HHD, elevated blood pressure can be very detrimental.

Although the mechanism for tourniquet-induced hypertension is unclear, two mechanisms are thought to be involved; the first is activation of C fibers, causing stimulation of N-methyl-d-aspartate (NMDA) receptors in the dorsal horn of the spinal cord, and the second due to sympathetic activity. It is well known that it is the activation of the sympathetic nerves in response to the onset of tourniquet pain. The plasma norepinephrine concentration increases in parallel with arterial pressure during tourniquet inflation.

Clonidine (dose 3 mcg/kg in 100 ml NS for 10 min) can attenuate sympathetic activity and if given before surgery, can blunt the hypertensive response. Clonidine reduces the release of presynaptic norepinephrine, and has a substantial analgesic and sedative effect. Clonidine also blunts sympathetic responses. In the above case, the patient was given IV clonidine, but no reaction was expected, possibly because clonidine was given after hypertension occurred, which is very difficult to reduce.[4]

The preoperative small dose of IV ketamine (0.25 mg/kgBW) significantly prevented the increase in systemic arterial pressure during prolonged tourniquet inflation in patients under general anesthesia. The mechanism of the tourniquet-induced arterial pressure increase has not been investigated in detail, but there are studies that suggest the involvement of NMDA receptor activation. Indeed, the activation of the NMDA receptor results in an increase in mean arterial pressure, and NMDA receptor antagonism may block cardiovascular responses in animals. This patient was not given preoperative ketamine so the effect could not be evaluated for this patient.[5]

An increase in arterial pressure caused by a tourniquet can occur even with adequate anesthesia. It will be very difficult to treat hypertension when the increased arterial pressure due to this tourniquet occurs, especially in patients with cardiovascular problems, such as essential hypertension and ischemic heart disease; with neurological diseases, such as intracranial aneurysms and increased intracranial pressure status; or with glaucoma. IV ketamine before tourniquet and skin incision inflation is expected to prevent tourniquet-induced hypertension.[4] In another study, intraoperative use of lidocaine bolus (1 mg/kg), followed by infusion (2 mg/kg/h), starting 10 min before tourniquet inflation may resolve tourniquet-induced hypertension in patients undergoing anterior cruciate ligament reconstruction under general anesthesia.[6]

The orthopedic surgeon's survey revealed two general practices regarding inflationary pressure: (i) to develop tourniquets to a fixed pressure (typically 250 mm Hg for the upper arm) and (ii) developing the tourniquet to a pressure higher than the systolic arterial pressure (usually +100 mm Hg for the upper limb and + 100–150 mm Hg for the thigh). Expanding the cuff to a fixed pressure has been criticized for not taking into account the patient's baseline arterial pressure.[7] Another recommendation is increasing tourniquets to a pressure based on limb occlusion pressure (LOP). If the LOP is <130 mm Hg then 40 mm Hg is added, 60 mm Hg is added if the LOP is 131–190 mm Hg, and 80 mm Hg is added if the LOP is >190 mm Hg.[8]

All tourniquets must be kept to the minimum possible time. In practice, the timing of safe inflation will be determined by the patient's age, physical health, and the vascular integrity of the limb. Most recommendations in the literature recommend a period of 1.5–2 h in healthy adults. If the duration of operation exceeds the maximum safe inflation time, the tourniquet must be deflated for a short time.[7],[8]

In this patient's surgeon increased the tourniquet cuff pressure to a fixed rate (about 240–250 mmHg) without measuring the LOP first as suggested in theory. The result of this increase can lead to the risk of local complications such as muscle injury, ischemia, nerve injury, and increase the risk of systemic complications to arise. In this patient, there was no nerve or muscle injury as known as posttourniquet syndrome.


  Conclusion Top


Any patient predicted to use a tourniquet during surgery should be better prepared preoperatively. Preoperative ketamine, clonidine, or lidocaine has been used to prevent tourniquet pain, which can lead to increased arterial pressure that is difficult to control. The anesthetist is also obliged to monitor the duration and pressure applied by the tourniquet so that detrimental complications can be prevented.

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

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Deloughry JL, Griffiths R. Arterial tourniquets. Contin Educ Anaesth 2009;9:56-60.  Back to cited text no. 1
    
2.
Kam PC, Kavanagh R, Yoong FF. The arterial tourniquet: Pathophysiological consequences and anaesthetic implications. Anaesthesia 2001;56:534-45.  Back to cited text no. 2
    
3.
Townsend HS, Goodman SB, Schurman DJ, Hackel A, Brock-Utne JG. Tourniquet release: Systemic and metabolic effects. Acta Anaesthesiol Scand 1996;40:1234-7.  Back to cited text no. 3
    
4.
Zalunardo MP, Serafino D, Szelloe P, Weisser F, Zollinger A, Seifert B, et al. Preoperative clonidine blunts hyperadrenergic and hyperdynamic responses to prolonged tourniquet pressure during general anesthesia. Anesth Analg 2002;94:615-8.  Back to cited text no. 4
    
5.
Satsumae T, Yamaguchi H, Sakaguchi M, Yasunaga T, Yamashita S, Yamamoto S, et al. Preoperative small-dose ketamine prevented tourniquet-induced arterial pressure increase in orthopedic patients under general anesthesia. Anesth Analg 2001;92:1286-9.  Back to cited text no. 5
    
6.
El-Sayed W, Hasanein R. Intraoperative lidocaine infusion attenuates tourniquet induced hypertension in patients undergoing anterior cruciate ligament reconstruction under general anesthesia. Egypt J Anaesth 2016;32:345-50.  Back to cited text no. 6
    
7.
Sharma JP, Salhotra R. Tourniquets in orthopedic surgery. Indian J Orthop 2012;46:377-83.  Back to cited text no. 7
[PUBMED]  [Full text]  
8.
Kumar K, Railton C, Tawfic Q. Tourniquet application during anesthesia: “What we need to know?” J Anaesthesiol Clin Pharmacol 2016;32:424-30.  Back to cited text no. 8
    




 

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