An Unusual Phenomenon of Tourniquet-induced Hypertension in a Young Adult Male undergoing Lower Limb Surgery under Subarachnoid Block: A Case Report

The employment of tourniquet to achieve bloodless surgical field is an essential step, especially in upper/lower extremity orthopaedic surgical procedures. However, tourniquet itself can lead to many possible problems, posing challenges to the anaesthesiologists. One such is exaggerated hypertensive response sometime after inflation of tourniquet, aptly termed as Tourniquet-induced Hypertension (TIH/T-HTN). It may not be evident in some patients, but if and once established, it becomes practically impossible to minimise/reverse it. This can be a nightmarish experience for the anaesthesiologist concerned. The authors hereby present one such case where, a young, healthy 25-year-old male posted for arthroscopy of right knee, who was administered subarachnoid block with dexmedetomidine as an adjuvant to bupivacaine. Within 35 to 40 minutes of inflating the torniquet, he developed severe hypertensive response, with blood pressures ranging from a Systolic Blood Pressure (SBP) of 190 to 210 mmHg and a Diastolic Blood Pressure (DBP) of 118 to 125 mmHg. It remained unresponsive to any form of treatment, including, the sedation with Inj. Midazolam or incremental doses of Inj. Labetalol. The hypertension persisted throughout the duration of surgery, while patient remained comfortably asleep. However, at the end of the surgical procedure, as soon as the tourniquet was deflated, the Blood Pressures (BPs), both SBP and DBP dropped to baseline values. Also, includes an in-depth review of the available literary evidence about this phenomenon and provided specific deductions and recommendations/remedial measures.

Anaesthesiologist,Hypertensive response,Knee arthroscopy,Spinal analgesia

A 25-year-old male weighing 72 kg presented with history of domestic fall one year back. There was no significant past medical history except for chronic alcohol consumption, about 250-300 mL daily for the last 4-5 years. Magnetic Resonance Imaging (MRI) confirmed Anterior Cruciate Ligament (ACL) tear with moderate effusion in the right knee joint and patient was posted for arthroscopic reconstruction of ACL.

Pre-anaesthetic examination was essentially normal, with Body Mass Index (BMI) of 22 kg/m² and blood pressure of 110/86 mmHg. All the routine investigations were within normal limits. He was considered as American Society of Anaesthesiologists (ASA) I and planned under subarachnoid block.

On the operating table, patient was comfortable, with pulse rate of 89/min and blood pressure of 180/109 mmHg. After waiting for five minutes, the BP came perceptibly down, to 134/88 mmHg. Intravenous access was secured with 20 G cannula. Patient was made to sit up and under all sterile precautions, with median approach in L3-L4 space with help of 25 G Quincke’s needle to subarachnoid block was achieved using Injection Bupivacaine 0.5% heavy (3.4 mL)+dexmedetomidine (12 micrograms) for a total volume of 3.6 mL. The patient was then made supine and level of sensory block was achieved up to T10 segment.

The pulse rate gradually dropped and settled down between 52-58/min. However, blood pressure remained slightly on the higher side (130-135/80-84 mmHg). This trend continued throughout, application of tourniquet on the right thigh (which was not inflated yet), as well as during the painting, cleaning and draping of the area. The tourniquet was inflated to 280 mmHg.

After 35-40 minutes, blood pressure began to rise, reaching levels up to 210/125 mmHg (ranging between, SBP of 190-210 mmHg and DBP of 118-125 mmHg). The pulse rate varied between 48-89/min. Inj. Midazolam was administered in the incremental doses of 0.5 mg up to a total of 1.5 mg. Inj. Labetalol 20 mg was given in titrated incremental doses of 5 mg each was given over nearly 30-35 minutes. There was absolutely no decrease in the BP levels; however, the patient was comfortably sleeping and snoring.

Blood pressure continued to rise relentlessly inspite the authors efforts to bring it down. At this point, the procedure was over and the tourniquet was deflated. Within 1-2 minutes, blood pressure decreased on its own to 136/78 mmHg and the pulse rate settled at 71/min [Table/Fig-1]. By the time the patient was shifted to Post Anaesthesia Care Unit (PACU), the BP and pulse had stabilised to 122/80 mmHg and 59/min, respectively.

[Table/Fig-1]:

Blood pressure normalising within few minutes of deflation of torniquet.

The patient was monitored for two hours and, after an uneventful recovery, was transferred out of PACU. The Visual Analogue Scale (VAS) at that time was two and the patient remained pain-free until late evening. The patient remained haemodynamically stable throughout the postoperative period and was discharged from the hospital next afternoon.

The process of exsanguination of the limb and an application of the tourniquet on the upper/lower extremity is an essential modality for minimising the blood-loss during surgery/trauma [1]. Originally, a screw-like device was invented in 1718 by a French surgeon Louis Petit to minimise blood loss during lower limb amputations. It derived the name from a French verb ‘tourner,’ which literally means ‘to turn [1,2].’ A version of rubber bandages was introduced in 1873 by Johann Friedrich August von Esmarch, which is still used today as Esmarch’s bandage [2,3]. The first pneumatic tourniquet was introduced by Harvey Cushing in 1904 and evolved into the modern-day pneumatic tourniquets [2]. In earlier years, tourniquets were also used for achieving Intravenous Regional Anaesthesia (IVRA/Bier’s Block) [4].

Few reported untoward effects are tourniquet pain, post-tourniquet-induced muscle/neurovascular injury, metabolic and electrolyte disturbances, rise in end-tidal Partial pressure of Carbon dioxide (PCO₂) and, most importantly, hemodynamic disturbances in the form of rise in SBP, DBP, Mean Arterial Pressure (MAP) and heart rate [1,5-7]. Recently, a study confirmed significant rise in Intracranial Pressure (ICP) after deflation of tourniquets in patients where the Tourniquet Time (TT) exceeded 67.5 minutes [8].

A severe intraoperative hypertensive response to inflation of torniquet especially under neuraxial (spinal) anaesthesia, is an uncommon phenomenon. The commonality of chronology of events, as observed in the present case, BP generally starts rising anywhere between 35 to 60 minutes after the inflation of the tourniquet. The rise is seen in all the three forms of blood pressure-SBP, DBP and MAP-as well as heart rate, by more than 30% from the baseline and is generally not amenable to routine measures like, sedation or antihypertensives like β-blockers, α and β-blockers, or even centrally acting α2 agonists.

The striking finding is the spontaneous and complete disappearance of this response within few minutes of deflation of tourniquet, as was evident in the present case. Factors like, TT, patient factors like older age and pre-existence of hypertension have been suspected to be contributory. Tourniquet Pressure (TP) may not have much role to play, especially in the rise in ICP [8].

Bradford EMW (1969) first reported “haemodynamic changes associated with the application of lower limb tourniquets in patients undergoing orthopaedic procedures.” Apparently, on application of a lower limb tourniquet, there was congestion in the neck and face. She concluded that there was significant rise in central venous pressure and there was mild to moderate rise in SBP/DBP (18-19 mmHg). However, it should be noted that the surgeries were completed within 60 to 90 minutes. So mild to moderate rise may have been just the beginning of the process, which was aborted by the release of the tourniquet at the end of relatively quicker surgical procedures [9].

The first reported study was by Kaufman RD and Walts LF (1982). A retrospective review of total of 600 lower limb surgeries with inflation of tourniquet after anaesthetic (n=500) concluded that 55 (11%) showed a hypertensive response irrespective of the anaesthetic used (halothane, enflurane, nitrous oxide, narcotic, or regional), which disappeared after deflation. In comparison, in the control group where the tourniquet was not used (n=100), only 1 (1%) of the patients showed a hypertensive response. They postulated that this might be due to tourniquet pain, because of occurrence of both phenomena occurred after 45 minutes of tourniquet inflation. However, they did not provide any pertinent explanation. Nonetheless, they coined the term ‘Tourniquet-induced Hypertension’ (TIH) [10].

After encountering TIH and facing the mortality in elderly, obese and hypertensive patient for lower limb surgery under General Anaesthesia (GA), Valli H et al., conducted a study on 699 patients and found higher incidence of TIH associated with the factors like, older age, lower limb surgery, longer duration, GA, or Intravenous Regional Anaesthesia (IVRA), rather than spinal or brachial block [11]. Tetzlaff JE et al., provided the definition of T-HTN as ‘rise of the BP (any parameter or all) by 30% above baseline after the inflation of the tourniquet’ [12].

Surprisingly, the modality of anaesthesia, such as GA, IVRA, or neuraxial block (subarachnoid/epidural or combination), does not have any effect on this phenomenon. These reports also describe administration of multiple drugs preemptively to control these untoward effects, like, preoperative or intraoperative infusions of low-dose ketamine [13-17], magnesium [17,18], lidocaine [19], amantadine [20], clonidine [21,22] and, latest the spate of reports on dexmedetomidine [23-27].

In spite of these and many other articles on this issue, there is no known aetiology. Some theories/hypotheses are as follows:

At present, preoperative infusion of dexmedetomidine is considered to be most effective panacea for tourniquet-induced reperfusion injury, tourniquet pain and everything related to tourniquets [23-27].

Against this background, the present case appears to be unique. The patient was a young male with no significant history or preoperative problems, except for a history of chronic alcohol intake. During administration of subarachnoid block, the authors added dexmedetomidine as an adjuvant to bupivacaine and as expected, all the features of dexmedetomidine-enhanced subarachnoid block began to establish until the onset of Tourniquet-Induced Hypertension (TIH). Therefore, even its presence could not prevent the process. One can deduce that dexmedetomidine acts purely centrally in subarachnoid block, with no systemic effects. This is corroborated by all the reported studies/reports where specifically, dexmedetomidine has to be infused preoperatively to have any effect.

It also confirms that once the process has been initiated, any drug-whether benzodiazepines, opioids, lidocaine, ketamine, β-blockers, even centrally acting α2 agonists, cannot reverse or control it. One might consider allowing the process to go on relentlessly without intervention, as that was the only alternative left to the authors and it is expected to reverse itself momentarily upon deflation of the cuff [26]. This approach may be feasible in young, healthy patients as in present case case, who came out unscathed and recovered well. However, it might have disastrous consequences the compromised patients, as has been reported [11].

Another striking feature in the present case was that, contrary to the common occurrence of TIH in patients under GA, the present case involved a subarachnoid block. The correlation between TT and TIH was confirmed, as the TT in the present case was nearly 90 minutes.

The TIH is a dreadful phenomenon and all the patients requiring use of a tourniquet, especially for lower limb surgeries, are potential victims. If it is going to happen, it will happen, 30-45 minutes after inflation of the tourniquet. Factors like age (including paediatric patients), gender and preoperative conditions (with a greater predisposition in hypertensive patients) do not seem to matter. The modality of anaesthesia has no control over it; TIH can occur under general, regional, neuraxial, or IVRA. It may not necessarily be due to tourniquet pain. However, TT is a very important factor. Once established, there is currently no treatment for TIH. The reported efficacy of various drugs is not curative or therapeutic in established TIH but may be preventive if infused before the establishment of TIH, especially dexmedetomidine. So, anaesthesiologists must be prepared for prevention rather than treating established TIH, which would be futile/fruitless. Lastly, Surgeon needs to be sensitised and made aware about TIH and specificity of TT.

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