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LETTER TO EDITOR
Year : 2011  |  Volume : 55  |  Issue : 3  |  Page : 318-320  

Tramadol-induced respiratory depression in a morbidly obese patient with normal renal function


1 Department of Anaesthesiology, A J Institute of Medical Sciences, Kuntikana, Mangalore, Karnataka, India
2 Department of Plastic & Reconstructive Surgery, A J Institute of Medical Sciences, Kuntikana, Mangalore, Karnataka, India

Date of Web Publication7-Jul-2011

Correspondence Address:
Thrivikrama P Tantry
Department of Anaesthesiology, A J Institute of Medical Sciences, Kuntikana, Mangalore - 575 004, Karnataka
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0019-5049.82667

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How to cite this article:
Tantry TP, Kadam D, Shetty P, Adappa KK. Tramadol-induced respiratory depression in a morbidly obese patient with normal renal function. Indian J Anaesth 2011;55:318-20

How to cite this URL:
Tantry TP, Kadam D, Shetty P, Adappa KK. Tramadol-induced respiratory depression in a morbidly obese patient with normal renal function. Indian J Anaesth [serial online] 2011 [cited 2019 Oct 22];55:318-20. Available from: http://www.ijaweb.org/text.asp?2011/55/3/318/82667

Sir,

Among opioids, tramadol hydrochloride is considered safer than other opioids with respect to its respiratory effects. Dose of tramadol in post-operative patient is up to 250 mg intravenous (i.v.) in initial hour and 600 mg in 24 h. [1] The metabolite of tramadol, O-desmethyl tramadol, (+ODT) has been shown to have an affinity for m opioid receptors (200 times) than that of parent drug and is responsible for analgesia. Tramadol-induced respiratory depression was reported previously in patients with altered renal function. [2] We report such an event in a morbidly obese patient but with normal renal and hepatic functions who received tramadol in clinical doses.

A 50-year male, weighing 143 kg (BMI: 50.7 kg/m 2 ), ASA 2 classification, was without any co-morbidity was scheduled for surgery for thigh reduction-plasty [Figure 1]. Nonsmoker nonalcoholic patient with good exercise tolerance reported two uneventful previous surgeries two years ago. He had no history suggestive of obstructive sleep apnoea (OSA) syndrome. Patient had normal renal, liver, cardiovascular function tests. Though pulmonary function tests [Figure 2] were suggestive of early minimal small air way obstruction, after consultation with pulmonologist, it was concluded as adequate. Pre-operative arterial blood gas (ABG) showed pH of 7.347, pCO 2 of 55.5 mmHg, pO 2 of 73.2 and saturation of 90%.
Figure 1: Morbidly obese patient under anaesthesia for thigh reduction plasty

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Figure 2: Preoperative pulmonary function testing curves. (FVC of 75% of predicted, FEV1 of 68% of predicted, FEF25-75 of 33% of predicted and FVV1/FVC ratio of 90% of predicted)

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Operating table width was adjusted with additional supports to accommodate hugely built patient. Anaesthesia was induced with fentanyl (150 μg i.v), inj. Propofol (2.5 mg/kg) and succynylcholine (1.5 mg/kg). Sevoflurane-vecuronium-fentanyl (150μg) was used for maintenance. During the uneventful surgery, patient received three units of whole blood, inj. diclofenac sodium 75 mg (i.m). Extubation was uneventful.

In the first hour of post-operative period, patient complained severe pain at the operating site. Inj. tramadol 200 mg i.v. was advised and ordered to repeat 8 th hourly. Four hours later, patient had adequate pain relief. Second dose of tramadol was administered at 8 th hour. Patient was found increasingly drowsy and further tramadol injection was omitted. Patient became unresponsive at 17 th hour with sluggish low respiratory rate breathing. ABG showed pH of 6.989, pCO 2 of 121.4 mmHg, pO 2 of 57.1 mmHg, HCO 3 of 28.6 mmol/l and SpO 2 of 65%. Emergency intubation was done and mechanical ventilation was started. Inj. Naloxone 0.4 mg i.v. was administered. Subsequently, patient was conscious with adequate mechanical ventilation. ABG parameters improved further. Patient was extubated at 28 th hour.

In clinical practice, respiratory depression by tramadol is extremely rare. [3] Previous studies shown unaltered end-tidal CO 2 changes or respiratory functions with tramadol usage in contrast to injection morphine [4] or pethedine [5] in spontaneously breathing patients. Further, the respiratory rate, arterial O 2 and CO 2 tensions were found normal in spontaneously breathing patients following upper abdominal surgeries who received epidural tramadol. [6] Teppema et al.[7] observed dose dependent respiratory depression due to tramadol in cats in doses 1-4 mg/kg and highlight the similar possibility in humans in the early postoperative period when residual anaesthetic effects still existing. However, our patient had dose of 1.5 mg/kg and the respiratory effects were observed in late post operative period where anaesthetic effects are ruled out.

Our patient had minimally altered but adequate pulmonary functions. Preoperative ABG showed minimally increased CO 2 levels, a significant increase in CO 2 level and unresponsiveness followed tramadol injections suggesting the possibility of respiratory depression by tramadol. Should the primary cause of respiratory depression be due to pulmonary insufficiency, then patient would have developed respiratory failure in the early post operative period itself when the residual anaesthetic effects still persist. Our patient had excellent recovery from anaesthesia. Conscious patient with complete cognitive and neuromuscular recovery usually need further sedation (and paralysis) for elective mechanical ventilation. Further, respiratory function was unaffected by the surgical incision. Thus, elective mechanical ventilation was not considered.

Respiratory depression following iatrogenic tramadol overuse can occur in individuals carrying CYP 2 D 6 duplication (ultrarapid metabolisers, UM). [8] These patients display increased enzyme activity for tramadol, resulting highly increased transformation to active metabolite (+)ODT. However, Asian population have the lowest incidence of 0.5%-2.5% of the CYP 2 D 6 UM genotype, compared to other continents, and the possibility of having such a genotype in our patient could be rare. Routine screening tests for UM genotyping (by polymerase chain reaction) may not be economically feasible, which is a limiting factor to investigate further in our clinical settings.

 
   References Top

1.Duthie DJ. Remifentanil and tramadol. Br J Anaesth 1998;81:51-7.  Back to cited text no. 1
    
2.Mattia C, Mazzaferro S, Coluzzi F, Luzi M. Respiratory depression following iatrogenic tramadol overuse in a patient with chronic renal failure. J Headache Pain 2004;5:137-9.  Back to cited text no. 2
    
3.Adams JP, Murphy PG. Obesity in anaesthesia and intensive care. Br J Anaesth 2000;85:91-108.  Back to cited text no. 3
    
4.Vickes MD, O'Flaherty D, Szekely SM, Read M, Yoshizumi J. Tramadol. Pain relief by an opioid without depression of respiration. Anaesthesia 1992;47:291-6.  Back to cited text no. 4
    
5.Tarrkkila P, Tuominen M, Lindgren L. Comparision of respiratory effects of tramadol and pethedine. Eur J Anaesthsiol 1998;15:64-8.  Back to cited text no. 5
    
6.Baraka A, Jabbour S, Ghabash M, Nader A, Khoury G, Sibai A. A comparision of epidural tramadol and epidural morphine for postoperative analgesia. Can J Anaesth 1993;40:308-13.  Back to cited text no. 6
    
7.Teppema LJ, Nieuwenhuijs D, Olievier CN, Dahan A. Respiratory depression by tramadol in the cat: involvement of opioid receptors. Anesthesiology 2003;98:420-7.  Back to cited text no. 7
    
8.Gan SH, Ismail R, Wan Adnan WA, Zulmi W. Impact of CYP2D6 genetic polymorphism on tramadol pharmacokinetics and pharmacodynamics. Mol Diagn Ther 2007;11:171-81.  Back to cited text no. 8
    


    Figures

  [Figure 1], [Figure 2]


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