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Year : 2019  |  Volume : 8  |  Issue : 1  |  Page : 73-74

Anesthetic dilemma in a case of tuberculoid leprosy

Department of Anesthesiology and Critical Care, INHS Asvini, Mumbai, Maharashtra, India

Date of Web Publication18-Feb-2019

Correspondence Address:
Dr. Vidhu Bhatnagar
Department of Anesthesiology and Critical Care, INHS Asvini, Near RC Church, Colaba, Mumbai - 400 005, Maharashtra
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ijhas.IJHAS_95_18

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How to cite this article:
Dwivedi D, Bhatnagar V, Karmarkar AA, Kanagraj M. Anesthetic dilemma in a case of tuberculoid leprosy. Int J Health Allied Sci 2019;8:73-4

How to cite this URL:
Dwivedi D, Bhatnagar V, Karmarkar AA, Kanagraj M. Anesthetic dilemma in a case of tuberculoid leprosy. Int J Health Allied Sci [serial online] 2019 [cited 2022 Dec 9];8:73-4. Available from: https://www.ijhas.in/text.asp?2019/8/1/73/252456


We intend to publish a report on anesthetic dilemma in a case of tuberculoid leprosy as a letter to editor. Leprosy or Hansen's disease is uncommon in developed countries, but around 80% of the worlds' cases are still reported from developing countries.[1] It is a chronic infectious disease caused by Mycobacterium leprae and involves mainly skin, peripheral nervous system, upper respiratory tract, eyes, and testes. The presence of any leprous reactions heralds serious complication as consequence of dynamic changes in the immune status of the patient. Clinical, bacteriological, pathological, and immunological spectrum of leprosy varies between tuberculoid and lepromatous leprosy.[1] In India, around 90% of cases are tuberculoid leprosy which remain confined to the skin and peripheral nerves. The skin lesions consist of anhidrotic, hyperesthetic, hypopigmented macules, or plaques. Peripheral nerve involvement leads to their enlargement in thickness and neuropathy and commonly involves the ulnar, posterior auricular, peroneal and posterior tibial nerves. While lepromatous neuropathy leads to insensitivity and myopathy which in turn, leads to plantar ulceration, foot drop, and joint deformities.[1],[2] Complications such as corneal ulceration, opacities, cataract or glaucoma, orchitis, and nerve abscess may also present. Early diagnosis and treatment with multidrug therapy (MDT: dapsone, rifampicin, and clofazimine) kills the pathogen and remains the key element in eliminating the disease.[1],[2],[3]

We present a case of a 24-year-old male, a diagnosed case of Hansen's disease (on basis of nerve biopsy) who came for surgery for ulnar nerve entrapment of the right hand [Figure 1]. The patient was on MDT (dapsone 100 mg BD + rifampicin 600 mg OD) for the past 2 years. During the early phase of treatment, the patient developed hypopigmented macules all over truncal area and right shoulder [Figure 2] and had leprae reaction 6 months back.
Figure 1: Ulnar nerve involvement

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Figure 2: Hypopigmented macules at the back

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The dilemma arose when we had to tailor an anesthetic plan for this patient; choice between deep sea and the devil: general anesthesia (GA) versus regional anesthesia (RA).

Cardiovascular system involvement in leprosy leads to dysautonomia causing bradycardia, hypotension, cardiac arrest, various arrhythmias, and other electrocardiogram changes. Respiratory complications lead to depressed cough reflex, alteration in pulmonary function test, and risk of aspiration. Autonomic neuropathy may manifest as orthostatic hypotension, altered baroreceptor reflex and impaired response to valsalva maneuver. Anemia, thrombocytopenia, and agranulocytosis due to leprosy lead to decrease in oxygen-carrying capacity, impaired coagulation, and increased chance of postoperative infection. Hepatorenal derangements, due to the disease process or due to chronic ingestion of rifampicin and dapsone may cause delayed recovery from anesthesia. Dapsone may also produce hemolytic anemia, methemoglobinemia, agranulocytosis, peripheral neuropathy, and leprae reaction.[1] These patients are prone to nerve damage and neuropathies, motor nerve function impairment observed as weakness/paralysis of muscles and loss of muscle mass, progressing to deformities if mixed nerve is involved.[1],[3],[4],[5] Although GA is not a very palatable choice due to long-standing MDT, history of leprae reaction, high chances of neurological deficit being accentuated, or new neurological deficits following after nerve blocks in the presence of nerve involvement make RA also a very debatable choice. Our patient had involvement of ulnar nerve, and we did not want the damage to increase on account of RA, thus chose GA.

We induced the patient with midazolam 1 mg, fentanyl 90 mcg, propofol 140 mg, and atracurium 35 mg intravenously (IV). The patient was endotracheally intubated and maintained on oxygen, air, and sevoflurane (minimum alveolar concentration 0.8–0.9). The standard monitoring continued. The patient remained hemodynamically stable intraoperatively; was uneventfully extubated postsurgery after reversal. Postoperative analgesia was maintained with IV Paracetamol 1 g 8 hourly. Keeping in view, the increased risk of cardiac, respiratory, and autonomic involvement in leprosy patients as well as the risk to nerves because of RA, a well thought of plan needs to be tailored for the patient for correct execution of anesthesia.

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.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Rao PN, Suneetha S. Neuritis definition, clinic pathological manifestation and proforma to record nerve impairment in leprosy. In: Kar HK, Kumar B, editors. IAL Texbook of Leprosy. 1st ed. New Delhi: Jaypee Brothers Medical Publishers Ltd.; 2010. p. 253-68.  Back to cited text no. 1
Mendiratta V, Khan A, Jain A. Primary neuritic lesion: A reappraisal at a tertiary care hospital. Indian J Lepr 2006;78:261-7.  Back to cited text no. 2
Smith EW. Diagnosis of pure neuritic leprosy. Neurol J Southeast Asia 2002;7:61-3.  Back to cited text no. 3
Scollard DM. The biology of nerve injury in leprosy. Lepr Rev 2008;79:242-53.  Back to cited text no. 4
Rai D, Malhotra HS, Garg RK, Goel MM, Malhotra KP, Kumar V, et al. Nerve abscess in primary neuritic leprosy. Lepr Rev 2013;84:136-40.  Back to cited text no. 5


  [Figure 1], [Figure 2]


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