Silent neuritis (Quiet Nerve Paralysis)

Leprosy Mailing List – March 9th, 2012 

Ref.:    Silent neuritis (Quiet Nerve Paralysis)From: H Srinivasan, Chennai, India

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Dear Dr Salvatore Noto,

Ref.: Query by Dr Narayanakumar (Kumbakonam, India) about “Silent neuritis”

Thank you, Dr Narayanakumar. My response is as follows :-

The term “Silent neuritis” is used by many to refer to the occurrence of nerve function deficit (NFD), usually motor paralysis, without concurrent or immediately antecedent episode of acute neuritis.  I preferred the term “Quiet Nerve Paralysis” (QNP) to refer to this phenomenon.

While leprologists were aware of its occurrence, I drew attention to the fact that it was associated with the occurrence of deformity in a significant proportion of patients [1].  Here I will not go into the reasons why I preferred the term ‘Quiet Nerve Paralysis’ to ‘Silent Neuritis’.  Interested colleagues may refer to reference [2].  

During the course of my investigations, in the field and in the sanatorium, on the origin and progress of deformities in leprosy patients, I found that motor paralysis and associated deformity was five times more common in patients giving a history of remembered attack(s) of acute neuritis of the concerned nerve trunk than in those not giving such a history.  However, I also found that such patients accounted for only about 20% to 25% of those showing paralytic deformity.  Even allowing for faulty memory, it appeared that a sizable proportion of patients developed deformity without developing acute neuritis.  We designated such patients as having ‘Quiet Nerve Paralysis’.

This group of patients comprised:
1). untreated or inadequately treated patients;
2).Patients adequately treated in the past and discharged as ‘cured’; as well as
3).patients still under treatment.
We hypothesized that uncontrolled leprosy was the cause of nerve paralysis in the first group and instituted proper anti-leprosy therapy in them.  We considered QNP as the manifestation of relapse of leprosy in the second group and treated them again with anti-leprosy treatment of the day.  As for the third group, we felt that, in the absence of other explanations, they probably had “subclinically operating reactional pathology” in them and so treated them with a standard course of prednisolone for three to four months or more depending on their response.  Varying proportion of patients showed partial or complete restoration of nerve function in all the three groups, indicating that our conjectures were probably correct, at least in those patients.  Those in the first two groups who did not show any sign of recovery of nerve function after three months of anti-leprosy therapy were given a standard course of steroid therapy for what it was worth.  If I remember right, there was no clinical evidence suggestive nerve compression in these patients and so nerve decompression was not offered to them.

We subsequently tried to carry out a prospective trial of steroid therapy for QNP in the field, but the results were not reliable due to operational problems.

I should also point out that the patients were from South India, and the study was done during the ‘dapsone era’ when dapsone monotherapy was the standard anti-leprosy treatment.  I do not know what the situation is like in present conditions of years of intensive coverage of the patient population with MDT and fewer cases of active leprosy in the environment.

H Srinivasan FRCS
Surgeon (Retd.)
25, First Seaward Road
Chennai - 600 041
India

[1] Srinivasan H, Rao KS, Shanmugam N (1982).  Steroid therapy in recent “quiet nerve paralysis” in leprosy. Leprosy in India  54(3) :  412 – 419.
[2] Srinivasan H, Gupte MD.  Experiences from studies on Quiet Nerve Paralysis, Ch. 3  in The Peripheral Nerve in Leprosy and Other Neuropathies, (pp 30 – 35), Ed. by Noshir H Antia & Vanaja P Shetty, Delhi, Oxford University Press, 1997.   

Acute abdomen in lepromatous (LL) leprosy

Leprosy Mailing List – November 3^rd, 2011

Ref.:   Acute abdomen in lepromatous (LL) leprosy.
From: Barreto J, Bauru, S. Paulo, Brazil

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Dear Salvatore, 

The questions that must be made about this case:

1. Is this patient with active (non treated) lepromatous leprosy?  If the answer is yes, Lucio's fenomenon must be ruled out; once it is not uncommom deep vascular trombosis in this type of leprosy.

2. Is this patient in erythema nodosum leprosum (ENL or type 2) reaction?  As well as in Lucio's fenomenon, deep trombosis also can occur during this reaction.  Dr Opromolla and Dr Raul Fleury published cases of deep vascular trombosis during type 2 reaction, in the past, in Hansenologia Internationalis (www.ilsl.br).  Some cases developed even myocardial infarction.

If the answer to both questions is no, other causes must be involved.

Regards,

Jaison 

“We changed and gave the clofazimine with a meal”

Leprosy Mailing List – November 3^rd, 2011 

Ref.:   “We changed and gave the clofazimine with a meal”.

From: G Warren, Sydney, Australia

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Dear Dr Noto,

Thank you for publishing that letter and picture by Dr Peton.  He does not mention what antileprosy medication the patient was on. -  was it multi-drug therapy (MDT)?  Was the patient on clofazimine – at what dose and for how long?

My comments are that in the early days we often used to use clofazimine as monotherapy (when doing the initial drug trials) and we used to give a dose of oil with each dose as initially recommended.  But we often gave it in 200 or 300m mgms daily.  Yes, it did produce a very dark skin in the Chinese patients.  A few of the patients did complain of abdominal discomfort if they did not take the oil. 

One patient was actually admitted to the major govt hospital and operated on for a suspected abdominal problem as he complained of persistent gastric discomfort.  From Memory (this was about 1970) they found very heavy pigmentation with clofazimine in the mucosa of the ileum and colon which were apparently very dark in colour (No I did not see it nor do I have a photo- good on you for getting the record).  But no evidence of gastric ulceration or other regular cause of gastric discomfort.  From that incident we changed and gave the clofazimine with a meal and had no further similar complaints.

Sometime in the 1980s an article appeared stating that clofazimine caused diarrhoea and similar problems but the case written up also had amoebic dysentery!  No we (treating literally hundreds of patients and doing regular path testing) found that clofazimine causes very few if any complications other than the discolouration of skin that fades within about a year of discontinuation.  But we did find that many of the biochemical abnormalities present (eg poor liver and kidney function) initially were corrected within the first year.- oh yes we treated any obvious abnormalities such as anaemia and parasites! 

I am sorry I cannot quote the publications concerned now-  but would be interested as to the symptoms of the patient he speaks about and recommend the clofazimine be given with his meals and or oil, in future.

Yours sincerely,

Grace Warren

Previously superintendent Hong Kong leprosarium 1960-75 and

Adviser for The Leprosy Mission In Asia for 1975-1994.

Unnecessary laparotomy for abdominal pain and fever due to clofazimine

Leprosy Mailing List – November 3^rd, 2011 

Ref.:   Unnecessary laparotomy for abdominal pain and fever due to clofazimine

From: Bryceson A, London, UK

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Dear Salvatore

I wonder if the patient was taking clofazimine.  If so, the red coloration might be due to clofazimine.  Clofazimine can cause abdominal pain, sometimes mimicking an acute abdomen.  The pain is thought to be due to an inflammatory reaction to crystals of the drug deposited in the small bowel mucosa and mesenteric lymph nodes.  For this reason the high starting dose (300 mg) of clofazimine that is used to control ENL (Type 2) reactions, should be reduced after 2 or 3 weeks.  References go back a long way, but here are some recent ones.

Jadhav MV, Sathe AG, Deore SS, et al. Tissue concentration, systemic distribution and toxicity of clofazimine--an autopsy study. Indian J Pathol Microbiol. 2004;47:281-283.

Mathew BS, Pulimood AB, Prasanna CG, et al. Clofazimine induced enteropathy--a case highlighting the importance of drug induced disease in differential diagnosis. Trop Gastroenterol. 2006;27:87-88.

Sukpanichnant S, Hargrove NS, Kachintorn U, et al. Clofazimine-induced crystal-storing histiocytosis producing chronic abdominal pain in a leprosy patient. Am J Surg Pathol. 2000;24:129-135.

I made the same mistake in 1979

Bryceson A. Unnecessary laparotomy for abdominal pain and fever due to clofazimine.  Lepr Rev. 1979 Sep;50(3):258-9.

Best wishes,

Anthony Bryceson

Abdominal complication of clofazimine

Leprosy Mailing List – November 3^rd, 2011 

Ref.:   Abdominal complication of clofazimine

From: W S C Smith, Aberdeen, UK

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Dear Dr Peton,

Thank you for circulating this photograph.  Had the patient been taking clofazimine – if so at what dose and for how long?

There are a few case reports in the literature of acute abdomen/abdominal pain associated with crystal formation due to clofazimine – I have attached reports from India, Thailand and Singapore – there are probably a few more.

Cairns Smith

http://informahealthcare.com/doi/abs/10.3109/00313029309068897

Acute abdomen in lepromatous (LL) leprosy. Request of information

Leprosy Mailing List – November 2^nd, 2011 

Ref.:   Acute abdomen in lepromatous (LL) leprosy. Request of information.

From: E Peton, Capital Federal, Argentina

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Dear Dr Noto,

I am a resident physician from an hospital in Argentina.  The last week a lepromatous patient was operated by an acute abdomen.  Nothing was found in the surgery, except a reddish discoloration of the colon (see attached picture).  I would like knowing if you have information about similar cases?
I hope in your answer. Thanks a lot in advance.

Best regards,

E Peton

Durand Hospital

Capital Federal

Argentina

Polymerase chain reaction in the diagnosis of paucibacillary leprosy in Colombia

Leprosy Mailing List – April 16^th, 2011 

Ref:     Polymerase chain reaction in the diagnosis of paucibacillary leprosy in Colombia
From: Cadorna-Castro N., Medellín, Colombia

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 Dear Dr. Noto,

 We have few but interesting experiences with the use of polymerase chain reaction (PCR) to help in the diagnosis paucibacillary (PB) leprosy.  However as you comment there is not a definitive concept about this technique.  

With the RLEP PCR we have detected new patients at early stage of disease; we do active search among high risk population: household contacts.  In our experience we could confirm several difficult cases of PB leprosy using PCR (RLEP 1-2 and RLEP 3-4), i.e:

1. Boy, 5 years old with a hipo-pigmented skin lesion on the leg, bacteriological index (BI) negative, both parents with multibacillary (MB) leprosy.  The PCR from skin biopsy was positive.

2. Boy 17 years old; contact of leprosy patient.  One skin lesion on leg.  It was difficult to evaluate sensitivity on the lesion; we concluded that there was no evident loss of sensitivity.  The BI was negative.  PCR from skin biopsy was positive.

We can use PCR as a complementary diagnostic tool for this kind of cases.  Kindly, find in attachment the paper of Donoghue et al:-

“PCR primers that can detect low levels of Mycobacterium leprae DNA”. 

Donoghue HD, Holton J, Spigelman M.

J Med Microbiol. 2001 Feb;50(2):177-182”.

Best wishes,

Nora Cardona-Castro.

MD. MSc.

Instituto Colombiano de Medicina Tropical.

Universidad CES.

A patient with leprosy who is awaiting renal transplant in the USA

Leprosy Mailing List – April 6^th, 2011 

Ref:     A patient with leprosy who is awaiting renal transplant in the USA

From: Laura O. Coster, George Town University, USA

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Dear Dr. Noto,

Dr Barbara Stryjewska from the Hansen's Institution recommended that I ask for your insight on a patient who is being evaluated at Georgetown University who was seen for pre-transplant Infectious Disease evaluation.  His previous medical care had been at an outside Hospital and Leprosy care through an outside Infectious Disease MD.  It is a very complicated case and I don't expect you to answer the below questions but if you could share your experience it would be very appreciated.

The major questions which are under debate:

1) Is his renal disease secondary to Leprosy;

2) Was Cryoglobulinemia responsible for his Renal disease;

3) Is there any contraindication to Renal Transplant;

4) Given his past history of Cytoxan (Cyclophosphamide. Also know as Endoxan) therapy which likely exacerbated his leprosy and substandard leprosy therapy how long should he be treated for Leprosy with traditional 3 drug therapy prior to transplant?

His story:

This 35 yr old man came from Bolivia in 2001 and was not diagnosed with Leprosy until 2007.  He developed endstage renal disease after 1 yr of Leprosy treatment in 2008, in detail:

- 2000: Diagnosed with "rheumatic fever" in Bolivia (the patient could not provide any details).  According to notes (but patient denies) he had recurrent pharyngitis from 2000- 2006.     

- 2001: Leg edema and elevated creatinine in the US.  Renal biopsy: Membrano-proliferative Glomerular Nephritis with crescent formation.  Significant mesangial capillary proliferation. 40% Crescent formation.  Staining of glomerular capillary walls and mesangium for IgG, C1a kappa and lamda.  Differential: cryoglobulinemia vs immunotactoid glomerulonephropathy vs. SLE.  At this time of this biopsy Cryoglobulins were negative and the diagnosis of Immunotactoid glomerulonephropathy was favored.  However, the staining pattern of both kappa and lambda light chain staining was atypical for Immunotactoid Glomerulonephritis.  Hand and arm warts were "diagnosed" at this time.

- December 2005: He presented with leg and facial swelling.  As per notes he had progressive neuropathy, splenomegaly, positive Cryoglobulins in blood (IgG kappa and IgM lambda) and his Creatinine was 2.1.  He was treated for "Essential mixed Cryoglobulinemia" with Cytoxan and Prednisone at least for a month.

- February 2006: Hospitalized for fever, tonsillitis, necrotic vasculitis of L ear and hands, new nephrotic syndrome and lower extremity.  At this point Cytoxan was stopped and patient was treated with plasmapheresis with good response.

Renal biopsy: "Immune complex-mediated glomerulonephritis with memrano-proliferative and focal crescentic patterns, most likely associated with Cryoglobulinemia".  At this hospitalization the patient had Cryoglobulins measurable in blood for some time.

Also patient had tonsillectomy which was read at the time as "actinomycetes structures".  (We recently sent the tonsillar biopsy to the Hansen's institute and it is actually c/w Lepromatous Leprosy).

- September 2007: Patient presented with nose bleed and a nasal biopsy and hand biopsy at this point were read as with Lepromatous Leprosy.

- September 2007/2008: Patient was initially treated with Dapsone/Rifampin for leprosy.  Because of non-hemolytic anemia on regimen he was changed to Minocycline/Rifampin x 12 months.  For unclear reasons the patient never received Clofazamine containing regimen.  During treatment for Leprosy his Creatinine increased from 2.1 to endstage renal disease by October 2008.

- February 2009: Patient was being evaluated for renal transplant so Hansen's Institute was involved.  A  forearm biopsy was compared to previous biopsy read Lepromatous Leprosy (LL-BL) in regression.  The Hansen's Institue recommended longer length of therapy given plans for renal transplant.  Again, for unclear reasons the patient was treated with non-Clofazamine regimen of Dapsone 25 mg qd/Rifampin monthly x 1 year.

- August 2010:  Skin biopsy of ear "Bacillary load within inflammatory area is decreased as compared to 04/09 arm biopsy. His first exam at Georgetown notable for Thinning eye brows, L ear pinna thinned, scattered macules on arm Hypertrophy on hand skin, bulla on palmar surface of distal digits, ballooning of digits. Decreased sensory sensation on face, arms (from biceps down) on legs (from thigh down). Multiple burn scars on legs.  He has a Peritoneal Dialysis catheter.

- January 2011: There was a National Teleconference through the Hansen's Institute where patient was treated  with the consensus that the patient should be treated at least 1 more year as he had substandard therapy.  The consensus was also that there was no contraindication to transplant as patients with leprosy did well if they were followed closely and new lesions were  treated.  At Georgetown, we started him on Dapsone, monthly Rifampin and Clofazamine in preparation for transplant. Unfortunately, he had non-hemolytic anemia again on Dapsone (he had not taken Rifampin yet) and will be changed to Minocycyline/Rifampin and Clofazamine.  It is thought that Cytoxan treatment in 12/05 increased the bacillary load and his 02/06 hospitalization with vasculitis could have been an ENL reaction.

Thank You for any thoughts on this difficult case, Laura

Laura O. Coster, M.D.

Assistant Professor of Medicine

Division of Infectious Diseases and Travel Medicine

Georgetown University Hospital

(202) 444-0153 (phone)

1-877-665-8072 (fax)

Case presentation (Perforation of the palate in leprosy)

Case presentation (Perforation of the palate in leprosy)

From: Theuvenet, J. Willem, Apeldoorn, The Netherlands

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Dear Dr. Krishna Bdr Tamang, Namasté!

Thank you for sharing the problems of this patient (LML Nov. 5^th, 2010). The perforation in his palate is the result of the chronic inflammation of the mucosa of his nose as often seen in multibacillary leprosy.  Is he not also having an erosion of his nasal septum?

The problems in eating and drinking can be partially elevated by a dentist/orthodontist who can make a removable palatal inlay for him that will cover his palate and should facilitate his eating and drinking.  It will take a while after finishing his MDT and before the nasal inflammation has completely subsided.  Only then it may be safe to make an attempt to reconstruct the palatal defect.  Depending on the condition of his palate and the size of the defect the solution may be in a reconstruction according to Langenbeck or coverage with a dorsal tongue flap.

As you now have an excellent hospital for reconstructive surgery in the Kathmandu valley, with plastic surgeons skilled in cleft lip and palate repair, I would suggest that your patient seeks their advice in due time!

Wih kind regards,

Dr. Willem J.Theuvenet,

Plastic Surgeon

Tourniquet in reconstructive surgery

Leprosy Mailing List – March 5^th, 2010

Ref.: Tourniquet in reconstructive surgery

From: T S Narayanakumar, Kumbakonam , India

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Dear Dr Noto,

I refer to “Nerve function loss after reconstructive surgery” by Angelica Piefer dated January 23, 2010. I have been following the communications regarding tourniquet in reconstructive surgery and I wish to add my observation.

I have used tourniquet in my patients both at Sacred Heart Leprosy Centre, Kumbakonam and Hoina Leprosy Research Centre, Muniguda. On few occasions, when I had extended tourniquet duration beyond 45 minutes, which is the usual, most of the patients used to complain of pain due to ischemia, especially when the duration exceed 50 to 55 minutes. That is the warning and indication to deflate the tourniquet at once.

Thanks,

With regards,

Narayanakumar

T S Narayanakumar ,

General and Hand Surgeon,

25, Gandhi Nagar,

Kumbakonam-612001

India

E mail drtsnkumar(at)yahoo.co.in

Tourniquet use in upper and lower extremity surgery

Leprosy Mailing List – March 1^st, 2010

Ref.: Tourniquet use in upper and lower extremity surgery

From: Antonio Salafia, Mumbai , India

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Dear Salvatore,

I would like to add my comments on the on-going discussion about tourniquet at its contraindications/side effects. As you know I am a trained hand-surgeon.

1.

In Legnano , Italy , where I trained under Prof. Morelli, we had an average of 40 major cases a day, in almost all cases a tourniquet was used.

2.

I have been following Prof. Morelli's teachings in all patients: leprosy and non-leprosy cases.
3.

I have operated a few hundred non leprosy patients (trauma, congenital) and more then 7000 leprosy cases.

In all the cases I have used the tourniquet, and so far, I have never had any compression/strangulation of nerves or any of the other side effects mentioned. I must add that when I operated on a nerve (be it the ulnar, the median or any other) I do not use a tourniquet except in a very few cases; most of the time there is no need; good hemostasis is all that it is required. Faulty technique, poor training are the reasons for these problems in most of the cases.

Dr. Antonio Salafia

Head of Dpt. Reconstructive Surgery

Vimala Dermatological Centre

Mumbai , India

Use of tourniquet in upper and lower extremity surgery

Leprosy Mailing List – March 1^st, 2010

Ref.: Use of tourniquet in upper and lower extremity surgery

From: James P. Wilton, Portsmouth , NH , USA

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Dear Dr. Noto,

I have read with great interest the ongoing commentaries regarding extremity tourniquet used in upper and lower extremity surgery. I can comfortably say after 25 years of lower extremity surgery both for reconstructive and peripheral neurological cases, that when a surgeon abides by the literature recommendations of releasing the tourniquet after 90 minutes for a 10 minute revascularization, that I have not seen any evidence of avascular necrosis or arterial compromise in the distal limb.

Studies have demonstrated that extremity hemostasis solely utilizing an Esmarch bandage can create internal pressure underneath the rubberized bandage well in excess of 300 mm of mercury. There is no way to clinically monitor the tissue pressure utilizing an Esmarch bandage as a tourniquet and this is not recommended or utilized either in the United States or South America where I perform surgery. Exsanguination of the limb with an Esmarch bandage prior to pressurization of a pneumatic limb tourniquet is preferred to help remove venous blood. This technique in no way creates vascular damage at the site of temporary application.

Advances in technology have allowed my surgical team to bring small digital tourniquets (Delphi Corporation) for our mission trips to South America . We utilized the use small digital tourniquet systems for major joint replacement surgery (TKR), pediatric orthopedic limb surgery and for both upper and lower extremity peripheral neurological surgery. With strict adherence to the above mentioned time frames for tourniquet application, we have not experienced any adverse vascular issues with these types of surgery.

Warmest regards,

Dr. James P. Wilton, FACFAS, FSPS
330 Borthwick Ave. Suite #112

Portsmouth , NH , 03801 -5102

USA

603-430-8505-Work

603-436-8381-Fax

603-502-8043-Cell

jpwilton(at)gmail.com

Comments on “tourniquet/strangulation” application and time in reconstructive surgery in leprosy

Leprosy Mailing List – February 27^th, 2010

Ref.: Comments on “tourniquet/strangulation” application and time in reconstructive surgery in leprosy.

From: Latif Ahmed, Karachi , Pakistan

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Dear Dr Noto,

I thank Dr Warren for her detailed explanation on nerve block anaesthesia (LML Feb. 1^st, 2010 and LML Feb 22^nd, 2010). I had an opportunity to assist her in some operations at Marie Adelaide Leprosy Centre (MALC) Karachi in the period between 1976 - 1993, only when her trainee doctor was not available. I also had an opportunity to work as a resident doctor in orthopaedics at Jinnah Postgraduate Medical Centre (JPMC) Karachi . I have nothing to add in nerve blocks as Dr Warren has covered all the aspects. However, if you allow me to put some points on tourniquet application and time, and please allow me to use the term "strangulation" in place for tourniquet.

Dr Warren used a maximum of 2 hours continuous strangulation in arms and legs in a cool atmosphere at MALC operation room, while at JPMC anaesthetists released strangulation intermittently every half an hour for few minutes to allow circulation. That also helped surgeons to clamp and ligate small bleeders. It is worth mentioning that atmospheric temperature remains 30 - 40 degrees C in Karachi for most of the year.

For upper limb sphygmomanometer cuff was used where it is easier to monitor pressure. At MA LC 100 mm Hg was added in systolic pressure while at JPMC 30 - 50 mm Hg was added especially in thin individuals. For lower limbs MALC used a rubber band which was applied spirally up from distal to proximal to squeeze blood out first and then applied circularly at mid thigh region. It was impossible to monitor pressure.

The operating team at MALC consisted of a trainee doctor, an inexperienced ward-girl and a girl from central sterilisation room (CSR). The trainee doctor took double the time for operations like tibialis posterior tendon transfer (TPT) and other tendon transfers, sequestrectomies, bone trim of foot etc. In this setting I had seen horrible results post operative, most of the patients developed avascular necrosis in and around operation field, few had to go for below knee amputations and very few (about 4) above knee amputations. I had see good results when duration of operation was short (less than 1 hour. I wonder why Dr Warren did not pick a surgeon to train in reconstructive surgery .

My fimal comment is: "USE INTERMITTENT RELEASE OF TOURNIQUET IF DURATION OF OPERATION IS MORE THAN 1 HOUR.

I hope that my observations will not offend anyone.

With regards,

Dr Latif Ahmed

Ex Medical Director MALC

Axillary blocks. Better to be sure than sorry!

Leprosy Mailing List – February 22^nd, 2010

Ref.: Axillary blocks. Better to be sure than sorry!

From: Grace Warren, Sydney , Australia

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Dear Dr Noto,

I appreciate the letter from Dr Wim Theuvenet (LML Feb. 11^th, 2010) regarding axillary blocks and all he says is very true! Careful anaesthesia and duration of torniquet should not produce a neural deficit. But it is easy for accidents to happen. As we have heard in Angelika’s case reports. Thanks Wim.

The tourniquet pressure and time is very true and can in theory cause problems. Yes, I have seen such occasionally but I must state that in 50 years of doing arm surgery in third world countries for leprosy and other disabilities I have never had one of my patients develop a neural deficit from the tourniquet. Yes, I must confess some of the patients had the tourniquet on for longer that I really wanted. But I have seen residual deficits in leprosy and in non neuropathic conditions from anaesthesia into the nerve directly as via axillary or brachial or cervical block and even from spinal anaesthesia. Devastating - especially in third world countries - especially when preventable by use of anaesthesia that does not require injecting into the nerve. Hence I have avoided such blocks since the 1960s.

Never forget that a nerve may appear to be functioning normally when up to 10% of the fibres for any one modality can be already non functioning and in many patients there is no way of telling clinically which nerves are partially damaged and which are not. Electrical tests are useful but cannot tell the whole story! So, a normal EMG or electrical sensory tests may not show how much damage is present. I would prefer not to risk causing more damage in a nerve that may already been affected.

I rarely if ever use the major nerve blocks, certainly not in neuropathy patients. Better to be sure than sorry! We want to improve the patients function. Not increase his disability.

Thanks Wim for the details.

Grace Warren

MD., MS., FRCS, Rehabilitation surgery, especially in Leprosy.

Axillary blocks

Leprosy Mailing List – February 11^th, 2010

Ref.: Axillary blocks

From: Wim Theuvenet, Apeldoorn, The Netherlands

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Dear Angelika,

Thank you very much for your message dated LML Jan. 23^rd, 2010. Please allow for an addition to some other comments:

1.

All problems arose in axillary blocks that were not succesfull! A rare complication even in the hands of a skilled anaesthesiologist is the creation of a big haematoma around the axillary artery of which the resorption may affect all the 3 peripheral nerves. Final recovery can take up to 12 months! Perhaps your anaesthesiologist should receive a copy of "Regional Block" written by D.C.Moore ?

2.
The tourniquet time should not be applied/ necessary longer than a 45-60 minutes, as the cuff can be removed immediately after the tunnelling, and thus long before the final suturing of all transferred slips.

3.
Did you check the pressure of the inflated cuff, this can be limited to the max. systolic pressure plus 100 mm Hg.? When using ketamine for a failed block the titration rate is often increased only when pain is noticed. This pain may cause a temporary increase of the systolic blood pressure which, when the cuff pressure is not corrected accordingly, may cause venous blood congestion which is worse than ischaemia.

Hope that your future patients will face less trouble!

With warm personal regards,

Wim Theuvenet, M.D., Ph.D.

Plastic and Reconstructive Surgeon.

Axillary block anaesthesia

Leprosy Mailing List – February 1^st, 2010

Ref.: Axillary block anaesthesia

From: Latif Ahmad, Karachi , Pakistan

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Dear Salvatore,

I agree with Dr Brandsma LML Jan 27th 2010 but, if I may add, all 3 patients had failure of axillary block anaesthesia. Such a skilled procedure by an unskilled operator is likely to cause damage to nerve trunks especially when repeated attempts are made.

Dr Latif Ahmad

Dermatologist and

Ex Medical Director Leprosy Hospital Karachi

In leprosy axillary and cervical nerve blocks are not recommended

Leprosy Mailing List – February 1^st, 2010

Ref.: In leprosy axillary and cervical nerve blocks are not recommended

From: Grace Warren, Sidney , Australia

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Dear Salvatore,

I note with interest the various responses to the letter from Angelika (LML Jan. 23^rd Jan. 2010). I am fascinated by the many suggestions and yes I understand that the tight tourniquet could be a problem and has caused many problems but, I would be grateful if this paper of mine could be included to show workers that they do not need to inject the nerves directly and in a patient with marked nerve damage the extra needle damage may well be the last straw and produce the paralysis. I have seen it in non-leprosy people with otherwise normal nerve function, sometime producing severe lasting pain sometime producing paralysis.

In Leprosy we can never be sure exactly how much of a nerve has been damaged or completely destroyed and/or if we have got rid of all the infection that is destroying or has destroyed that group of nerve fibres, and hence if there is ever likely to be a further neural deficit in the future.

For good rehabilitation as soon as diagnosis is made, we should strengthen every muscle in the limb to its maximum and assess the detailed function of all nerves affected. Some nerve may have been damaged and yet may recover with time and good medication. Every patient with nerve damage in the arm, ought to be taught full hand exercises. Details of these exercises, are given in my book “The care of the neuropathic limb” (Parthenon – 1999). I will ask Dr Noto to publish a revision of those exercises in the LML. The idea is to help physiotherapists and other involved health workers in restore fuction in weak intrinsics etc.

After the disease is controlled and the muscle function has plateaued we can then assess what measures, surgical or otherwise can assist that person to rehabilitation.

In leprosy the nerves are involved very early in the disease but may not show a deficit for a prolonged period of time. When the nerve is damaged it does not show obvious deficient function until about 10% (some say 15%) of the nerve fibres of any one modality are damaged, so palpating a nerve may suggest it is OK but in fact some 6-8-10% of its fibres may be NON functioning and yet there is no obvious sign of the functional deficit.

Even skilled technicians cannot detect the functional deficit, initially, and may say ”No obvious deficit”- so when assessing a hand with a weakness of thumb opposition for example, one must assume that there is a weakness of the other medially innervated intrinsic muscles and even if not detectable at present there will be some deficit of the other modalities of that nerve in the future or there will be some sensory abnormality even if one cannot record anything definite. All the nerves in the arm are likely to be affected to some degree even if we cannot record it.

It is also wise to remember that in lepromatous leprosy the nerve damage is not obvious early and I have had patients who were initially “ cured” of the active infection before 1960, and recorded as “No neural deficit” and developed a neural deficit in the 1970s! Was this just that the continuation of the “healing” fibrosis in the nerves from the disease has eventually squeezed the life out of the remaining fibres or was it relapse? It was not obviously relapse as no other lesions were found just a progressive (usually ulnar) palsy! So One should bear this in mind when planning surgery so that one selects muscles for transfer carefully so that there are possibilities available if something further is needed in future.

The basic treatment of the patient is important in the long term rehabilitation of the patient. If the patient has any other disease like tuberculosis, typhoid or just a septic foot, anaemia, some intercurrent disease. Is he malnourished? We cannot expect good recovery for the malnourished!

When a nerve block is put in it is aimed at defunctioning some of the nerves, albeit temporarily. However in most nerve blocks one manages to damage some nerves permanently! I assume just by the needle hitting the nerve and I realised this to my disgust many years ago (in the i960s!). When I had two patients, within a few months, who developed radial nerve palsy from brachial plexus anaesthesia. As a medical student I had discovered that a cervical plexus block was more likely to produce problems and it is also much more difficult to put in for people who are not yet fully experienced. When I have to use an arm block now I use an upper arm or brachial block, which is much easier to insert and just as good for anything below the elbow.

For operations on leprosy patients the use of general sedation and ketamine is usually more than adequate, supplemented by a little local at incision sites if needed. Most of them if they have a paralysis due to leprosy also do have reduced sensory perception, and a good sedative plus ketamine is usually effective. However for that, one needs a suitable assistant to give the anaesthetic as he may need respiratory assistance or other medication. In many situations there is not other “doctor” to help.

An excellent alternate method is a “Biers Block” using a tourniquet on the arm and then injecting local anaesthetic into the vessels distal to the tourniquet . This is effective if one knows one can do the surgery within the hour or so .

The good old Karigiri Cocktail is excellent requiring NO injection of nerves and I still use that when a good anaesthetic doctor is not available. In many centres that I have visited teaching over the years, I have used Karigiri Cocktail by choice as I know it well and the patient has no post op discomfort from the anaesthetic! Again a good sedative with properly given preoperative sedation, seconal and phenergan and later morphine and scopolamine and Intravenous pethedine and largactil! (I wrote it up in Leprosy review in 1974!).

Second I note two of the hands used Palmaris tendon as the transferred tendon . We know it is never very strong . Sometimes I suspect the patient can never use it in isolation. I rarely if ever use it as an active transfer . If they can work it, it is very weak and not really strong enough to give a good thumb opponents as the patient needs a strong grip and Palmaris will never give that! Nor will the Extensor Pollicis Longus. Yes I have used it as a tenodesis for an intrinsic replacement when there is nothing else one can steal!

The object of the operation is to improve function and many of our patients need a strong grip . I often used is as a graft when it was not convenient to get a piece of leg fascia . I wonder what graft the surgeon used to extend Palmaris so it would reach the thumb? (aH I see fascia lata for at least one case) . So I would recommend that before any surgery the patient does 3 months of good physio under supervision (but he or she does it all himself) strengthening every muscle available and then make the assessment as to what to use. If you do not want a sublimus for opponens of thumb (it is the best usually I think) then the Flexor carpi radialis muscle can be quite effective or a wrist extensor (NOT flexor carpi ulnaris) that is too important in stabilising the wrist) - but in leprosy I rarely use Extensor carpi radialis longus or Extensor carpi radialis Brevis as the chances of needing an intrinsic is great- also the Pronator teres is excellent if done the correct way!, even brachioradialis in a very bad arm!

We always have to take into consideration the possibility that there is further progression of the neural deficit and be prepared to deal with it! Patients may have multiple bouts of paralysis because of relapses and inadequate therapy in the initial stages. The MDT regimens as suggested by WHO may be inadequate.

Now, in the first case mentioned I see weak thumb muscles I wonder how weak? And I wonder if intensive exercises would have restored enough function to have eliminated the need for surgery.

I note he used fascia as graft would have been easier to use Flexor carpi radialis as motor and palmaris as graft! Sounds now as if he will need a full radial nerve reconstruction . It is unlikely that the nerve will recover from the block injection . The steroids not much use, certainly do not give for more that 6 weeks at the most and as the nerve only regenerates at 1 inch per month it will be many months before one can say nothing doing! I advise all patients have Multivits with at least 10mgms Vit B and Vit C and zinc before and after surgery and for a t least a few months after .

Case two . Horrors high medial palsy as well, that arm is going to be a real challenge . No use giving steroid to long! That result means that the transfer does not work and apparently there is no long muscle left that is going to be worth transferring . Work with him 6 months to maintain mobility and then re-assess .

I do not mind if you write then and say what muscles do function and their strength I use the 0-5 voluntary muscle test (VMT) scale . Electrical tests do not really help . It is what the patient can do himself that counts . A wrist brace all the time now (in the post operative period). It may help him to try and use the fingers to encourage reuse of any nerve/muscle fibers still intact . I have produced some amazingly functioning arms is cases like this if the patient is realty prepared to persist and we get tensions etc correct ..

Case three is much the same. Do not try and rush. Remember the nerves re-grow at one inch per month! And from an axillary damage it is many inches to the muscle affected!

I hope this will warn THAT IN LEPROSY (and some other diseases) AXILLARY AND CERVICAL NERVE BLOCKS ARE NOT RECOMMENDED for reconstructive surgery . And people on poor diets or with other diseases need all the assistance they can get medically to encourage return of function of partly affected nerves .

Dr Grace Warren

The Hong Kong Leprosy Hospital., Hay Ling Chau 1959-1975;

Adviser in Leprosy and Reconstructive Surgery for The Leprosy Mission in Asia 1975-1994.