Clinical experiences with Acupuncture: failures and successes

FAILURES IN AP PRACTICE

Idealists may reject definition (c) as too soft, a cop-out for charlatans and incompetent clinicians. I suggest that it is a realistic recognition of the frailty of human endeavour and of the final and inevitable degeneration of human and animal life. In spite of decades of study of conventional and complementary diagnostic and therapeutic methods, the most skilled, sensitive, loving and intuitive of clinicians will still have failures, even under definition (c).

If we define success as in (c) above (medium-term elimination of most of the severe signs and symptoms, with restoration of body-mind functions to the extent possible under prevailing circumstances), clinical failures may be due to professional error; patient/owner error (non-compliance with advice given); coincidental disorders and inability of target organs to respond. Some patients may be "non-responders".

PROFESSIONAL ERROR

There are five main sources of professional error: (1) faulty diagnosis, (2) incorrect choice of points, (3) inadequate stimulation, (4) failure to use supportive therapies, (5) premature withdrawal of therapy.

1. Faulty diagnosis

Accurate diagnosis is needed for optimum results to any form of therapy. The cause, nature, location and extent/severity of the dis-ease/lesion/dis-order should be known. First-degree therapy aims to remove/alleviate the cause, to enhance the adaptive response and to provide supportive/symptom-atic relief during recovery.

In practice, many of us have not the training, skill or equipment to make a precise and detailed diagnosis in a conventional sense. Even if we have back-up services, we may put undue emphasis on laboratory or radiological findings. For instance non-clinicalmineral deficiency and non-clinical radiological lesions are commonplace and their correction will not improve the health/productivity of the "patient".

I am a Vet who has worked in nutritional/metabolic research (herd or flock disorders) for over 32 years. I think that I am very good at this ! My greatest weakness as a clinician is in the area of diagnosis of individual cases and my failure to keep abreast of developments over the past decades in practice general diagnostics, medicine and pharmacology.

My AP practice is extra-mural (after-hours, weekends). Most of my animal patients are horses (plus a few dogs), usually presented with pain or lameness. About 30% are referred by a colleague and 70% are referred by owners/trainers. Many of my equine cases are not clinically lame but have a history of poor limb action, reduced stride at the gallop, "hanging" to one side or poor racing performance. Most of these would have been seen by one or more colleagues who had made no specific diagnosis. As a result, unless there are visible or palpable lesions, my diagnosis is doubtful in many cases. If the patient has been referred by a colleague who has made a specific diagnosis (based on X-ray, nerve block etc), I usually accept that diagnosis. However, most of my cases have some abnormality of the muscular system (with 1-8 TPs present). Some have bone, joint, periosteal or tendinous problems. Less than 10% have definite muscle atrophy (poor prognosis; see below).

Some of my clinical failures (due to faulty diagnosis on my part) were: in carpitis(carpal chips missed); in septic tendinitis (sesamoideal chips missed); in canine posterior ataxia (degenerative myelopathy missed); in equine cervical ataxia(irreparable myelopathy missed); in equine severe hindlimb lameness (sacroiliac subluxation missed).

Carpitis (carpal chips missed): A gelding was treated successfully for sacro-iliac lameness by injection of AP points in February 1989. In late February, chip-fractures of the both carpi developed. A colleague used arthroscopy on both carpi to remove the chips. The horse was rested until August, when training recommenced. By early September he was in full training and was working well. Suddenly his action became poor and tenderness in the left lumbar area was noted.

Hoof marks on the wall of his box suggested that he had been cast in his box before the lumbar injury. Point injection of TPs and AP points for lumbar lameness between 5/10 and 17/10 had little effect. On 17/10, laser was used on the points, plus the arthroscopy scars. Marked and visible relaxation of the back muscles occurred within 5 minutes. On 18 and 19/10, his hind action was improved but his front action was short and he was hanging on the rein. Further sessions between 20/10 and 4/11 eliminated all TPs but, meanwhile, the carpal area became swollen and hot. X-rays were not taken at the time. Between 4/11 and 11/11, laser (local points plus Ting points) did not help the carpitis. Advised carpal X-ray and Animalintex plaster. On 18/11, X-ray by colleague showed carpal chips. Colleague operated to remove chips. Prognosis poor (second time surgery done).

Septic tendinitis (sesamoideal chips missed): On 11/11, horse with severe lameness due to tendinitis, with marked infection and oedematous swelling of the lower part was presented. The condition had been treated by poulticing and parenteral ampicillin and other antibiotics over three weeks. Laser was applied for 12 seconds to many points over the tendon (medial, posterior and lateral) and to ST36, LI11, LI 4, VG14 and SI, HC and LU Ting points. Five sessions of laser between 14/11 and 18/11 gave a definite decrease in soft tissue swelling but the infection persisted. On 23/11, X-rays showed bone sequestra in the sesamoid area. They were removed surgically. On 9/12/89, the referring vet reported that the prognosis was poor and euthanasia was being considered. Laser gave initial success in reducing soft tissue swelling in < 9 days (6 sessions) but necrotic bone sequestra required surgical operation and laser was discontinued.

Canine posterior ataxia (degenerative myelopathy missed): A German Shepherd was referred in 1986 by a colleague for gold-bead implant treatment of hip dysplasia. (There was pain on compression of the hip area). I assumed that the diagnosis was correct and did not conduct a full clinical/neurological examination. Gold bead (1 mm diameter) implants were inserted "between 9 and 3 o'clock" around the acetabulum, under general anaesthesia. (In hip dysplasia, the response to this treatment is usually marked in the days following implants). In this case, there was no improvement and the dog's ataxia deteriorated in the next few weeks. On re-examination, a diagnosis of degenerative myelopathy was made and euthanasia was advised.

Equine cervical ataxia (irreparable myelopathy missed): In my early days of equine AP, I attempted to treat cervical ataxia (wobbler syndrome) in horses. Diagnosis of the degree of pathology was not attempted. Treatment consisted of needling (usually with electro-stimulation) of TPs, neck points (including GB20, 21, TH and SI points) plus distant points (including SI 3, BL23, VG 3, GB34). In foals with recent signs, the outcome was good to excellent. However, in cases with long-standing clinical signs (> 3 months duration) in older animals, the outcome (in spite of initial and stable improvement, which would have been most welcome if the case was a human or family pet) was unsatisfactory. Most cases were shot eventually. If race-horses cannot race their future is grim, unless they are very well-bred mares. I attribute failure in older horses/chronic cases to irreparable myelopathy.

Equine severe hindlimb lameness (sacroiliac subluxation missed): In 1988, a horse with recent severe bilateral hindlimb lameness following a race and transport in a horse-box was found to have marked tenderness over both sacro-iliac joints. I diagnosed muscular strain in the sacro-iliac area. (In the previous months, I had treated successfully 2-3 similar clinical cases by point injection (5 ml of 0.5% procaine-saline) at 3-4 points over both sacro-iliac joints, plus all TPs, plus BL23, VG 3, GB30). 2-3 sessions of point injection was not successful in this case. I changed the diagnosis to sacro-iliac subluxation and recommended manipulation of both joints. Within days of one session of manipulation (by a human "bone-setter"), the horse became sound. (In April 1990, I met another case. I treated it with laser on presentation, in an attempt to provide some temporary analgesia, but recommended immediate manipulation. The result was dramatic improvement within days).

Now, in cases of sacro-iliac pain, if the height of the sacro-iliac area is the same on both sides (as the horse stands square), I diagnose the case as muscle-strain (likely to respond to AP). If the height is not the same, I diagnose sacro-iliac subluxation(poor prognosis to AP) and I suggest manipulation as the best option.