Trigger thumb

CONGENITAL TRIGGER THUMB

Introduction

It is tenosynovitis of flexor pollicis longus with stenosis at A1 pulley. It simply means the tendon meant for bending the thumb is swollen and finds itself difficult to glide in its tunnel because of a smaller tunnel entry. Though this condition is congenital but usually diagnosed later. It must be differentiated from contractures in Arthrogyrposis and spastic thumb in Cerebral palsy.

Its incidence is 2-3 for every 1000 births. It presents as a bent thumb which sometimes becomes straight when forced but with a sudden release. A small swelling can be noted ocasionally at the base of thumb which is called Notta nodule. It is due to ganglion or cyst formation along the tendon near the metacarpal neck. It is also seen bilaterally in many cases.

Natural history

 Most cases get resolved spontaneously with age. If the triggering doesn't resolve by 3years or if thumb is not extending then surgical intervention is necessary to prevent permanent deformity.

Diagnosis

Clinical examination is sufficient for a diagnosis. Presentation gets delayed till child is 6months to 1 year.

Management

Initially stretching might help but if it fails to resolve then surgery is gold standard. If not corrected by the age of 3 years spontaneous resolution is not expected to happen. The procedure involves release of A1 pulley. There is no evidence that meddling with the nodule or cyst helps. Care must be taken to protect digital nerves to thumb especially the radial one. Sometimes a hyperextension develops after a late release, in such cases proximal advancement of volar plate at PIP joint with A1 pulley release works well.

Attitude of left trigger thumb 

Normal right thumb can extend fully

On manipulation also left thumb fails to straighten out preoperatively 

Notta's nodule seen near base of thumb intraoperatively 

Intraoperative video showing smooth gliding of tendon after A1 pulley release

Surgical scar after 3 months of release and free thumb extension

Cerebral palsy

Cerebral palsy

It is a upper motor neuron disorder due to hypoxic or ischemic injury to the brain of a child during pregnancy or delivery or postnatal period. It results in altered tone in limbs. Early signs include delayed milestones, abnormal posture and gait. As child grows, spastic muscle tendon units fail to catchup with bone growth. So as age advances especially, during periods of rapid growth there can be a deterioration in ambulatory status due to contractures. 

Most of my patients are brought by parents who are aware of the name of the problem but don't know its implications. They continue to think that there is an issue with the upper limb or legs. I always make them understand that the real problem is, in the damaged brain which sends disturbed signals to hands and legs, which result in abnormal posture and gait. Joints and muscles are basically normal, its culprit is the damaged area in brain which controls them. Now that does not mean whole of the brain is damaged. Our brain is magnificently divided in such a way that each of the different part of brain  controls a specific organ or a part or a function. For this reason we may see many variations in presentation of our patients, depending on the part of brain involved.

The numerous causes of this condition are described in literature, a few important ones are mentioned below:

•  Prenatal (75% cases) 

  Maternal infection during pregnancy ex: CMV, rubella
  Cerebral ischemia
  Maternal drug intake
  Congenital cerebral malformation or abnormalities
  Pre-eclampsiais a risk factor

• Perinatal (6 - 8% cases)

  Cord prolapse
  Obstructed labour
  Abruptio placenta
  Meconium staining of amniotic fluid

• Postnatal (10-18%cases)

  Jaundice
  Hypoglycemia
  Neonatal infection ex: meningitis, septicemia

  CP has been classified based on the extent of body involvement, tone, functional and ambulatory capacity. 

  Physiotherapy for keeping the joints free and mobile is mainstay during growth period.  Pharmacological therapy for muscle relaxation to reduce tone may be necessary. When there is a dynamic deformity Botox, casts and stretching might help. However once muscle groups become contracted our physiotherapy, botox and casts may not work efficiently. In severe cases selective posterior rhizotomy may become desirable.  Simultaneously bowel and bladder, speech, intellectual level, oromotor function, hearing, occupation, needs assessment and training to improve it.

  Muscle relaxants are generally used to decrease tone. Baclofen is commonly preferred.

  Botox injections reduce spasticity and effects are temporary and reversible. No major side effects are noted with it and is FDA approved. It must be realized that it is not an isolated treatment and must be integrated with proper rehabilitation. The effect kicks in about 2 weeks after injection and lasts for 3-6 months.

  Doses are again based on weight of the child and muscle group it is intended to be used on. 10 IU/kg per setting is maximum dose to be given. Larger muscles especially biarticular ones in lower limb need 3-6 IU/kg whereas for small muscles of arm and forearm, 1-2 IU/kg may suffice. Botox is available in a freeze dried vial, which needs normal saline for reconstitution. In India vials are available in 200, 100 and 50 IU dose. The site of injection is determined by a qualified physician either clinically, EMG or by ultrasound guidance. Paracetamol or topical local anaesthetic cream if given before botox injection may help reduce the pain after the procedure.

  Soft tissue surgery is key once contractures develop. In olden days single level surgery used to create imbalance as problems in other joints were not dealt with simultaneously. Present trend is to do a single time multilevel surgery (SEMLS), right from hips to ankles that will allow them to balance efficiently. It is necessary to have a video gait analysis done before surgery for better understanding of complex gait patterns.

  They include Psoas lengethening, Adductor release, Hamstrings fractional lengethening, rectus release with or without transfer to hamstrings, Gastronemius recession, Tendoachillis lengethening, Tibialis anterior or tibialis posterior split transfer.

  
  Bony procedures may be required in cases which do not yield to soft tissue surgery. 

  These include pelvic osteotomy, varus osteotomy, derotation osteotomy, Femur extension supracondylar osteotomy,calcaneal lengthening osteotomy, griece green subtalar arthrodesis.

  It is important to understand that all these will improve the child functionally but never cure the basic problem. Physiotherapy must be continued till skeletal maturity, as after that worsening of contractures rarely occurs.

  7 yrs old girl with spastic hemiplegia and equinus gait, she was treated with perutaneous tendoachillis lengthening.

  

  Postop cast in place

  
  

  

  AFO after cast removal for couple of weeks later only night time

  

  8 weeks postop without AFO, plantigrade foot

  Gait after 6 months

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  Fixed knee deformity in CP in 15yr old boy with crouch gait

   

  

  Incision for Distal femoral extension osteotomy, inferiorly insicion for hamstring lengethening can be seen.

  AP view of supracondylar dital femoral extension osteotomy

  
  

   

  

  Lateral view of supracondylar extension osteotomy of femur

  
  

  

  
  

  

  Healed osteotomy after 8 weeks post op

   

  

  Calcaneal lengethening osteotomy with tricortical bone graft insitu for correction of pes planovalgus

   

   

Clubfoot

CLUBFOOT / CTEV

 Introduction

This is a very common deformity noticed immediately at birth and can be diagnosed in pregnancy time through repeat ultrasound examination. It might inadvertently be a cause for parents worry, if diagnosed during pregnancy. It is a surprise that many such parents come to me for advice on termination of pregnancy. I want to make it very clear that it is a 100% treatable condition and such dramatic decisions are not warranted. In India and other developing countries this perfectly treatable condition is commonly neglected, especially in rural setups. Over a period it becomes less amenable to conservative treatments and may result in a rigid foot, whereon surgery becomes a must.

Etiology and Incidence

Prevalence is 1 in 1000 in Indian population, with male child more commonly affected and in approximately 50% cases it is bilateral. Intrauterine overcrowding due to less amniotic fluid, twins, large baby, associated uterine fibroid can cause clubfoot due to mechanical pressure. There is no true reason for this deformity but there is an association with hip and spine disorders. It can also be found with multiple joint contractures or constriction band syndrome. Family history is also a predisposing factor. All babies born with CTEV must be screened on day 1 for Developmental hip dysplasia, spinal disorders or other syndromic associations.

USG study of a clubfoot baby

 Management

Initial treatment is conservative with plaster casts. It must be started as early as possible preferably on day 1. These casts are above the knee level to prevent slipping out of plaster while the baby kicks and to control rotations.  Parents have to be cautious regarding care of casts. They must keep them clean and dry by avoiding spilling of water or urine over the cast. These casts are put after gentle passive manipulation of foot and ankle to a corrected position, gradually the correction is achieved and sometimes even exaggerated to achieve slight over correction. It is important that weekly casts are changed for 4-6 weeks till only equinus deformity is remaining, which can be corrected by a percutaneous tenotomy followed by again casting, this last cast is continued for a total of 3 weeks. Later after removing the cast baby is put on a foot abduction orthosis for 23hrs a day till 3 months after which the splints are worn only at night times. Initially it is important to ensure compliance with braces and their fitting, so your doctor may advise you to come frequently for a month, once all is well followup once in every 3 months is sufficient. These shoes may need change frequently as the baby grows. Followup is necessary till 3-4 years of age to check compliance and detect recurrence early. For residual deformity various surgical procedures are available which can be done at appropriate age. In neglected and rigid clubfoot surgery is required. It can be done before walking age at around 9 months. Surgery involves soft tissue procedures to  release the tight medial and posterior structures. Bony surgery may be needed at later age for residual deformities. Sometimes a tendon transfer is needed to correct a flexible adduction deformity. For more resistant and delayed cases an external fixator in the form of Rings or small rods are applied to slowly correct the deformity by gradual distraction.

Bilateral CTEV 

First Casting in supination  to correct cavus

2nd cast put in abduction to correct forefoot adduction

3rd cast for further abduction

4th cast for still more abduction

Last cast after percutaneous tenotomy in 15* dorsiflexion and 70* abduction

Skin complications due to tight plaster

A fully corrected foot after cast removal

Example of foot abduction orthosis used after final correction for 23 hours per day

Another type of Foot abduction orthosis worn by baby