Learn medicine the easy way.

Dupuytrens disease

Dupuytrens disease is one of those diseases which present to our Plastic Surgery OPD frequently.Most of the patients come to us, when they are unable to work.So it is the functional limitation due to this disease that forces the person to consult expert help.Let us see what this disease is about.

What is dupuytrens disease?

Dupuytren’s disease is a progressive disease of the palmar and digital fascial structures characterized by nodular thickening and subsequent contracture. Deformity of the hand occurs primarily at the metacarpophalangeal (MCP) and proximal interphalangeal (PIP) joint level.This results in functional limitations to the patient.

Dupuytrens disease is closely related to Peyronie’s disease (penile fibromatosis) and Ledderhose’s disease (plantar fibromatosis).It is  most prevalent in populations with a strong northern European ancestry. Men are six times more likely to develop Dupuytren’s disease than are women.It usually begins in 5th decade in men and 6th decade in women.It has an autosomal dominant inheritance pattern.


Repetetive trauma,chronic obstructive pulmonary disease, human immunodeficiency virus, malignancy (paraneoplastic manifestation), and epilepsy have been associated with Dupuytrens contracture.

Palmar fascia and its role in Dupuytrens disease

Dupuytren’s disease is ultimately manifest as the transformation of the normal palmar and digital fascial structures to thickened diseased cords through the deposition of type I and type III collagen and the contractile forces generated by myofibroblasts.

The palmar fascia provides a flexible yet firm framework for the soft tissues of the palm, tethering the skin to the underlying musculoskeletal structures.

Layers of Palmar fascia

The palmar fascia consists of two distinct layers: the deep fascia and the superficial fascia or palmar aponeurosis. The deep fascia covers the interosseous muscles and is not involved in Dupuytren’s disease. The superficial fascia, in contrast, is affected by the pathologic progression of Dupuytren’s disease.

Pathogenesis of Dupuytrens disease

The pathogenesis of Dupuytren’s contracture in pathologic terms is divided into proliferative, involutional, and residual phases.

Proliferative phase

The proliferative phase is characterized by nodule formation within the palmar fascia and biochemically by increased fibrinolytic activity.

Involutional phase

Marked nodular thickening and signs of early joint contracture characterize the involutional phase. Throughout the involutional phase, type III collagen is synthesized and the myofibroblasts reorient along the lines of tension within the palm.

Residual phase

Type III collagen deposition continues and is gradually replaced with type I collagen throughout the residual phase.Myofibroblasts disappear leaving predominantly Type I and Type III collagen.

Signs in Dupuytrens disease

1.  Hugh Johnson sign- Widening of the skin crease in Dupuytrens disease

2. Short–Watson sign- A soft palpable fullness immediately adjacent to the cord at the level of the MCP joint may indicate displacement of the neurovascular bundle by a pathologic spiral cord



a)Non Operative

Extension splinting to prevent prevent contracture.

Ultrasound therapy has been reported to soften palmar nodules but has not been effective in the treatment of cords or contracture.

b)Injection treatment

Steroids have demonstrated a restrictive effect on the formation of fibrous tissue and scar.Steroids are effective in treating palmar nodule.

Enzymatic fasciotomy-Injection in enzymatic fasciotomy is performed with 0.58 mg clostridial collagenase diluted in 0.25 mL (MCP joint) or 0.20 mL (PIP joint) of sterile diluent. The cord is
located by manual palpation and injection is performed at three points along the length of the cord via a single puncture with a 25-gauge needle.

Injection is done at 1 month intervals, injection is followed by manual manipulation and night splinting.

c) Surgical Treatment of Dupuytrens contracture

Surgical treatment of Dupuytren’s disease consists of both fasciotomy and fasciectomy. Fasciotomy involves division of the diseased cords without excision and may be performed
via an open technique or percutaneously. Fasciectomy involves excision of the diseased cords.

Surgical treatment of dupuytrens in itself is a vast topic, and will be delt with in the next post.

Layers of SCALP ,blood supply and nerve supply

SCALP has 5 layers and it can be memorized by a simple mnemonic SCALP

Layers of SCALP-Mnemonic

S -Skin

C-Connective tissue


L-Loose areolar tissue


Blood supply of scalp

The Internal carotid and External carotid artery which together give 5 branches to scalp.

Internal carotid artery

1.Supratrochlear artery- Supplies the midline of forehead.It is the branch of he ophthalmic branch of the internal carotid artery.

2Supraorbital artery- Supplies the lateral forehead and scalp as far up as the vertex. The supraorbital artery is a branch of the ophthalmic branch of the internal carotid artery.

External carotid artery

1.Superficial temporal artery- frontal and parietal branches of Superficial temporal artery supply much of the scalp

2.Occipital artery-supply  the posterior aspect of the scalp

3.Posterior auricular artery- It ascends behind the auricle to supply the scalp above and behind the auricle.

Nerve supply of scalp

1.Ophthalmic division of the Trigeminal nerve-via Supratrochlear nerve and the supraorbital nerve

2.Greater occipital nerve (C2)- Supplies the area posteriorly up to the vertex

3.Lesser occipital nerve (C2) -Supplies behind the ear

4. Maxillary division of the trigeminal nerve-Via zygomaticotemporal nerve supplies hairless temple

5.Mandibular division of the trigeminal nerve-Supplies via Auriculotemporal nerve

The mnemonic which can be used to learn the innervation of scalp is:


Zygomaticotemporal nerve

Greater occipital nerve

Lesser occipital nerve,

Auriculotemporal nerve

Supratrochlear nerve

Supraorbital nerve

Lymphatic drainage

Posterior half of the scalp drain to occipital and posterior auricular nodes. Anterior half drain to the parotid nodes,eventually draining into submandibular and deep cervical nodes.

Some general concepts in medicine and ways to learn

English: Planes of human anatomy.

English: Planes of human anatomy. (Photo credit: Wikipedia)

If basic anatomy and physiology is not mastered well the rest of medical studies is bound to fail.So refreshing and relearning some basic concepts in medicine will be a great idea.

We are going to learn the human anatomy, physiology and diseases affecting different organs and structures in a step by step manner.

 How topics are going to be covered.

Human body can be covered from surface to deep and from top to bottom.From skin to bone and from head to foot.

The basic structure


2.Subcutaneous tissue



5.Blood vessels, nerves


Although this is the basic structure of human body, the different layers can vary in different parts of human body. For example, the skin of scalp and other areas are different and likewise the structure and formation of bones can also vary. Mastering the anatomy of the human body is not an easy task, it is difficult but can be made easy by combining the anatomy with physiology and surgical anatomy. So we are starting a journey which is going to extend from head to foot.



Achalasia Cardia


Megaesophagus (Photo credit: Wikipedia)

Failure of LES to relax. LES remains in a constant state of tone with periods of relaxation.


Neurogenic degeneration
Chagas disease


Young women, middle aged men and women are affected. Primary pathology is destruction of nerves to LES and failure to relax leading to esophageal dilation and loss of progressive peristalsis

Achalasia is a premalignant condition and in 20 year period chance of carcinoma is 8%.
SCC is the most common type of carcinoma seen in Achalasia.It is due to long standing air fluid levels, mucosal irritation leading to metaplasia. Adenocarcinoma affects middle 1/3 rd of esophagus.

Clinical features

Triad of dysphagia(begins with liquids and progress to solids), regurgitation and weightloss.

Lung abscess


Barium esophagogram
Characterised by
1.Distal natrowing- Birds beak appearance
2.Absence of gastric air bubble
3.Later stages massive esophageal dilatation, tortuosity and sigmoidal esophagus(mega esophagus)

Motility study
Lack of peristaltic waves in the body of esophagus and failure of LES to relax.

Esophageal Manometry

Gold standard. Characterised by

1.LES hypertension- pressure more than 35mmHg
2.Failure of LES to relax with deglutition
3.Pressurisation of esophagus due to incomplete air evacuation
4.Simultaneous mirrored contractions with no evidence of progressive peristalsis
5.Low amplitude wave forms due to lack of muscle tone

To evaluate mucosa for esophagitis or carxinoma.

All treatment is aimed at relieving obstruction caused by LES contraction
1.In early stages sublingual nitroglycerine, nitrates or calcium channel blockers.
2.Bougie dilatation up to 54Fr
3.Botox injection to LES


1.Surgical esophagomyotomy is superior to balloon dilatation
2.Modified laparoscopic Hellers myotomy is the operation of choice.It may be combined with an antireflux surgery like fundoplication
3.Esophagectomy is done in mega esophagus, sigmoid esophagus, failure of more than one myotomy,undilatable reflux stricture.




Congenital develoental disorder characterised by the absence of ganglion cells in myenteric(Auerbach’s)plexus and aubmucosal Meissner’s plexus.


Occurs in 1 in 5000 childbirths, more common in males and m:f ratio is 4:1.


Family history of HIrschsprungs, 3-5 percent of HIrschsprungs disease are associated with downs disease, Abnormal locus in Chromosome 10, RET oncogene, MEN 2 are the etiological factors


Hirschsprungs disease is characterised by muscular spasm of the distal colon and rectum upto internal anal sphincter, leading to functional intestinal obstruction.Abnormal bowel appears distally and appears contracted whereas the proximal normal bowel appears dilated. This usually begins at anorectal line and rrctosigmoid is affected in 80% splenic flexure in 17% and entire colon is affected in 8%

According to length of bowel involved HIrschsprungs is divided into 4/types
1.Ultra short segment- Analcanal and terminal rectum
2.Short segment- Anal canal and rectum
3.Long sefment- Anal canal and up to splenic flexure
4.Total xolonic- Involving entire colon

Clinical features

More than 90% infants present with abdominal distsion and bilious vomiting along with failure to pass meconium in first 24 hours after birth.Diarrhoea may develop due to enterocolitis.
MISSED HIRSCHSPRUNG’S – In some infants Hirschsprung may be missed in infancy and may be diagnosed in childhood and early adulthood.It is characterised by poor feeding,abdominal distension, constipation and passage of goat pellet like stools. In young adults it presents as intestinal obstruction.

Intestinal obstruction


Barium enema

Characterised by

1.Rectum is normally more dilated compared to sigmoid, but in HIrschsprungs disease, sigmoid has increased calibre compared to rectum.

2.Failure to evacuate instilled contrast after 24 hours


Failure of internal sphincter to relax when rectum is distended with balloon is the characteristic finding

Rectal biopsy

This is the gold standard test in HIrschsprungs disease
In infants rectal biopsy is taken using special suction rectal biopsy instrument. Biopsy should be taken from 2 cm above dentate line. In older children full thickness biopsy is taken under GA

Histopathologic criteria

Absent ganglia
Hypertrophied nerve trunks
Robust immunostaining for acetyclcholinesterase
Loss of calretinin staining


Initial treatment is diversion colostomy which can be by loop or end colostomy done at ganglionic segment
Nutritional supplementation incliding and elecrolyte imbalance correction should be done
Followed by definitive procedures like
1.Swenson procedure – Resection of aganglionic bowel up to internal sphincter followed by colonial anastomosis

2.Modified Duhamel’s procedure – Resection of bowel leaving a distal rectal stump, followed by colon pill through posterior to rectal stump and stapler anastomosis between rectum and colon leaving a posteriror wall formed by ganglionic colon.

3.Suave procedure – Endorectal mucosal resection followed by colon pull through and colo anal anastomosis

Post operative complications

Fecal fistulas

Undescended testis

English: The route of the vas deferens from te...

English: The route of the vas deferens from testis to the penis. (Photo credit: Wikipedia)


Incomplete descent of testis occurs when testis is arrested in some part of its normal path to scrotum.

Development and descent of testis

Testis develops from genital ridge in 7th week of intrauterine life, in the retroperitoneum below the kidneys at around 10th thoracic level.It gets covered by processus vaginalis which is a fold of peritoneum which aids in the  descent of testis into the scrotum.
By the 3rd month testis lies at the level of internal inguinal ring, and up to 7th month it stays there, descent of testis into scrotum occurs between 7 to 9th month of intrauterine life.
The testis is supplied by testicular arteries which arises from abdominal aorta below renal arteries. Left testicular vein drains into left renal vein and right vein drains into IVC.


4% boys are born with undescended testis.In 2/3rd of these cases descent occurs by 3rd month. The incidence of UDT by 1 year of age is 1%.If descent does not occur by 3 months it is unlikely to descent.

Undescended testis is more common in the right side. Bilateral UDT is seen in 20%.
Sites of UDT are
1.Intra abdominal – Lying extra peritoneally just inside internal inguinal ring
2.Intracanalicular- May or may not be palpable.
3.Extracanalicular- At neck of scrotum
Ectopic testis may be seen in sites other than the line of descent of testis. MC site is superficial inguinal pouch.It can also be found in femoral triangle, root of penis, perineum.

Though undescended testia has the same size in childhood compared to the descended testis, UDT gets atrophied by puberty.

Histological changes occuring in UDT are

1.Loss of leydig cells
Degeneration of sertoli cells
Decreased spermatogenesis
These changes start to occur from 1st year.
2.Malignancy – 5-10 times greater chance compared to normal.Seminoma is the mc variety of cancer
3.Hernia – 90% UDT have patent processus vaginalis
4.Testicular torsion


Treatment of UDT is mainly surgical. procedure is done before 1 year so that fertility can be preserved.
1.Palpable testis – Testis mobilised and processus vaginalis ligated and divided and orchodopexy is done with placement of testis in subdartos pouch.
2.Impalpabe testia- Testis is localised by USG if Intracanalicular or by laparoscopy if intraabdominal.

If there is insufficient length of cord, lengthening of cord can be done by
1.Ligating and dividing processus vaginalis.
2.Coverings of spermatic cord including cremasteric muscles is divided
3.Lateral fibrous bands inside the internal ring should be divided.

If sufficient length cannot be obtained even after performing these steps, orchiopexy can be done as a 2 stage procedure.

1.Testis mobilised as far as possible and is anchored with suture and mobilisation is completed after 6 months.
2.An alternative approach involves initial division of gonadal artery( it is tighter than the vas) so that the testis become dependant on vasal artery for its blood supply. The second stage involves conventional orchiopexy

Orchidectomy should be considered in atrophic testis, if the other testis is found to be normal in a post pubertal boy.

Below Knee Amputation-Burgess Long posterior flap technique

The Burgess technique is the most frequently used technique in BK amputation.The well vascularized myocutaneous flap consists of gastrocnemius, partial soleus and posterior skin.



Anterior skin incision should be located 12 cm (one handbreadth) below tibial tuberosity, skin incision should be continued transversley for a distance approximately 1/3rd of calf circumference to minimize formation of dog ears. Skin incision should be extended vertically for a distance approx one and half times the length of transverse incision. The posterior flap is then completed with a transverse incision at this level.The skin incision is then extended through the fascia throughout, with division of great saphenous vein.

Division of muscles

The anterior compartment muscles(Tibialis anterior.EHL,EDL and fibularis longus) are divided at the same level as the anterior incision.Central in the anterior compartment is anterior tibial artery and vein and deep peroneal nerve.The vessels are suture ligated and nerve is transected under tension.The tibia is then cleared and interosseus membrane is incised sharply.The tibia is divided at or just proximal to the skin incision with an anterior bevel.The lateral compartment muscles(fibularis longus and brevis) are divided to expose fibula.Fibula is divided 1-2cm proximal to level of  tibial transection.

Flap closure

The posterior compartment muscles( Soleus and Gastrocnemius) are divided obliquely to create a posterior muscle flap.Enough soleus should be removed to allow flap closure. The posterior tibial and peroneal vessels are suture ligated .The fascial edges are closed with interrupted sutures and skin closed with mattress sutures.Elasto crepe bandage should be applied to mould the stump.

Load time improved by PHP Speedy Load time improved by PHP Speedy