April, 2015 | Master Of Medicine

Monthly Archives: April 2015

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 theĀ  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.

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