Surgery | Master Of Medicine

Category Archives: Surgery

Achalasia Cardia

Posted by on April 14, 2015 No comments
Megaesophagus

Megaesophagus (Photo credit: Wikipedia)

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

Etiology

Idiopathic
Infectious
Neurogenic degeneration
Stress
Trauma
Chagas disease

Pathophysiology

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.

Complications
Pneumonia
Lung abscess
Bronchiectasis

Diagnosis

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

Endoscopy
To evaluate mucosa for esophagitis or carxinoma.

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

Surgical

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.

 

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HIRSCHSPRUNGS Disease

Posted by on April 14, 2015 No comments

Definition

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

Epidemiology

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

Etiology

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

Pathophysiology

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.

Complications
Intestinal obstruction
Hematochezia
Perforation
Peritonitis
Sepsis

Diagnosis

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

Manometry

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

Treatment

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

Constipation
Soiling
Incontinence
Enterocolitis
Fecal fistulas

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Undescended testis

Posted by on April 12, 2015 1 comment
English: The route of the vas deferens from te...

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

Definition

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.

Incidence

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.

Pathophysiology
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.
Consequences
1.Infertility
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

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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Below Knee Amputation-Burgess Long posterior flap technique

Posted by on February 8, 2015 No comments

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.

Technique

Incision

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.

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Skin Grafting-Types of skin grafts

Posted by on January 30, 2014 No comments
Anatomy of the human skin with English languag...

Anatomy of the human skin with English language labels. Arabic language description translated by: Tarawneh (Photo credit: Wikipedia)

Split thickness skin grafts

 

Also known as thiersch graft,split-thickness grafts consist of epidermis and a variable thickness of dermis. Thinner grafts (<0.016 in.) have a higher rate of engraftment, whereas thicker grafts, with a greater amount of dermis, are more durable and aesthetically acceptable. Common donor sites are the thigh, buttock, and scalp.

 

Full thickness skin grafts

 

Also known as Wolfe graft ,full-thickness grafts include epidermis and a full layer of dermis. Common donor sites include groin and postauricular and supraclavicular sites, but the hypothenar eminence and instep of the foot can also be used. The donor site is usually closed primarily. These grafts are generally used in areas for which a high priority is placed on the aesthetic result (e.g., face and hand).

 

Thinner grafts have greater secondary contraction and do not grow commensurate with the individual. They have fewer adnexal cells and therefore have variable pigment, less hair, and less sebum, with a proclivity toward dryness and contractures. Full-thickness grafts, with more dermis and the requisite adnexal structures, exhibit less contraction and better cosmesis.

 

Graft meshing

 

Grafts can be meshed in expansion ratios from 1.5:1 to 6:1. Meshing a graft allows coverage for a wider area using the same-size donor site and decreases the risk of serous fluid accumulating under the graft without a method of egress. The interstices are covered within 1 week by advancing keratinocytes. However, because the entire area is not covered by dermis, meshed grafts are less durable, and the meshing pattern remains after healing, making them inappropriate for aesthetically important areas, such as the face.
Graft healing.

 

Factors affecting graft take

 

Initial metabolism is supported by imbibition or diffusion of nutrients from the wound bed. Revascularization occurs between days 3 and 5 by ingrowth of recipient vessels into the graft (inosculation).

 

Therefore, for a graft to take, the bed must be well vascularized and free of infection, and the site must be immobilized for a minimum of 3 to 5 days. Prevention of shear forces is particularly important during this period of inosculation.

 

Although bare bone and tendon do not engraft, periosteum and peritenon can support skin grafts, especially if they are first left to form a layer of granulation tissue. Graft failures are most often the result of hematoma, seroma, or shear force prohibiting diffusion and vascular ingrowth.

 

Source:Washington manual of surgery

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Classification of nerve injuries

Posted by on January 30, 2014 No comments
Sunderlanda Seddonb Structure injured Prognosis
First degree Neurapraxia Schwann cell (demyelination) Complete recovery within 12 wk
Second degree Axonotmesis Axon (wallerian degeneration) Complete recovery regeneration 1 mm/day
Third degree Endoneurium Incomplete recovery
Fourth degree Perineurium No recovery
Fifth degree Neurotmesis Epineurium No recovery
Sixth degree Mixed injury, neuroma, incontinuity Unpredictable recovery

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Compartment Syndrome

Posted by on January 30, 2014 No comments
English: This is a picture of compartment synd...

English: This is a picture of compartment syndrome of the lower leg (Photo credit: Wikipedia)

Compartment syndrome results from increased pressure within an osseofascial space, leading to decreased perfusion pressure. If it is left untreated, muscle and nerve ischemia may progress to necrosis and fibrosis, causing Volkmann ischemiccontracture.Compartment syndrome is usually seen in hand and forearm

  • Etiology. Fractures that cause bleeding, crush and vascular injuries, circumferential burns, bleeding dyscrasias, reperfusion after ischemia, or tight dressings can lead to the syndrome.
  • Diagnosis is based on a high index of suspicion, clinical examination, and symptoms of pain that are exacerbated with passive stretch of the compartment musculature, paresthesias, paralysis, or paresis of ischemic muscles. Pulselessness may occur and indicates a late finding (and is usually also a sign of irreversible damage) or the presence of major arterial occlusion rather than compartment syndrome. Measurement with a pressure monitor of a compartment pressure of greater than 30 mm Hg confirms diagnosis.
  • Treatment for incipient compartment syndrome involves close observation and frequent examinations and should include removal of tight casts and dressings. Elevation of the extremity to, or slightly above, the level of the heart is recommended. Acute or suspected compartment syndrome requires urgent fasciotomies of the involved areas. Decompression within 6 hours of established compartment pressures is necessary to prevent irreversible muscle ischemia. Forearm fasciotomies involve volar, carpal tunnel, and dorsal compartments. Hand fasciotomies include dorsal incisions for interossei and adductor pollicis, thenar, and hypothenar compartments, as well as midaxial incisions of the digits (ulnar for the index, long, and ring fingers and radial for the thumb and small finger).
Source:Washington Manual of surgery

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