TRACHEO-ESOPHAGEAL FISTULA - A case Report

This was a case of a 65 year old female who came to our department with dysphagia for Barium Swallow.

Upon doing the investigation, a tracheoesophageal fistula was detected and the patient was rushed to the casulaty for further management.
The patient had probably developed the fistula due to pressure necrosis by a tracheostomy tube as she had given history of being applied a trachestomy tube for quite some time.


X-Ray Images

DISCUSSION


A tracheoesophageal fistula is an abnormal connection (fistula) between the esophagus and the trachea. TEF is a common congenital abnormality, but when occurring late in life is usually the sequela of surgical procedures such as alaryngectomy.

Causes

Congenital TEF can arise due to failed fusion of the tracheoesophageal ridges during the third week of embryological development.

A fistula, from the Latin meaning ‘a pipe,’ is an abnormal connection running either between two tubes or between a tube and a surface. In tracheo-esophageal fistula it runs between the trachea and the esophagus. This connection may or may not have a central cavity; if it does, then food within the esophagus may pass into the trachea (and on to the lungs) or alternatively, air in the trachea may cross into the esophagus.

TEF can also occur due to pressure necrosis by a tracheostomy tube in apposition to a nasogastric tube (NGT).

Associations

Babies with TEF or esophageal atresia are unable to feed properly. Once diagnosed, prompt surgery is required to allow the baby to take in food. Few TEF children have problems after surgery, however a number develop feeding difficulties and chest problems. Some TEF babies are also born with other abnormalities, most commonly those described in VACTERL association - a group of anomalies which often occur together, including heart, kidney and limb deformities. 6% of babies with TEF also have a laryngeal cleft

Clinical presentation

Tracheoesophageal fistula is suggested in a newborn by copious salivation associated with choking, coughing, vomiting, and cyanosis coincident with the onset of feeding. A fistula may also be a the cause of polyhydramnios while in utero.

Treatment

It is surgically corrected, with resection of any fistula and anastomosis of any discontinuous segments. Surgical repair is associated with complications, including

• Stricture, due to gastric acid erosion of the shortened esophagus.
• Leak of contents at the point of anastomosis.
• Recurrence of fistula.

RICKETS - A Case Report

This is a case of Rickets which presented to our department with swelling of joints. The baby was 3 years old.

Clinical Images :

Hypertrophy of jointsBow legs

Harrisons Groove

Upon evaluation of the case X-Ray was done on the wrist joints which revealed Cupping and Fraying of the metaphyseal ends of radius and ulna with widening of the metaphysis.

DISCUSSION :

Rickets is a softening of bones in children potentially leading to fractures and deformity. Rickets is among the most frequent childhood diseases in many developing countries. The predominant cause is a vitamin D deficiency, but lack of adequate calcium in the diet may also lead to rickets (cases of severe diarrhea and vomiting may be the cause of the deficiency). Although it can occur in adults, the majority of cases occur in children suffering from severe malnutrition, usually resulting from famine or starvation during the early stages of childhood.Osteomalacia is the term used to describe a similar condition occurring in adults, generally due to a deficiency of vitamin D.^[1] The origin of the word "rickets" is probably from the Old English dialect word 'wrickken', to twist. The Greek derived word "rachitis" (ραχίτις, meaning "inflammation of the spine") was later adopted as the scientific term for rickets, due chiefly to the words' similarity in sound.

Signs and symptoms

Signs and symptoms of rickets include:

• Bone pain or tenderness
• dental problems
• muscle weakness (rickety myopathy or "floppy baby syndrome" or "slinky baby" (where the baby is floppy or slinky-like)
• increased tendency for fractures (easily broken bones), especially greenstick fractures
• Skeletal deformity
  
  
  
  • Toddlers: Bowed legs (genu varum)
  • Older children: Knock-knees (genu valgum) or "windswept knees"
  • Cranial, spinal, and pelvic deformities
• Growth disturbance
• Hypocalcemia (low level of calcium in the blood), and
• Tetany (uncontrolled muscle spasms all over the body).
• Craniotabes (soft skull)
• Costochondral swelling (aka "rickety rosary" or "rachitic rosary")
• Harrison's groove
• Double malleoli sign due to metaphyseal hyperplasia
• Widening of wrist raises early suspicion, it is due to metaphysial cartilage hyperplasia.

IMAGING FINDINGS

Plain radiograph findings include the following:

• Widening and cupping of the metaphyseal regions
• Fraying of the metaphysis
• Craniotabes
• Bowing of long bones
• Development of knock-knees, or genu valgum 
• Development of scoliosis
• Impression of the sacrum and femora into the pelvis, leading to a triradiate configuration of the pelvis
• In healing rickets, the zones of provisional calcification become denser than the diaphysis. In addition, cupping of the metaphysis may become more apparent.

A useful mnemonic for remembering the findings of rickets is as follows:

• Reaction of the periosteum (may occur)
• Indistinct cortex
• Coarse trabeculation
• Knees, wrists, and ankles affected predominantly
• Epiphyseal plates, widened and irregular
• Tremendous metaphysis (cupping, fraying, splaying)
• Spur (metaphyseal)

Treatment and prevention

The treatment and prevention of rickets is known as antirachitic.

[]

Diet and sunlight

Treatment involves increasing dietary intake of calcium, phosphates and vitamin D. Exposure to ultraviolet B light (sunshine when the sun is highest in the sky), cod liver oil, halibut live oil are all sources of vitamin D.

A sufficient amount of ultraviolet B light in sunlight each day and adequate supplies of calcium and phosphorus in the diet can prevent rickets. Darker-skinned babies need to be exposed longer to the ultraviolet rays. The replacement of vitamin D has been proven to correct rickets using these methods of ultraviolet light therapy and medicine.

Recommendations are for 400 international units (IU) of vitamin D a day for infants and children. Children who do not get adequate amounts of vitamin D are at increased risk of rickets. Vitamin D is essential for allowing the body to uptake calcium for use in proper bone calcification and maintenance.

[]Supplementation

Sufficient vitamin D levels can also be achieved through dietary supplementation and/or exposure to sunlight. Vitamin D₃ (cholecalciferol) is the preferred form since it is more readily absorbed than vitamin D₂. Most dermatologists recommend vitamin D supplementation as an alternative to unprotected ultraviolet exposure due to the increased risk of skin cancer associated with sun exposure. Note that in July in New York City at noon with the sun out, a white male in tee shirt and shorts will produce 20000 IU of Vitamin D from 20 minutes of non-sunscreen sun exposure.^{[citation needed]}

According to the American Academy of Pediatrics (AAP), infants who are breast-fed may not get enough vitamin D from breast milk alone. For this reason, the AAP recommends that infants who are exclusively breast-fed receive daily supplements of vitamin D from age 2 months until they start drinking at least 17 ounces of vitamin D-fortified milk or formula a day.^[2] This requirement for supplemental vitamin D is not a defect in the evolution of human breastmilk, but is instead a result of the modern-day infant's decreased exposure to sunlight (i.e. breast-fed infants who receive adequate sun exposure are less likely to develop rickets, though supplementation may still be indicated in the winter, depending on geographical latitude).

CHILAIDITI SYNDROME

This patient was a 55 yr old female who presented to our department with acute onset of abdominal pain and shortness of breath. Upon chest X-Ray it was found out that her Transverse Colon was interposed between the Liver and the diaphragm which gives rise to a condition called Chilaiditi Syndrome.

DISCUSSION

Chilaiditi syndrome is a rare condition when pain occurs due to transposition of a loop of large intestine (usually transverse colon) in between the diaphragm and the liver, visible on plain abdominal X-ray or chest X-ray.

Normally this causes no symptoms, and this is called Chilaiditi's sign. The sign can be permanently present, or sporadically. Thisanatomical variant is sometimes mistaken for the more serious condition of having air under the diaphragm (pneumoperitoneum) which is usually an indication of bowel perforation. This may lead to unnecessary surgical interventions.

Chilaiditi syndrome refers only to complications in the presence of Chilaiditi's sign. These include abdominal pain, torsion of the bowel (volvulus) or shortness of breath.

Causes

The exact cause is not always known, but it may occur in patients with a long and mobile colon (dolichocolon), chronic lung disease such as emphysema, or liver problems such as cirrhosis and ascites. Chilaiditi's sign is generally not associated with symptoms, and is most commonly an incidental finding in normal individuals.

Absence or laxity of the ligament suspending the transverse colon or of the falciform ligament are also thought to contribute to the condition. It can also be associated with relative atrophy of the medial segment of the left lobe of the liver. In this case, the gallbladder position is often anomalous as well - it is often located anterior to the liver, rather than posterior.

Epidemiology

The occurrence (incidence) on abdominal or chest X-rays is around 0.1% but it can be up to 1% in series of older adults. It has also been reported in children.

Synonyms

Synonyms include interpositio hepatodiaphragmatica, subphrenic displacement of the colon and subphrenic interposition syndrome.