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Supracondylar Fractures of the Humerus in Children

Anatomy:

The distal humerus resembles a triangle, with the medial and lateral columns making up the sides and the trochlea forming the base (270° arc). The lower end of the humerus is expanded from side to side, and has articular and non-articular parts. The articular part includes the Capitulum which articulates with the head of the radius and the Trochlea which articulates with the trochlear notch of the ulna. The non-articular part includes: the medial epicondyle (related to the ulnar nerve), the lateral epicondyle, the medial and lateral supracondylar ridges, the coronoid fossa, the radial fossa, and the olecranon fossa.

Supracondylar fractures of the humerus are common in young age. They are produced by a fall on the outstretched hand. The distal fragment is mostly displaced backwards, so that the elbow is unduly prominent, as in dislocation of the elbow joint. However, in a fracture, the three bony points of the elbow form the usual equilateral triangle.

Ossification:
The humerus ossifies from one primary center and 7 secondary centers. The primary center appears in the middle of the diaphysis during the 8th week of development.
The upper end ossifies from 3 secondary centers: one for the head, one for the greater tubercle, and one for the lesser tubercle. These 3 centers fuse together during the sixth year to form one epiphysis, which fuses with the shaft during the 20th year. The upper end is the growing end of the humerus.

The lower end ossifies from 4 centers which form 2 epiphysii. The centers include: one for the capitulum and the lateral flange of the trochlea (first year), one for the medial flange of the trochlea (9th year), and one for the lateral epicondyle (12th year). All three fuse during the 14th year to form one epiphysis, which fuses with the shaft at about 16 years. The center for the medial epicondyle appears during 4-6 years, forms a separate epiphysis, and fuses with the shaft during the 20th year.


Supracondylar Humeral Fractures:

Much of the difficulty encountered in treating distal humerus fractures lies in the complex anatomy of the elbow joint. The highly constrained nature of the elbow joint causes it to absorb energy following direct trauma. Consequently, articular comminution may occur.
The following observations were made in a study by Wilkins studying 4,520 fractures:
1) 97.7% of the fractures were of the extension type, and only 2.2% were of the flexion type; 2) most occurred in males and especially in between the ages of 5 and 8 years; 3) Volkmann’s ischemic contracture occurred in 0.5% of the fractures; and 4) the radial, median, and ulnar nerves were involved in that order of frequency.

Dameron has listed, depending on the type of fracture, four basic types of treatment: 1) side arm skin traction; 2) overhead skeletal traction; 3) closed reduction and casting, with or without percutaneous pinning; and 4) open reduction and internal fixation.

Classification:
Most distal humerus fractures can be classified into 2 etiologic groups: those resulting from a high-energy mechanism, such as a motor vehicle accident, and those resulting from a low-energy injury, such as a fall while walking.

Gartland has proposed a further classification for supracondylar fractures: Type I, undisplaced; Type II, displaced with intact posterior cortex; and Type III, displaced with no cortical contact; his classification also notes whether the fracture is displaced posteromedially or posterolaterally.

The type I undisplaced fracture can be satisfactorily treated closed with external fixation, such as a plaster cast. The type II fracture is displaced and is difficult to reduce and to hold reduced by external methods. The type III fracture is displaced posteromedially or posterolaterally with no cortical contact and the periosteum may be stripped; reduction is difficult, and maintaining reduction is almost impossible without some form of internal fixation. The fracture should be reduced in extension and reduction should be maintained through the use of the triceps bridge by holding the elbow in flexion if the pulse and vasculature tolerate it.


Angular Deformities associated with Supracondylar Humeral Fractures:

Previously cubitus varus or cubitus valgus were thought to occur because of growth arrest of the distal humeral epiphysis, rather than because of malreduction of the fracture.

Cubitus varus is the most common angular deformity that results from supracondylar fractures in children. Cubitus valgus, although causing tardy ulnar nerve palsy, is rarely seen and occurs more often from nonunion of lateral condylar fractures.

Cubitus varus and cubitus valgus should be prevented by obtaining proper anatomic reduction. Of the two, cubitus varus produces a distasteful cosmetic deformity, yet only rarely any limitation of motion. A big problem noted in the prevention of these abnormalities is obtaining satisfactory roentgenograms to determine whether any cubitus varus or valgus is present.

The three most common reasons for residual cubitus varus or valgus deformity are:
1) the inability to interpret poor roentgenograms and therefore, acceptance of a less than adequate reduction; 2) the inability to interpret good roentgenograms because of a lack of knowledge of the pathophysiology of the fracture; 3) loss of reduction.
Whether external mobilization or pin fixation is used, the forearm should be placed in the pronated position to decrease the lateral tilt and resultant cubitus varus.


Imaging Studies:

The bone quality, fracture pattern, level of comminution, articular involvement, displacement, and associated injuries, must be understood completely before treatment is attempted. Multiplane radiographs, including anteroposterior (AP) and lateral views, are appropriate.



AP radiographs should be obtained with the elbow flexed approximately 40° and with the radiographic beam directed perpendicular to the distal humeral surface. This allows disengagement of the olecranon from its fossa and permits a better view of the distal humerus.

In the pediatric population, the Baumann angle (the angle between the lateral condylar physeal line and the axis of the humerus) is often measured using AP radiographs. It must be compared to the contralateral side.

A computed tomography (CT) scan can be obtained of the distal humerus to further analyze the fracture pattern. Duplex Doppler ultrasonography or angiography can be performed to check vascular status.


Closed Reduction and Percutaneous Pinning:

Closed reduction is difficult not only to achieve, but also to maintain because of the thinness of bone of the distal humerus between the coronoid and olecranon, where most supracondylar fractures occur.

Fowles and Kassab noted that ulnar nerve lesions are common in displaced flexion fractures. The reduction is more difficult, the results are worse than in extension fractures, and these anteriorly displaced fractures should be considered for accurate reduction and percutaneous pinning.

Percutaneous fixation after closed reduction has the advantage of providing excellent stability of the supracondylar fracture in any position of the elbow. However, the ultimate result will be only as good as the initial reduction, and does not depend on the placement of the pins. If the fracture is not satisfactorily reduced and is held in an unsatisfactory position with pins, the outcome will be unsatisfactory, just as if no pin fixation were used.



A 5-year-old girl fell onto her outstretched hand and sustained a Gartland Type II supracondylar humerus fracture with medial impaction. (A) Lateral preoperative radiograph. (B) Anterior/posterior (A/P) preoperative radiograph. (C) Lateral radiograph after closed reduction and percutaneous pin fixation (cross-wire technique). (D) A/P postoperative radiograph. (E) Lateral radiograph taken four weeks postoperatively. (F) A/P follow-up (4 wks) radiograph. There is good evidence of healing.


Technique:
Place the patient prone or supine on a fracture table. Prepare and drape the elbow. Outline the posterior triangle of the elbow joint (the medial and lateral epicondyles and the olecranon). Reduce the fracture by applying longitudinal traction, extending the fracture, and manipulating with the thumbs to correct lateral tilt, medial impactation, or posterior displacement. Flex the elbow to neutral. Crisscross two smooth Steinmann pins through the condyles and metaphysic, one to exit above the medial epicondyle and one to exit above the lateral epicondyle. Be careful to avoid the ulnar nerve. Following engagement of the shaft, use an image intensifier to make sure the pin engages the opposite cortex proximally. Cut the pins off beneath the skin and bend their ends so they will not migrate proximally but can be easily retrieved in the office. Check and note radial pulse.

Aftertreatment:
A long arm posterior plaster splint is worn for 3 weeks. Ulnar, radial, and median nerve function should be checked after anesthesia. The pins are removed at 3 weeks and another posterior splint is applied. At 4 weeks, intermittent active range of motion exercises are started at home after being taught by a physical therapist to the child and parent. Passive motion or forceful manipulative motion must be avoided in children because they will decrease the range of motion and may frighten the child.


Open Reduction and Internal Fixation:

Open reduction and internal fixation of supracondylar fractures are indicated when closed reduction is unsatisfactory. In a type III displaced fracture with no cortical contact and completely detached periosteum, and with the fracture fragment penetrating the skin (compound fracture), a satisfactory closed reduction may not be possible, if, after one or two attempts at closed reduction with the child under general anesthesia, the fragments cannot be reduced and held by percutaneous pinning, open reduction and internal fixation are indicated. Also if the elbow is so severely swollen that a closed reduction cannot be maintained, then olecranon traction may be used for several days, followed by closed or open reduction as necessary. Other indications for O.R.I.F. include open (compound) fractures that require irrigation and debridement and those fractures complicated by vascular injury, mysositis ossificans excessive callus formation with residual stiffness, and decreased range of motion.

If open reduction and internal fixation are to be carried out, they should be performed after the swelling has decreased, but no later than 5 days after that time because the possibility of mysositis ossificans increases after that time.

Gruber and Hudson treated 31 difficult fractures with open reduction and internal fixation and observed satisfactory results even in the most severe ones.

Technique:
Prepare and drape the arm in the usual fashion with the patient supine. Make a curved incision over the lateral humeral epicondyle. Dissect the soft tissue, including the anconeus and common extensor origins, and retract these anteriorly and posteriorly respectively. Make sure the radial nerve is retracted posteriorly to avoid injury. Observe the supracondylar fragment, and note its alignment with the proximal fragment. Use a small curet to remove any hematoma at the fracture site. Note any interdigitations on the ends of the bone and by matching them, reduce the fracture. Use two crossed Steinmann pins in a manner similar to that described for percutaneous pinning. Cut the pins percutaneously for easy removal later. Close the incision in layers.

Aftertreatment:
A posterior plaster splint is applied and the radial pulse and neurological function are checked following anesthesia. The pins are removed at 3 to 4 weeks and an active, not passive, range of motion program is started.


Complications:

Supracondylar fracture of humerus being the most common fracture in children needs proper treatment to prevent complications like compartment syndrome, neurovascular compromise (Volkmann’s ischemic contracture), elbow stiffness (mysositis ossificans) and angulations.




Injuries to nerves or blood vessels are much more serious than the fracture itself. The early recognition of such complications is imperative. Early and adequate treatment of acute vascular complications is necessary, even though it means surgical exploration of the antecubital fossa and resection of the injured segment of the brachial artery. Adequate and early treatment of acute vascular injuries usually ensures a good prognosis, but delay may lead to serious and permanent disability.

Gartland type I supracondylar fracture can be early treated with casting alone but displaced (Gartland type II, III) can be treated with casting, ORIF or percutaneous Pinning (PCP). Close reduction and casting is an old treatment modality that is still practiced in developing countries due to limited facilities. Close reduction and casting has its own advantages and disadvantages. Its advantages are no need of metal insertion, least costly, safe, time effective, bearing less morbidity. Disadvantages are loss of reduction, compartment syndrome and cubitus varus.

References:

Campbell’s Operative Orthopedics, 4 volume set
Human Anatomy: Regional and Applied. B.D. Chaurasia
www.emedicine.com
www.wikipedia.com

The Diabetic Patient: A Clinical Approach

Diabetes Mellitus is a metabolic disorder affecting millions of people across the globe. We as doctors and medical students should know these patients from A-Z. The following is a quick review of points to remember when approached by someone with diabetes in your clinic.

History: Take a normal history as with any other patient, but keep these points in mind...

Hypoglycemia- tremors, fatigue, palpitations, sesting, coma
Neuropathy- calf muscle pain, burning muscles, "losing shoes"
Nephropathy- decreased urine output, frothy urine, periorbital swelling, recurrent UTI
Cardiovascular- pain, dyspnea, loss of breath
Retinopathy- blurry vision, halos, spots
Autonomic- orthostatic hypotension, GIT disturbances, recurrent infections
Dermopathy- poor wound healing


Investigations: (for the known diabetic)

Fasting blood sugar- <110>125 is established diabetes
Lipid profile- ALT and SGPT every 6 months
Urine DR in special regards for microalbuminuria (<200>200 is irreversible).
Creatinine clearance
Serum creatinine and Urea
ECG
Fundoscopy


Examinations: Perform foot, abdominal, CVS, respiratory, 3rd 4th 6th 7th cranial nerves, and check of dehydration.

Particularly in Foot examination:
Inspection- look for discoloration, ulcers, callus', skin changes, loss of shin hair, cuts, and bruises. Pay special attention to the intertarsal spaces.
Palpation- pedal edema, vibration (this is usually the first sense to be compromised in 'diabetic foot'- diabetic neuropathy), proprioception, temperature, touch, reflexes, pulses.


Diet: The following diet pertains particularly to those patients from the Indian subcontinent. Please refer to a diabetic book for patients of other ancestry.

Contraindications- bakery sweets, white bread, white a'ata (use chokaar instead), rust, cold drinks (sodas), sharbaats, gosht, biryani, mattar plow, biscuits, jam, jelly, honey, red meat.

Foods that help- chaana with chai, boiled eggs, akhroat, dhalia, omega 6 fatty acids (fish and walnut).

Keep in mind- eating 1/2 cup rice is okay but only once a day, oil should be decreased in all foods, dhai with no sugar or malai, only 1 fruit is allowed per day.


Management:
Management of diabetes varies from patient to patient. Please refer to medicine books for details.


Diabetic Emergencies:

Diarrhea and vomiting can cause uremia leading to hiccups.
Acute renal failure
Diabetic ketoacidosis- Patient is usually young with Type I DM.
Hyperosmotic nonketotic diabetic coma causes high bloog glucose levels and dehydration

Plasma osmolarity can be calculated by the following equation: (normal is 275-290 mmol)
Plasma osmolarity = (sodium x 2) + (BUN / 2.8) + (blood glucose / 18)

Managed initially by I/V insulin and isotonic saline. Followed by dextrose with insulin to allow for intracellular free water absorption.
Check blood pressure for orthostatic hypotension.

Further investigations: CBC, blood culture, urine culture, head to toe examination for signs of infection.


Note: The following was just a quick review of what to expect when dealing with a patient with known diabetes mellitus. Please refer to a textbook for further details.

Pathology- Female reproductive MCQ's

1) Which one of the following endometrial lesions is associated with the highest risk of developing endometrial carcinoma?

A. Chronic endometritis
B. Complex hyperplasia with atypia
C. Complex hyperplasia without atypia
D. Simple hyperplasia
E. Squamous metaplasia



The correct answer is B. In general, any condition characterized by excessive estrogenic stimulation is associated with some degree of endometrial hyperplasia and increased risk of endometrial cancer. Endometrial hyperplasia is a histologic precursor of endometrial adenocarcinoma.The most severe changes are present in complex hyperplasia with atypia. Disorganization and crowding of glands, high mitotic activity, and nuclear atypia characterize this change. 25% of women with this form of hyperplasia develop adenocarcinoma.



2) a 36 year old gravid female notes vaginal bleeding. Ultrasound reveals small grape-like cystic structures witout evidence of a developing embryo. A diagnosis of complete hydatidiform mole is made at the hospital. Further analysis is most likely to reveal that:

A. hCG levels are markedly increased
B. serum levels of alpha fetoprotein are elevated
C. the genotype of the mole is 46,XX and is completely paternal is origin
D. the genotype of the mole is triploid
E. two or more sperm fertilized the ovum



The most correct answer is C. A complete hydatidiform mole is characterized by elevated hCG and grape like cystic structures filling the uterus with no detectable embryo on ultrasound. The genotype of a complete hydatidiform mole is purely paternal, caused by fertilization of an egg that has lost its chromosomes. Hydatidiform mole is associated with increasing maternal age, and may be a precursor to choriocarcinoma.

hCG levels are increased relative to normal values for dates, rathar than decreased, in a molar pregnancy (choice A).

Alpha fetoprotein (choice B) is a marker for endodermal yolk sac tumors, embryonal tumors in men, and hepatocellular carcinoma. It is made by the fetus, hence not detectable in a complete hydatidiform mole.

Triploidy and even tetraploidy are characteristics of partial moles (choice D). Partial moles are thought to be due to fertilization of an egg with two different sperm, one with an X and one with a Y chromosome, typically leading to triploidy.

Two or more sperm may fertilize an ovum, leading to a triploid fetus and a partial mole (choice E).



3) A 37 year old woman complains to her gynecologist of discomfort during intercourse and placement of a tampon. Physical examination demonstrates flocculent swelling below the skin of the posterolateral part of one labium majora. Which of the following is the most likely diagnosis?


A. Bartholin's gland cyst
B. Condylomata acuminatum
C. Lichen sclerosis
D. Vestibular adenitis
E. Vulvar squamous hyperplasia



The correct answer is A. This is a Bartholin's gland cyst, which is a relatively common lesion occurring when Bartholin's duct becomes obstructed, typically a sequela to a previous infection. The cysts can enlarge to 3 to 5 cm in diameter.They are lined by either transitional or metaplastic squamous epithelium. Treatment is by excision or marsupialization (permanent opening).

Condylomata acuminatum (choice B) usually produces a papillary lesion (venreal wart).

Lichen sclerosis (choice C) usually produces gray, parchment-like thinned epidermis.

Vestibular adenitis (choice D) usually produces an exquisitely tender posterior introitus with focal ulcerations.

Vulvar squamous hyperplasia (choice E) usually produces a white plaque.



4) A 39 year old woman has cyclical premenstrual pain. Her breasts have a "lumpy bumpy" texture on palpation. A biopsy is performed. The histopathologic features include small cysts lined by epithelial cells with apocrine metaplasia, calcium deposits, areas of fibrosis, increased number of acini (adenosis), and foci of florid hyperplasia of ductal epithelium. Which of these changes increase the risk of breast cancer?

A. Adenosis
B. Apocrine metaplasia
C. Calcium deposits
D. Cysts
E. Epithelial hyperplasia



The correct answer is E. Fibrocystic changes usually come to clinical attention by causing pain (often cyclical, in premenstrual phase), palpable lumps, or mammographic densities and calcifications. A "lumpy-bumpy" texture is caused by cysts and fibrosis. Epithelial hyperplasia is defined as an increase in the number of epithelial cell layers in the ductal epithelium. Florid epithelial hyperplasia leads to an increased risk of developing carcinoma, especially is these is associated cellular atypia (atypical ductal hyperplasia).

Adenosis (choice A) refers to an increase in the number of acini and can be observed in fibrocystic changes as well as in other breast conditions, such as sclerosing adenosis.

Apocrine metaplasia (choice B) describes a benign change of breast epithelial cells that come to resemble the apocrine epithelium of sweat glands.

Calcium deposition (choice C) is a nonspecific finding that mar occur in a number of both benign and malignant breast change, including fibrocystic changes, ductal carcinoma in situ, and invasive carcinoma. Calcification is not clinically significant except for its diagnostic value.

Cysts (choice D) are frequent in fibrocystic changes and result from dilatation of ducts. A classic gross description is that of blue-dome cysts, which appear brown to blue because of their turbid fluid content.




5) An 83 year old female has a biopsy of an ulcerated nipple lesion that is interpreted as Paget's disease. A biopsy of the underlying breast tissue will most likely show which of the following?

A. Acute mastitis
B. Ductal carcinoma in situ
C. Intraductal papilloma
D. Invasive lobular carcinoma
E. Normal breast tissue



The correct answer is B. Paget's disease of the breast is a form of ductal carcinoma in which neoplastic cells involve the squamous epithelium of the skin by direct extension through the lactiferous ducts.

Acute mastitis (choice A) is a disease of nursing women in which bacteria (S. aureus) gain entry to the breast tissue via cracks in the traumatized nipple. It is characterized by acute inflammation and tissue necrosis.

Intraductal papilloma (choice C), a papillary mass arising within the ducts, usually presents as a single subareolar tumor that may produce a bloody or serous nipple discharge.

Invasive lobular carcinoma (choice D) is a tumor of the terminal ductules of the breast. It presents as a poorly circumscribed, rubbery breast mass. Lobular carcinoma does not produce Paget's disease.

Paget's disease of the breast always reflects underlying ductal cancer. This is in marked distinction from extramammary Paget's disease, which may arise without an identifiable malignancy (choice E).

GLAUCOMA

Glaucoma: group of diseases in which increased IOP (intraocular pressure) in an eye produces optic disc cupping and visual field defects.

Normal IOP: 10-21 mm Hg
- Usually slightly high in the morning and slightly deceased at night.


PRODUCTION OF AQUEOUS HUMOR:
(a) Active Secretion: 80% ultrafiltration & 20% diffusion
(b) Drainage: 90% through the Trabecular pathway & 10% through the Uveo-scleral pathway
(c) Level o episcleral venous pressure


CLASSIFICATION:
A. Developmental aka. Congenital: Children present with BUPTHALMOS (increased corneal diameter)
- Primary
- Rubella
- Secondary to other ocular causes such as aniridia
B. Acquired
1. Open angle
- Primary – chronic open angle
- Secondary
2. Closed angle
- Primary – Acute and Chronic closed angle
- Secondary – Due to trauma, raised episcleral venous pressure, steroid induced, associatd with other ocular disease such as uveitis


TONOMETRY (measurement of tension or pressure, particularly IOP)
1. Goldmann tonometer
2. Schiotz tonometer
3. Perkin’s tonometer
4. Air Puff tonometer
5. Tono pen

EYE EXAM:
1. Check IOP
2. Look for optic disc cupping
3. Test field of vision

GONIOSCOPY (examination of anterior chamber of the eye to demonstrate ocular motility and rotation)
- Done to identify structures in the irideo-corneal angle.
- Use a triple-mirror GONIOLENS to visualize the angle and the periphery of the retina
- Opening of the angle is graded (Grades 0-4)
Grade 0: Closed angle
Grade 1:Narrow angle
Grade 2: Moderately narrow angle
Grade 3: Open angle
Grade 4: Widest angle


OPTIC NERVE HEAD CHANGES SEEN IN GLAUCOMA:
1. Retinal nerve fiber changes
2. Concentric expansion of optic disc cup
3. Localized expansion of optic disc cup (notching at inferior or superior pole)
4. Narrowing of neuro-retinal rim
5. Pallor
6. Splinter hemorrhages on disc margin
7. Deepening of optic cup
8. Nasalization of vessels
Note: Papillomacular area is spared and tunnel vision is preserved!!


PERIMETRY:
Visual field: an island of vision surrounded by a sea of darkness.
Normal visual field:
- Superiorly 50 degrees
- Inferiorly 70 degrees
- Nasally 60 degrees
- Temporally 90 degrees

VISUAL FIELD DEFECTS SEEN IN GLAUCOMA:
1. Arcuate Scotomas
2. Isolated paracentral scotoma
3. Nasal step
4. Temporal wedge
5. Ring scotoma


PRIMARY OPEN ANGLE GLAUCOMA:
1. Adult onseT
2. IOP > 21mm Hg at some point in the course of the disease
3. An open angle of normal appearance
4. Glaucomatous optic nerve damage
5. Visual field defect


RISK FACTORS for the development of glaucoma:
1. Age > 40 years
2. Race (higher incidence in Black people)
3. Family history
4. Diabetes
5. Hypertension
6. Myopia
7. Prolonged use corticosteriods (oral or topical)


SYMPTOMS: Usually symptomless & diagnosed on routine eye examination!!
- Patient with Acute closed angle Glaucoma may present with : photophobia, and painful eye, loss of vision, watering of the eye

SIGNS:
1. Increased IOP
2. Fluctuating IOP
3. Optic disc changes
4. Glaucomatous field change


TREATMENT:
1. Medical :
- Alpha-2 agonists eg. Apraclonidine
- Beta Blockers eg. Timolol, Carteolol
- Carbonic anhydrase inhibitors eg. Brinzolamide, Dorzolamide
- Prostaglandins eg. Latanoprost, Travaprost
- Sympathomimetic and Parasympahtomimetic agents eg. Adrenaline, Pilocarpine

2. Laser cyclophotocoagulation

3. Surgery (has a lot of complications and is therefore the last resort of treatment!)
- Argon Laser trabeculoplasty
- Trabeculectomy (a fistula is created between the angle of the anterior chamber and sub Tenon’s space to allow drainage of the fluid)
- Cryotherapy of ciliary body

Management of TRABECUECTOMY FAILURE:
1. Adjunctive Antimetabolites- such as 5-FU and Mitomycin
2. Artificial drainage shunts
3. Cyclodestructive procedure using Lasers OR Cryotherapy


LOW-TENSION GLAUCOMA:
- Also known as Normotensive Glaucoma
- The intraocular pressure is normal but optic disc cupping and field defects are present


OCULAR HYPERTENSION: IOP > 21 mm Hg but there’s no cupping and visual field defects