Corns, Calluses and Properly Fitting Children’s Shoes

Patient Presentation
A 6-year-old male came to clinic for his health supervision visit. His mother had no concerns but had noticed some intermittent mild limping. He denied any problems and his mother denied any fever, muscle aches, back pain, or trauma. She thought it had been occurring for a few weeks or “since the spring started.” The past medical history was negative for any trauma, orthopaedics or neuromuscular problems. The review of systems was negative.

The pertinent physical exam showed a healthy-appearing boy with normal vital signs and growth parameters in the 75-90%. His musculoskeletal examination was normal except that he had calluses on the lateral 5th metatarsalphalyngeal bones of both feet and along the edge of the heels.

The diagnosis of a healthy male was made. The pediatrician looked at the child’s shoes and noted that they seemed worn. When placing them against his feet they were obviously too small. His mother said that they would look into getting new shoes right away. “I’m also going to check his soccer shoes. I bet those are small too,” she said.

Discussion
Probably the most common foot problem is foot pain or skin problems. This can be due to chronic and acute trauma, mobility issues, normal development, activities and footwear.

Common foot problems include:

  • Acute trauma is probably one of the most common reason patients and families seek care for is pain after acute trauma. Children prior to full puberty with acute trauma may have a growth plate fractures or Salter-Harris fractures which can be reviewed here.
  • Apophysitis and tendonitis are common overuse injuries where there is irritation of the tendon and its insertion points. Chronic overuse can also lead to fracture. A review can be found here.
  • Hallux valgus or bunion is caused mainly by restrictive footwear. It is very common in patients with Down Syndrome. A review can be found here.
  • Plantar fasciitis is pain in the plantar area with its dense connective tissues due to overuse. Stretching exercises, a heel cup, supportive shoes and nighttime splinting can help with the pain. It can be a slow heaing process though. A review can be found here.
  • Pes Planus or flat foot is a common presentation in children and is the absent or diminished longitudinal medial foot arch. Flexible flat feet occur in children < 6 years and should be painless. History of pain makes this diagnosis less likely. A review can be found here
  • Plantar warts caused by viruses can be irritating and quite painful for patients. There are numerous treatments including debridement, local acid treatments or cryotherapy as common mainstays. There are potential complications that need to be considered though. A review of treatments can be found here. A review of potential cryotherapy treatment problems can be found here.
  • Tinea pedis and onychomycosis are common skin and nail infections due to exposure to humid environments and exposure to fungal infections, including that of shoes themselves. Treatment is increased air exposure and topical or oral anti-fungal medications. Prevention measures can be reviewed here.
  • Immersion injury – most people are well aware of experiencing wrinkled skin after being exposed to water due to hyperhydration of the plantar stratum corneum. Immersion injuries occur after extended or repeated exposure to water in warm or cold environments. Treatment is mainly preventative but severe problems can occur. A review can be found here.

Learning Point
Corns and calluses are other common foot problems. Both are thickened skin caused by friction or pressure. It is the skin’s protective mechanism to protect the underlying tissues. They are usually due to increased activity, ill-fitting shoes or anatomic foot problems. Calluses are not painful usually unless they themselves are injured (e.g. cracked skin) and are located in places of high movement and pressure (such as hands and feet). Corns are smaller than calluses. They have a hardened center and can be painful when palpated. They are located in non-pressure areas such as between toes.

Treatment includes:

  • Decreasing pressure or friction. Using appropriate footwear along with socks can decrease the friction. Socks can also wick moisture away.
  • Padding of the area to allow it to heal
  • Over the counter or customized orthotics and shoes to decrease pressure and friction
  • Salicylic acid, urea and similar products can soften and diminish the thickened tissue
  • Scalpel debridement is also sometimes used

Shoes are judged by their form, fit and function with fit usually governing how they function. Therefore fit is very important. In a systemic review, it was estimated that 63-72% of people had improperly fitted shoes. A study of children with Down Syndrome found shoes that were too narrow.

Proper footwear should:

  • Be usable right out of the box. It should not need to be “broken in.”
  • Shoes should be fitted when feet are the largest which is at the end of the day. They should be fitted while weight-bearing on both feet. This allows the foot to spread. Walking or running can also cause the foot to spread and shoewear should be tested doing these activities as well.
  • Shoes should fit snugly and not slip off. The heel needs to be able to move but should fit snugly
  • Length should be ~ 10 mm from the longest toe for general shoes with athletic shoes up to 1 inch. Width should allow for adequate space across the entire ball of the foot (usually < 10 mm extra space).
  • If orthotics or other appliances are used, they should be in place while fitting shoes as they will change the fit.
  • Specialty shoes usually need activity/occupational specialists to fit such shoes. For example, pointe shoes for ballet dancers or skates for skaters. A review can be found here.

Foot professionals may characterize general foot and toe morphology as Egyptian (first toe is the longest), Greek (second toe is the longest), and square (first and second toes are of equal length). These can be important as most children’s shoes are developed on adult foot templates which are developed usually from square toed morphology. Children’s feet grow faster than most parents realize and they need new shoes often. Toddler and young preschoolers may need new shoes 3-4 times/year, those 4-6 years about 2 times per year and those 6-12 years about 3 times per year. Adolescents may need them more frequently depending on age of puberty.

Questions for Further Discussion
1. What are the most common foot problems in your clinic?
2. What are your favorite treatment choices for corns and calluses?
3. What causes limping? A review can be found here

Related Cases

To Learn More
To view pediatric review articles on this topic from the past year check PubMed.

Evidence-based medicine information on this topic can be found at SearchingPediatrics.com and the Cochrane Database of Systematic Reviews.

Information prescriptions for patients can be found at MedlinePlus for these topics: Corns and Calluses and Foot Injuries and Disorders.

To view current news articles on this topic check Google News.

To view images related to this topic check Google Images.

To view videos related to this topic check YouTube Videos.

Buldt AK, Menz HB. Incorrectly fitted footwear, foot pain and foot disorders: a systematic search and narrative review of the literature. J Foot Ankle Res. 2018;11:43. doi:10.1186/s13047-018-0284-z

Becker BA, Childress M. Common Foot Problems: Over-the-Counter Treatments and Home Care. AFP. 2018;98(5):298-303.

Gonzalez Elena ML, Cordoba-Fernandez A. Footwear fit in schoolchildren of southern Spain: a population study. BMC Musculoskelet Disord. 2019;20:208. doi:10.1186/s12891-019-2591-3

Corns and Calluses Cedars-Sinai. Accessed November 23, 2021. https://www.cedars-sinai.org/health-library/articles.html

Author
Donna M. D’Alessandro, MD
Professor of Pediatrics, University of Iowa

What Are Potential Physical Examination Findings for Patients with Atrioventricular Canal Defects?

Patient Presentation
A 7-day-old male came to clinic for routine followup. He had Trisomy 21 with an atrioventricular canal heart defect. Additional evaluations during the newborn stay did not identify other congenital anomalies including no heterotaxia. He had been bottle feeding well without cyanosis or tachypnea, and taking the bottle within 15 minutes.

The pertinent physical exam showed a well-appearing male with Trisomy 21 facial features. His weight was down 3% from birthweight and was 15% on the Trisomy 21 growth chart. His lungs were clear and his heart had a normal S1, S2 but with a systolic murmur heard best toward the left sternal border to the apex. He had no hepatosplenomegaly. Femoral pulses were strong. He had mild hypotonia.

The diagnosis of a patient with Trisomy 21 and atrioventricular canal defect was confirmed. His mother asked good questions about how to continue monitoring him at home. The patient’s clinical course the following week showed he had passed birth weight but was decreasing in weight gain per day. The mother was instructed to increase the calories per ounce of formula. At return the following week the infant still was not showing signs of fatigue or difficulties with feeding but weight gain per day continued to decline. Cardiology was called and arranged to have him be seen the following day, where they began diuretic therapy. Over time he needed more ionotropic support before he had successful surgical correction at 4 months of age.

Discussion
Atrioventricular canal defects (AVCD) are a heterogeneous range of congenital heart defects (CHD) arising from malformations of intracardiac septal development. Essentially the location where the 4 corners of the 2 atria and 2 ventricula meet is abnormally formed. There is partial or complete fusion of the mitral and tricuspid valves along with atrial (ASD) and ventricular septal defects (VSD). Fusion of the endocardial cushions occurs around 4-5 weeks gestation. The anatomy for an individual is bespoke as the variations of the valve leaflets, chordal attachments and variations in ASD and VSD are numerous. This pathology causes fluid overload and left-to-right shunting and resulting pulmonary overcirculation.

AVCDs occur in ~3-7% of CHD patients or in about 3.5/10,000 live births. Patients with AVCDs often have extracardiac anomalies (75%). AVCDs are common in patients with Trisomy 21 (40-45% of Trisomy 21 patients have AVCD) but also with heterotaxy (15%). Non-syndrome patients are observed in about 25% of AVCD patients. Other genetic syndromes associated with AVCD include “CHARGE,…, Ellis-van-Creveld, Ivemark, Kaufman McKusick, Ritscher-Schinzel, Smith-Lemli-Opitz, and 3p.”

Patients are often identified prenatally on prenatal ultrasound or karyotype. Others are identified soon after birth with abnormal physical examination. Others may not present until 1-2 months of life when pulmonary overcirculation occurs. Diagnosis is made by echocardiogram.

In 1955, Dr. Walton Lillehei of the University of Minnesota successfully surgically treated a patient with AVCD. Patients are surgically treated usually between 3-6 months before pulmonary overcirculation is severe. Presurgery this includes proper weight management but also may need diuretics, angiotensin-converting enzyme inhibitor, angiotension 2 receptor blockers and/or digoxin. The surgical technique involves patches to vertically separate the ventricles and the atria along with creating separate mitral and tricuspid valves horizontally. Because of the location the main potential post-procedure problems include heart block as the coronary sinus is located close to this area, and valvular competence and adequacy. Intraoperative mortality is cited at ~3% and 10-year survival rate is ~90%. Re-operation occurs in about 5-10% of people usually because of mitral regurgitation.

Learning Point
In patients with suspected AVCD, the general physical examination should look for dysmorphic features especially those associated with Trisomy 21, but also evaluation of other mid-line defects such as cleft lip/palate and musculoskeletal abnormalities. Signs of heterotaxy should also be looked for. Signs and symptoms of AVCD are usually associated with congestive heart failure including increased work of breathing, sweating with activities such as eating, sleepiness and lethargy. Tachypnea, tachycardia, wheezing and poor weight gain can be noted. Patients may also have pulmonary rales, hepatomegaly, jugular venous distention and apical displacement of the apical impulse. Generally AVCD is acyanotic as it is has left-to-right shunting, but during crying or other circumstances can cause right-to-left shunting and cyanosis for a period of time. Auscultation may show a wide split S2 because of the left-to-right shunting, and an S3 gallop again because of increased flow. There may be a holosystolic murmur that is best at the apex or a mid-diastolic murmur because of valvular regurgitation.

Questions for Further Discussion
1. What are the 5 “C’s” of cyanotic congenital heart disease? A review can be found here
2. What are common acyanotic congenital heart diseases? A review can be found here
3. What other extracardiac problems are common in patients with Trisomy 21?

Related Cases

To Learn More
To view pediatric review articles on this topic from the past year check PubMed.

Evidence-based medicine information on this topic can be found at SearchingPediatrics.com and the Cochrane Database of Systematic Reviews.

Information prescriptions for patients can be found at MedlinePlus for this topic: Congenital Heart Defects

To view current news articles on this topic check Google News.

To view images related to this topic check Google Images.

To view videos related to this topic check YouTube Videos.

Malik M, Khalid Nuri M. Surgical Considerations in Atrioventricular Canal Defects. Semin Cardiothorac Vasc Anesth. 2017;21(3):229-234. doi:10.1177/1089253217708622

Digilio M C., Pugnaloni F, De Luca A, et al. Atrioventricular canal defect and genetic syndromes: The unifying role of sonic hedgehog. Clinical Genetics. 2019;95(2):268-276. doi:10.1111/cge.13375

Knatterud M. C. Walton Lillehei, PhD, MD. Medical School – University of Minnesota. Published November 24, 2020. Accessed November 16, 2021. https://med.umn.edu/lhi/about/c-walton-lillehei

Rigby M. Atrioventricular Septal Defect: What Is in a Name? J Cardiovasc Dev Dis. 2021;8(2):19. doi:10.3390/jcdd8020019

Umapathi KK, Agasthi P. Atrioventricular Canal Defects. In: StatPearls. StatPearls Publishing; 2021. Accessed November 15, 2021. http://www.ncbi.nlm.nih.gov/books/NBK557511/

Author
Donna M. D’Alessandro, MD
Professor of Pediatrics, University of Iowa

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Polyuria, Polydipsia and Possible Diabetes Insipidus?

Patient Presentation
A 20-month-old male who had just moved to the area came to clinic with a history of several months of polyuria and polydipsia. He demanded to drink all the time and would gulp 4+ ounces at a time and didn’t care what type of fluid it was. He would seek out other fluid such as drinking from water hoses and pet water bowls if he was denied fluid. His mother described 20-25 diapers/day that would be soaked with urine. At night the mother would set up several bottles of fluid for the boy and would need to change his diaper several times which disrupted their sleep. He was otherwise well and had normal growth and development when his medical records were reviewed.

The past medical history showed a full term infant with no trauma, significant illnesses, hospitalizations or surgery. The family history was negative for any early childhood illnesses or deaths. The mother denied any central nervous system, endocrine or kidney problems. Most people in the family died of heart disease or stroke. The review of systems was negative including any fevers, weight or growth problems, sleep, or elimination.

The pertinent physical exam showed normal growth in a happy playful child who drank 4 ounces of fluid and had 2 wet diapers during the visit. There were no obvious midline defects including no hypertelorism, high arched palate etc. Heart revealed no abnormal sounds or rhythms. Abdominal and genitourinary systems were normal.

The diagnosis of ongoing probable polyuria and polydipsia was made. The laboratory evaluation included a normal basic metabolic panel, glucose and hemoglobin A1c, calcium and thyroid tests. The urinalysis showed a specific gravity of 1.060, pH of 7 and was otherwise normal. Urine osmolality was 162 mOsm/L and spot urine sodium was 24 mEq/L. Given the fluid seeking behaviors, normal physical examination and laboratory findings, the diagnosis of diabetes insipidus versus a primary polydipsia was strongly considered. During a telephone consultation, the endocrinologist agreed with the general pediatrician and the patient was scheduled to be seen with a water deprivation test at that time.

Discussion
The body is smart. It has mechanisms for maintaining balances within the body in a closely controlled manner but allows for a variety of states. This is very true for fluid balance in the body which is highly controlled between almost all of the major body organ systems. When fluid is low, the sensor sends signals for us to drink, and conserves fluid until we can. When the fluid is high, the kidneys excrete the excess and sends signals not to drink. Usually it works very well. While there are many pathological states that can cause polyuria and/or polydipsia, the most common reason is excessive fluid intake because of habit or behavioral causes.

Polyuria is an excessive production of urine. Normal urination varies by age and decreases as the kidneys mature. Polyuria needs to be distinguished from frequent toileting, nocturia and enuresis, and just plain urinary frequency. Anatomic abnormalities such as meatal stenosis, posterior urethral valves, or labial adhesions may also appear to cause frequent urination. Additionally, some normal fluids such as caffeine can have a short term diuretic effect.

Normal urine volume is:

  • Birth – 150 ml/kg/day
  • 2 years – 100-110 ml/kg/day
  • 2 years 40-50 ml/kg/day

Causes of polyuria include:

  • Fluid excess
    • Polydipsia
    • Intravenous fluid overadministration
  • Diabetes mellitus and hyperglycemia
  • Diabetes insipidus
  • Diuretics
  • Electrolyte abnormalities
    • Hypercalcemia
  • Nocturnal polyuria
    • Enuresis

Confirmation of polyuria can usually be accomplished by a 24-hour urine collection. For diapered children, weights of diapers before and after use can give the volume.

Polydipsia is excessive thirst which causes consumption of larger than normal volumes of fluid.
Polydipsia needs to be distinguished from habitual drinking or fluid preferences.
Normal fluid intake is usually calculated by the child’s weight:

  • 0-10 kg = 100 ml/kg
  • 10-20 kg = 1000 ml + 50 ml/kg
  • > 20 kg = 1500 ml + 20 ml/kg

Note that the amount of fluid intake is also dependent on environmental temperature and physical activity.
Fluid intake will necessarily exceed fluid out because of incessant losses.

Causes of polydipsia include:

  • Inadequate intake or dehydrated state
  • Diabetes mellitus and hyperglycemia
  • Diabetes insipidus
  • Excessive exercise
  • Excessive water drinking as it causes increased fluid output

With true polydipsia, patients will have an insatiable thirst and will seek fluid wherever they can if denied access to usual sources. These would include drinking from pet bowls, toilet bowls, mop heads, water hoses, etc. These behaviors can cause risks of water intoxication and also safety risks for drinking inappropriate fluids such as bleach, coolants, etc. Confirmation of polydipsia usually can be accomplished by a diary of fluid intake and type of fluid.

A differential diagnosis of presentation of polyuria and/or polydipsia includes:

  • Excessive water drinking
  • Central nervous system
    • Head trauma
    • Neurosurgery
  • Electrolyte abnormalities
    • Hypercalcemia
    • Hypokalemia
  • Endocrine
    • Diabetes mellitus
    • Diabetes insipidus
    • Adrenal insufficiency
    • Congenital adrenal insufficiency
    • Cushing’s
    • Renal tubular acidosis, Type 4
  • Genetic/congenital
    • Familial
    • Kabuki syndrome
    • Septo-optic dysplasia
  • Iatrogenic
    • Intravenous fluid overadministration
    • Diuretic medication
    • Other drugs
  • Infection
    • Urinary tract infection
    • Meningitis/encephalitis causing central diabetes insipidus
  • Renal
    • Polycystic kidney disease
    • Sickle cell nephropathy
    • Renal tubular acidosis (Bartter or Gitelman syndromes)
    • Renal failure
  • Tumor/infiltrative
    • Catecholamine secreting tumor
    • Craniopharngioma
    • Germinoma
    • Histiocytosis
    • Pituitary adenoma
    • Sarcoidosis
  • Other
    • Malnutrition

Baseline evaluation for polyuria/polydipsia often includes:

  • Urinalysis
  • Urine sodium and osmolality
  • Urine glucose
  • Basic metabolic panel
  • Calcium
  • Glucose
  • Other possibilities include cortisol, thyroid function tests

Learning Point
Diabetes insipidus (DI) is a syndrome where there is chronic excretion of excessive amounts of dilute urine. Diagnosis is made using measurements of 24-hour urine volume, osmolality, and glucose and sodium values. Additional testing including water deprivation testing and desmopressin testing may be necessary. Vasopressin, copeptin levels and magnetic resonance imaging of the head may also be employed. Specialized testing should be performed by appropriate specialists because of the potential risks involved with these tests in addition to necessary lab conditions and cost. In DI, the urine volume is high, urine osmolality is low, urine glucose is negative, urine specific gravity and sodium will vary depending on conditions. It is also important to remember that the vasopressin levels or insensitivity to them may be partial and not absolute. Therefore some of the presenting symptoms or laboratory values can vary.

There are 4 types of DI

  • Central or pituitary DI
    • Caused by inadequate vasopression production or secretion by the pituitary gland
    • Causes include
      • Genetic/congenital – autosomal dominant, recess or X-linked recessive, holoproencephaly
      • Acquired – problems that destroy or invade the pituitary such as trauma, neoplasms, infections, CNS vascular problems
    • Treatment is desmopressin, vasopressin
  • Nephrogenic DI
    • Caused by renal insensitivity to vasopressin
    • Causes include
      • Genetic – autosomal dominant, recessive or X-linked recessive
      • Acquired – problems that change the renal function such as drugs, electrolyte abnormalities (hypercalcemia, hypokalemia), neoplasms, renal vascular problems
    • Treatment is diuretics and/or indomethacin
  • Primary polydipsia
    • Abnormal thirst (dipsogenic) or abnormal cognition (psychogenic) causes an increased secretion of vasopression
    • Treatment is environmental changes, education and potentially psychotherapy
  • Gestational DI
    • Increased degradation by the placenta of vasopression during pregnancy
    • Usually begins in 3-4 month of gestation and resolves within 4-6 weeks after delivery
    • Treatment if needed is desmopressin

Questions for Further Discussion
1. How does diabetes mellitus present?
2. What causes urinary frequency?
3. What causes syndrome of inappropriate antidiuretic hormone? A review can be found here

Related Cases

To Learn More
To view pediatric review articles on this topic from the past year check PubMed.

Evidence-based medicine information on this topic can be found at SearchingPediatrics.com and the Cochrane Database of Systematic Reviews.

Information prescriptions for patients can be found at MedlinePlus for this topic: Diabetes Insipidus

To view current news articles on this topic check Google News.

To view images related to this topic check Google Images.

To view videos related to this topic check YouTube Videos.

Robertson GL. Diabetes insipidus: Differential diagnosis and management. Best Practice & Research Clinical Endocrinology & Metabolism. 2016;30(2):205-218. doi:10.1016/j.beem.2016.02.007

Mahon M, Amaechi G, Slattery F, Sheridan AL, Roche EF. Fifteen-minute consultation: Polydipsia, polyuria or both. Arch Dis Child Educ Pract Ed. 2019;104(3):141-145. doi:10.1136/archdischild-2018-315486

Kavanagh C, Uy NS. Nephrogenic Diabetes Insipidus. Pediatric Clinics of North America. 2019;66(1):227-234. doi:10.1016/j.pcl.2018.09.006

Patti G, Ibba A, Morana G, et al. Central diabetes insipidus in children: Diagnosis and management. Best Pract Res Clin Endocrinol Metab. 2020;34(5):101440. doi:10.1016/j.beem.2020.101440

Author
Donna M. D’Alessandro, MD
Professor of Pediatrics, University of Iowa