Falcon Reviews

Five Critical Diagnoses Not to Miss on a Chest X-ray

by : William Herring, MD, FACR

It’s 3:00 a.m. Mr. Smith is in Room 2, and is extremely short of breath, with a falling blood pressure. You are reviewing his chest x-ray. Here are five critical diagnoses you don’t want to miss:

Tension Pneumothorax

When air enters the pleural space, the lung and visceral pleura collapse toward the hilum. The visceral pleura then becomes visible as a thin, white line marking the lung’s outer border (visceral pleural line). If air loss into the pleural space occurs with a check-valve mechanism, the intrapleural pressure continues to rise, leading to a shift of the heart and trachea away from the side of the pneumothorax. This can lead to cardiopulmonary compromise, by impairing venous return to the heart (tension pneumothorax). Tension pneumothoraces require emergent decompression. (Fig. 1)

Aortic Dissection

Conventional radiographs are not sensitive enough to be diagnostically reliable, but they can suggest the diagnosis when several imaging findings occur together, especially in the proper clinical setting. Look for (1) a widening of the mediastinum — a subjective and often over-interpreted finding; (2) a left pleural effusion; (3) a left apical pleural cap of blood or fluid; (4) loss of the normal aortic knob shadow, and (5) deviation of the trachea or esophagus to the right. MRI and CT are more sensitive in making this diagnosis, by demonstrating the intimal flap separating the true (original) lumen from the false lumen created by the dissecting blood. (Fig. 2)

Ruptured Esophagus

Rupture of the distal esophagus can occur with increased intra-esophageal pressure in Boerhaave’s Syndrome. Think of Boerhaave’s Syndrome when the x-ray displays (1) a pneumomediastinum and/or (2) a left pleural effusion (3) in a patient with a history of retching or vomiting. Pneumomediastinum produces linear, streak-like lucencies associated with a thin white line paralleling the left heart border, spine or great vessels. Sometimes, pneumomediastinum outlines the central portion of the diaphragm beneath the heart, producing an unbroken diaphragmatic contour extending from one lateral chest wall to the other (continuous diaphragm sign). (Fig. 3)

Pulmonary edema

Unfortunately, congestive heart failure is frequently over-diagnosed on chest radiographs.  Stick to these four, key radiographic signs to recognize pulmonary interstitial edema: (1) thickening of the interlobular septa Kerley B lines ─ visible at the lung bases as 1-2 cm, thin, horizontally-oriented lines perpendicular to the pleural surface; (2) peribronchial cuffing – tiny “doughnuts” visible in the lung, due to fluid-thickened bronchial walls visualized en face; (3) fluid in the fissures ─ opacification and thickening of the major and minor fissures, and (4) pleural effusions ─ usually bilateral but, when unilateral, usually right-sided. As pulmonary venous pressure increases, fluid spills into the alveoli, producing pulmonary alveolar edema, which is characterized by perihilar, fluffy airspace densities frequently having an angel-wing or butterfly configuration and sparing the outer third of lungs. (Fig. 4)

Pneumoperitoneum

Free intraperitoneal air will frequently be first visualized on an upright chest x-ray. In the upright position, free air will usually reveal itself under the right hemidiaphragm as a crescentic lucency that parallels the undersurface of the diaphragm. The size of the crescent is roughly proportional to the amount of free air. Free air can be due to trauma, either accidental or iatrogenic, or rupture of a loop of bowel, mostly from gastric or duodenal ulcer disease. Remember that small amounts of free air will not be detectable in a supine view of the chest (or abdomen), and will require an upright view to be visible. (Fig. 5)

William Herring, MD, FACR, is the Radiology Residency Program Director at Albert Einstein Medical Center in Philadelphia, Pennsylvania, and the author of Learning Radiology: Recognizing the Basics, a fundamental radiology text.

 

OPTHALMIA NEONATORUM

On September 17, 2010, in COMLEX, USMLE Step 1, USMLE Step 2, by admin

A USMLE/COMLEX Overview by Michael Lloyd, MD

The beautiful thing about questions regarding neonatal conjunctivitis (ophthalmia neonatorum) on the USMLE/COMLEX is that you really only have to remember the three main causes, and how to tell them apart. Ophthalmia neonatorum describes conjunctivitis that occurs within a baby’s first month of life. The USMLE/COMLEX usually places the setting as a newborn screening, or two-week checkup following delivery. The infant will always present with discharge, swollen eyelids, and erythematous conjunctiva (see Figure 1).

Figure 1. Opthalmia neonatorum

Thinking about the source of the conjunctivitis will help you remember the possible causes. As in cases with adult patients, neonatal conjunctivitis is mainly caused by infectious agents such as bacteria or viruses, or by irritation (such as hay fever, allergic conjunctivitis, etc). The overwhelming majority of newborn conjunctivitis cases are caused either by infectious agents, such as Nisseria gonorrhea or Chlamydia trachomatis, or a chemical irritation from the prophylactic antibiotic put in the eyes of newborns to prevent gonococcal conjunctivitis. Of course, other etiologies, including herpes simplex virus, Pseudomonas species, and group B strep (strep mitis) can cause disease as well, but these are less commonly asked about on the USMLE/COMLEX.

The timing of onset is your biggest clue in discriminating among these different choices.   Chemical conjunctivitis (due to irritation from the silver nitrate or erythromycin ointment) has the fastest onset, and will have a clear, rather than purulent discharge.  Chlamydia has a longer incubation period than gonococcus, and therefore has a later onset, as shown in Table 1.

Table 1. Causative Agents in Neonatal Conjunctivitis

AgentChemicalGonococcalChlamydial
Timing of onsetWithin the first day2-5 days after birth5 days to 2 weeks after birth


Other clues will often be given to solidify your hunch. For example, the mother may have an active case of purulent urethritis (gonococcal), swabs may show elementary bodies (Chlamydia), or discharge may resolve in 24 hours after stopping the antibiotic (chemical). Although gonococcal conjunctivitis should not occur in newborns who have received prophylaxis, chlamydia conjunctivitis is not prevented by the antibiotic, and may still occur.

Other important points include the following:

  • Chlamydia conjunctivitis requires systemic erythromycin, in addition to erythromycin eye ointment. This is to prevent chlamydial pneumonia, which would otherwise develop.
  • Gonococcal conjunctivitis can become serious if it penetrates the cornea or becomes systemic — watch for fevers, a rash, or sepsis. Treat with topical erythromycin and systemic IV cefotaxime.
  • For infants with chlamydial and gonococcal conjunctivitis, parents should be treated, as well.

References:

  1. Brochert, A. Crush Step 2, The Ultimate Step 2 Review. 2003. Hanley & Belfus, Philadelphia, PA.
  2. Marino, B. Blueprints Pediatrics: Fourth Edition. 2007. Lippincott Williams & Wilkins. Philadelphia, PA.
  3. http://www.meduni-graz.at/augenheilkunde/ahk_site/systematik/bh/bh_conju_neona/bh_conju_neona.html
 

Retinoblastoma

On September 14, 2010, in COMLEX, USMLE Step 1, USMLE Step 2, by admin

A USMLE/COMLEX Overview by Michael Lloyd, MD

The USMLE/COMLEX often tests your knowledge of some less common, but life-threatening disorders, and retinoblastoma is a perfect example. Although there are only about 300 new cases of retinoblastoma in the U.S. each year, it is the most common intraocular tumor of childhood, and the second most common primary intraocular malignancy in all age groups (Uveal melanoma is the most common in adults). It is a curable disease that can be fatal if not recognized and diagnosed at an early stage.  Retinoblastoma is a neuroblastic tumor caused by a mutation in the long arm of chromosome 13, which can be inherited (one third of cases) or spontaneous (two thirds of cases). The retinoblastoma gene is a tumor suppressor gene; and in familial cases, one defective copy is inherited, and a somatic mutation is required for tumor growth. Thus, the genetic inheritance is autosomal recessive; but the tumor behaves clinically as an autosomal dominant trait.

Presentation

Retinoblastoma can occur unilaterally (in either eye) or bilaterally. The bilateral cases are usually diagnosed at one year of age, while the unilateral cases are not detected until 24 months or so. The most common presentation is a complaint of leukocoria — a white, rather than red, reflex from the eyes (see Figure 1).

Figure 1 Leukocoria

Parents often notice a difference in the appearance of their child’s eyes in photographs, and this brings them to the pediatrician or family practitioner. Checking for leukocoria is an important step in every well-child exam because it is quick, easy, and can catch devastating diseases.  Table 1 lists the differential diagnosis for leukocoria – you will not likely be asked about any of the other causes on the USMLE.

Table 1. Differential Diagnosis for Leukocoria

RetinoblastomaStrabismus (ocular misalignment)
Congenital cataractRetinopathy of prematurity
Infectious causes (endophthalmitis, toxocariasis, toxoplasmosis)

Diagnosis and Management

You will not be asked on the USMLE how to manage retinoblastoma, but you should know some of the following important characteristics.

  • Imaging (CT or ocular ultrasound) will often show calcium deposits within the tumor mass itself.
  • CT or MRI of the brain is required in bilateral cases to rule out involvement of the pineal gland (the so-called trilateral retinoblastoma).
  • Family members should be evaluated, as the inheritance is clinically described as autosomal dominant.
  • Localized, unilateral tumors are managed by enucleation (removal of the eye), with attention to the optic nerve, to evaluate for any tumor involvement.
  • The management of bilateral, localized tumors is beyond the scope of the USMLE, but options include systemic chemotherapy, localized radiation therapy, and bilateral enucleation.
  • Histologic characteristics include Flexner-Wintersteiner rosettes in well-developed tumors (can also be seen in other neural tumors such as ependymomas or neuroblastomas).

Figure 2. Flexner-Wintersteiner Rosettes

References:

  1. Gallin, PF, Pediatric Ophthalmology: A Clinical Guide. 2000 Thieme Medical Publishers, Inc. New York, NY.
  2. http://www.oftalmo.com/publicaciones/pediatrica/cap31.htm
  3. http://www.bangkokhealth.com/eye_htdoc/eye_health_detail.asp?number=9705
  4. http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=180200
  5. http://www.thefreedictionary.com/Flexner-Wintersteiner+rosette
 

PEDIATRIC RHEUMATOLOGY

On September 13, 2010, in COMLEX, USMLE Step 1, USMLE Step 2, by admin

A USMLE/COMLEX Overview by Michael Lloyd, MD

Pediatric Rheumatology can seem daunting because of the variety of diseases (see Table 1) and the numerous diagnostic criteria. Fortunately, these various disorders have enough unique characteristics to distinguish themselves from one another, and USMLE/COMLEX exams tend to describe them in their classical settings. This article will review the characteristics found in each of the following diseases, so you can easily recognize them on Steps 1 and 2 or Levels 1 and 2. As with most autoimmune disorders, girls are affected more frequently with rheumatologic disease than boys.

Juvenile Rheumatoid Arthritis (JRA)

Inflammatory joint disease (arthritis) is defined as decreased range of motion, pain, warmth, or swelling in an affected joint. Patients who have JRA must be under sixteen years old at diagnosis, and have six weeks of arthritis in at least one joint that is not due to any other etiology. Synovial joint analysis will reveal many WBCs without bacteria or blood (the presence of these in a joint analysis should lead you to another cause of the arthritis).

JRA comes in three distinct forms, which are detailed in Table 2.

Table 2. Juvenile Rheumatoid Arthritis

SubtypeSystemic "Still's disease"~15% of all casesPauciarticular~50% of all casesPolyarticular~35% of all cases
Clinical characteristicsAbrupt onset of high fever spikes, a salmon-colored evanescent rash, hepatosplenomegaly, and pericarditis, followed by arthritis.Arthritis in four or fewer joints; usually large joints below the waist. High risk for asymptomatic uveitis.Arthritis in five or more joints. Includes small and large joints.
Laboratory characteristicsAnemia & thrombocytosis. Negative ANA and RF.Frequently have positive ANA, but RF is negative.Similar to adult RA, there is usually positive RF.

Some physicians argue these should be called “juvenile idiopathic arthritis,” because the rheumatoid factor is negative in most cases. Those patients with positive RF often go on to develop rheumatoid arthritis, in a similar fashion to the adult-onset version.

ANA positivity is a risk factor for iridocyclitis or uveitis (ocular inflammation), which is often asymptomatic, but can cause irreversible blindness and severe visual disability.  These patients should be frequently screened by an ophthalmologist, to evaluate for ocular inflammation.

Management of JRA includes the use of systemic anti-inflammatory agents, including corticosteroids, methotrexate, and some of the newer anti-TNF agents.

Systemic Lupus Erythematosus

Lupus is a systemic autoimmune disorder characterized by immune complex deposition, which leads to an arteriolar vasculitis. The diagnosis is made when four of eleven possible diagnostic criteria have been met (see Table 3).

Table 3. Diagnostic Criteria for SLE (Four out of eleven are required)

Malar rashDiscoid rash
PhotosensitivityOral Ulcers
Arthritis (nonerosive)Serositis (pleuritis, pericarditis)
Neurologic symptoms (seizures, psychosis)Hematologic abnormalities (anemia, thrombocytopenia)
Renal manifestations (nephritic or nephritic syndromes)Positive ANA
Positive anti-dsDNA, anti-smith, or anticardiolipin tests

The kidneys are one of the most commonly involved organ systems, and — as in adult-onset SLE — there are grading systems that are used to measure the severity of disease.

Diagnosis is based on a careful history (to recall episodes of psychosis or seizures, oral ulcers or photosensitivity), physical exam (to diagnose the rash, arthritis, or serositis), and by an appropriate laboratory workup (to check for anemia, thrombocytopenia, ANA, and other immunologic tests.

Treatment is based on the presenting symptoms and the current amount of inflammation.  Nephrology is often involved in management of lupus nephritis, but anti-inflammatory medications and common sense measures (avoid the sun, manage HTN, monitor for petechial bleeding, etc) are also helpful. Oral corticosteroids are useful, but steroid-sparing agents (methotrexate, cytoxan, cellcept) are also frequently used, to avoid the side effects of prednisone.

Other rheumatologic disorders to think about include the following:

  • Dermatomyositis – proximal muscle weakness, joint deformities on the fingers (Gottron’s papules), and a characteristic violacious (heliotrope) rash on the eyelids. Elevated CK – treat with steroids.
  • Polyarteritis nodosa – multiple systemic complaints, with an elevated ESR.  Diagnose based on biopsy results. Treat with immunosuppressives.
  • Henoch-Schonlein pupura – upper respiratory infection, followed by palpable purpura on the lower extremities and buttocks, IgA mediated damage to the GI tract, and glomerulonephritis. Treat with corticosteroids and supportive therapy.
  • Kawasaki disease – watch for a young child with a high fever, desquamating rash, and conjunctivitis. Get a 2-D echo to evaluate for coronary artery aneurysms, and treat with aspirin (an unusual recommendation in the pediatric population) or IVIG.

References:

  1. Brochert, A. Crush Step 2, The Ultimate Step 2 Review. 2003. Hanley & Belfus, Philadelphia, PA.
  2. Marino, B. Blueprints Pediatrics: Fourth Edition. 2007. Lippincott Williams & Wilkins. Philadelphia, PA.
  3. http://www.stillsdisease.org/
  4. http://www.niams.nih.gov/hi/topics/juvenile_arthritis/juvarthr.htm
  5. http://www.niams.nih.gov/hi/topics/lupus/slehandout/
  6. http://www.myositis.org/about_myositis/juvenile_dermatomyositis.cfm
  7. http://vasculitis.med.jhu.edu/typesof/polyarteritis.html
  8. http://www.nlm.nih.gov/medlineplus/ency/article/000425.htm
  9. http://www.kdfoundation.org/
 

Hyperthyroidism

On September 11, 2010, in COMLEX, General, USMLE Step 1, USMLE Step 2, Vignettes, by admin

A USMLE/COMLEX Overview by Michael Lloyd, MD

What do the following vignettes all have in common?

  • A fast-talking, 40-year-old woman complains that she isn’t sleeping much, and that she’s hot all the time. She appears to be staring intently at you.
  • A 38-year-old woman presents with fatigue, weight loss, and infrequent, spotty periods. On exam, she has neck pain and a fever.
  • A 25-year-old man with an irregular heartbeat has the following lab results: a low TSH, and normal levels of T3 and T4.

In addition to being common USMLE/COMLEX presentations, the previous three patients could all be diagnosed with some form of thyroid dysfunction. Thyroid disease often shows up on the USMLE/COMLEX. Following is a review of the aspects of hyperthyroidism that most frequently generate questions.

Figure 1: Thyroid Hormone Axis

Cause and Commonality

Thyroid disease is very common (second only to diabetes in terms of endocrine diseases), and occurs more often in women than in men. It has many causes, but they all work by increasing the amount of thyroid hormone available for the body to use. The hypothalamic-pituitary-thyroid axis is shown in Figure 1. Causes of hyperthyroidism are listed in Table 1.


Table 1. Causes of Hyperthyroidism
Etiology Mechanism of Action Symptoms

Tumors

Multinodular goiter

Toxic adenoma

Pituitary adenoma (rare)

Tumor production of hormone (multinodular goiter and toxic adenoma) or of TSH (pituitary adenoma) Heat intolerance, palpitations, weight loss, nervousness, weakness, fatigue, loose stools, oliogmenorrhea
Graves’ disease (most common) Thyroid stimulating immunoglobulins (TSI) are formed, which bind to and stimulate the TSH receptor on the thyroid gland. All of the above, plus Exophthalmos and pre-tibial myxedema

Subacute thyroiditis

Hashimoto’s disease (autoimmune)

de Quervain’s (granulomatous thyroiditis)

lymphocytic thyroiditis

Inflammation or infection of the thyroid gland stimulates release of pre-formed thyroid hormone. Neck pain, can follow a viral URI

Clinical Presentation

As noted in Table 1 and the vignettes above, patients can present with a variety of symptoms. Only Graves’ disease patients get the “thyroid stare” seen in Figure 1. On physical exam, look for tachycardia, atrial fibrillation, warm, moist skin, and a fine tremor as clues to let you know your patient may have a thyroid problem. The neck exam may reveal a diffusely enlarged gland with a thyroid bruit (as in Graves’ disease), or one or more nodules. The thyroid gland may be tender to the touch in subacute thyroiditis.

"The Thyroid Stare"

Workup and Diagnosis

Laboratory workup is essential to determining the cause of your patient’s thyroid disease.  An elevated T4 and a low level of TSH (except in rare TSH-secreting pituitary tumors) are good steps in the right direction. The USMLE will have normal values available for your reference. A thyroid scan helps evaluate how the thyroid gland takes up iodine, and will help you tell Graves’ disease (diffusely hot gland) from a toxic adenoma (single hot spot), and from toxic multinodular goiter (many spots of varying uptake amounts). Assaying for thyroid-stimulating antibodies or antithyroid peroxidase antibodies can also be helpful. Fine needle biopsies are infrequently used, since most tumors are hypofunctional.

Management

Therapy for hyperthyroidism depends on the etiology. Most cases of inflammatory hyperthyroidism will resolve spontaneously, or will respond to a brief course of anti-inflammatory therapy (NSAIDS, or corticosteroid). Obviously, a pituitary adenoma needs neurosurgical intervention.

Graves’ patients have three viable options, depending on their situation: medications, radioablation, and surgical removal. All will leave them hypothyroid, following successful treatment. Medications include propylthiouracil and methimazole — but watch out for side effects, including hepatitis and agranulocytosis. Radioablation involves uptake of radioactive iodine, and should not be considered in pregnant women (due to the risk of fetal hypothyroidism). Surgery is recommended for young patients, pregnant patients, and those with respiratory difficulty, or with a multinodular goiter. There is a risk of removing the small, nearby parathyroid glands, so watch for postoperative hypercalcemia.

In addition to these treatments, many patients respond well to symptomatic treatment with beta blockers (for tachycardia, arrhythmias). Propanolol is a good initial treatment for thyroid storm (an extreme state of hyperthyroidism associated with atrial fibrillation, shock, mental status changes, etc).

One more note:

Watch out for the patient with who is not symptomatic for hyperthyroidism, but has a low (or undetectable) TSH and a normal T4 and T3: this patient has subclinical hyperthyroidism, and is at risk for developing atrial fibrillation and bone density abnormalities. Management is controversial, and not likely to be the subject of questions on the USMLE/COMLEX exams.

References:

  1. Brochert, A. Crush Step 2, The Ultimate Step 2 Review. 2003. Hanley & Belfus, Philadelphia, PA.
  2. Young, V. Blueprints Medicine: Fourth edition. 2007. Lippincott Williams & Wilkins. Philadelphia, PA.
  3. http://www.ophthalmic.hyperguides.com/default.asp?section=body.asp
  4. http://www.dpcweb.com/medical/thyroid/thyroid_function.html
  5. http://www.aafp.org/afp/20020201/431.html
 

A USMLE/COMLEX Overview by Michael Lloyd, MD

Any half-decent pediatrician could generate a list a mile long for the causes of pediatric abdominal pain. Having so many possible etiologies can be daunting, and the writers of USMLE Step 1 and Step 2 exams and COMLEX Level 1 and Level 2 exams are banking on your anxiety over this endless list, making you feel like every question will be similar to the one below:

1-  A child has abdominal pain. Your most likely treatment is:

A)  Open laparotomy

B)  A popsicle for rehydration

C)  A pat on the back

D)  Convince the parents that a transfusion is necessary, despite their religious beliefs.

In fact, such questions wouldn’t be very productive on the USMLE/COMLEX; and in reality, the test writers will give you a few characteristics in each question, which will point you in the right direction. A close look at the age, gender, quality, location, associated symptoms and timing of the pain should assist you in making the diagnosis with confidence. For example, look at this USMLE question:

2-  A 5-week-old male infant develops nonbilious projectile vomiting, and you palpate an olive-shaped, nontender mass in the upper middle abdominal quadrant. There is an associated hypokalemic hypochloremic metabolic alkalosis, and dehydration. What is the likely diagnosis and appropriate initial management?

A)  Gastroenteritis, intravenous antibiotics

B)  Hirschprung’s disease, obtain radiographs and surgical consultation

C)  Choanal atresia, pass a nasogastric tube

D)  Pyloric stenosis, intravenous fluids and electrolytes followed by surgical consultation

As you see in the question above, you need to know some of the distinguishing features of each disease so you can tell them apart. There are few causes of projectile nonbilious vomiting, and only one of them is associated with an olive-shaped mass in the epigastrum. At this point in the question, the writers have already given you all you need to make the diagnosis — now it’s up to you to start fluid resuscitation, and call the surgeon.

A systematic approach to abdominal pain in the pediatric patient will help you in your quest to make the correct diagnosis. It will also help you avoid missing less common — and possibly fatal — disorders.

On the USMLE Step 1 and Step 2, or the COMLEX Level 1 and Level 2, when you are presented with a question describing a pediatric patient with abdominal pain, look for the distinguishing features, and see which ones fit best with the various categories of disease listed below. Each category is followed by a short list of disorders, with a brief description of some characteristic features. The purpose of this list is to provide a framework for you to think about abdominal pain. Use it to guide further studies into each of the listed disorders below.

INFECTIOUS

  • Gastroenteritis – one of the most common causes of abdominal pain, nausea, vomiting, and sometimes diarrhea. Rotavirus and Norwalk          virus are the most common viral etiologies, and are commonly passed via daycare facilities.
  • Food poisoning – with toxins from clostridium, bacillus, salmonella species, and staph aureus, is likely if others who ate the same food are                    similarly affected.
  • Viral hepatitis, pancreatitis

INFLAMMATORY

  • Inflammatory bowel disease – children can present with Crohn’s disease and Ulcerative Colitis (UC). Look for erythema nodosum, iridocyclitis, and sclerosing cholangitis. X-rays may show skip lesions (indicating Crohn’s) or toxic megacolon (indicating UC).
  • Necrotizing enterocolitis – common in preterm infants, presents with bilious vomiting, fevers, and rectal bleeding. CT scans show air in the gut wall. Treat with IV antibiotics, IV fluid resuscitation, and surgical intervention, as needed.
  • Henoch-Schonlein Purpura – GI bleeding, hematuria, palpable purpural rash on lower extremities and buttocks. Look for a history of recent URTI.
  • Mesenteric lymphadenitis – enlarged lymph nodes following a viral infection.
  • Vasculitides (PAN, Kawasaki disease, SLE, JRA) – most have many systemic manifestations. Look for coronary artery aneurysms in Kawasaki disease, and treat with aspirin. Still’s disease is the systemic form of juvenile rheumatoid arthritis, and presents with high fevers and a salmon-colored, evanescent rash. SLE should present with joint disease, a malar rash, serositis, and psychiatric complaints, as well.

MALIGNANCY

  • Tumors of solid organs – such as neuroblastoma, Wilm’s tumor (associated with Von Willibrands’ disease, aniridia and hemihypertophy), and      retroperitoneal rhabdomyoscarcoma.
  • Leukemia – may also have bone pain, malaise, petechial rash, and hepatosplenomegaly.
  • Lymphoma – especially Burkitt’s lymphoma, Hodgkin lymphoma, and anaplastic large cell lymphoma.

DEVELOPMENTAL

  • Pyloric stenosis – as described above, within the first two months, commonly in males. Nonbilious vomiting, olive-shaped epigastric mass, sucussion splash on abdominal exam, hypokalemic, hypochloremic metabolic alkalosis and deyhdration. Surgical treatment.
  • Intestinal atresia – presents within the first week of life with bilious vomiting and a double bubble sign on KUB.
  • TE fistula – early presentation of choking during feedings and food regurgitation. You can’t pass an NG tube – surgical intervention.
  • Hirschprung’s disease – can present any time within the first year, with feculent vomiting. There is a lack of ganglia seen on colonic biopsy.
  • Gastroschisis – anterior abdominal defect present at birth. Off the midline, with small bowel exposed; low incidence of associated abnormalities.
  • Omphalocele – anterior abdominal defect present at birth that is midline through a defective umbilical ring. Other abdominal organs may be contained within the hernia sac; many associated anomalies.
  • Intussuseption – telescoping of the colon onto itself; presents in young childhood with bilious vomiting, colicky abdominal pain, and currant-jelly stools. Palpable mass on abdominal exam. Barium enema is diagnostic and therapeutic.
  • Meckel’s diverticulum – presence of ectopic gastric tissue; usually within two feet of the ileocolic junction, has two layers of tissue, presents within two years of life, 2% of the population affected. Technetium “Meckel’s” scan to diagnose; surgical removal is curative.
  • Midgut volvulus – sudden onset of pain and bilious vomiting, due to malrotation of abdominal organs around the ligament of Trietz. Upper GI series helpful in diagnosis, and surgery can be curative.

METABOLIC

  • Inborn errors of metabolism – check urine and serum amino acids, and look for syndromic features; there may be a history of seizures or mental retardation; can present at any time during childhood.
  • Diabetic ketoacidosis – history of polyuria, polydipsia, vomiting. Ketones in the urine and an anion-gap acidosis. Treat with volume replacement and insulin.
  • Lactase deficiency – bloating, cramping, diarrhea, and vomiting after ingestion of meals containing lactose – can run in families. Treat with avoidance of dairy products.

PSYCHIATRIC

  • Depression – can be common in adolescent range. Look for anhedonia, poor concentration, and changed behaviors. Treat with therapy or medications as needed.
  • Somatoform disorders – various presentations involving the transfer of anxiety, anger, or other feeling to a physical symptom. Treat with counseling and family therapy.
  • Functional abdominal pain – a wastebasket diagnosis. You should rule out common and dangerous etiologies of abdominal pain first.

APPENDICITIS

  • The most common surgical cause of abdominal pain. RLQ pain, nausea, vomiting, rebound tenderness at McBurney’s point. Negative “hamburger sign” (offer the patient a hamburger – if they want to eat it, they don’t have appendicitis). Surgical treatment.

TRAUMA

  • Treat according to Pediatric acute life support guidelines. Use imaging (Focused Abdominal Ultrasound for Trauma, CT abdomen, neck and pelvis), and physical exam findings to diagnose. Surgery is often indicated.

REPRODUCTIVE-RELATED

  • Pelvic inflammatory disease – find in sexually active young women; positive chandelier’s sign, look for cervicitis and tests to show Chlamydia or gonococcal infection. Treat with antibiotics (ceftriaxone, doxycycline). Admit if systemically ill.
  • Testicular torsion – sudden abdominal/groin pain and vomiting in a young man. Swollen, erythematous scrotum on exam. Ultrasound to distinguish from epididymitis. Prompt surgical intervention is crucial. Fixation of the other testis is often performed during surgical intervention.
  • Ectopic pregnancy – positive β-HCG, ultrasound to reveal tubal or mesenteric gestational sac. Watch for rupture with associated hemorrhage and shock. Surgical treatment is often required.
  • Ovarian cysts – intermittent pain, with cysts seen on pelvic ultrasound. Conservative management is usually adequate.

UROLOGIC

  • Nephrolithiasis – presents with flank pain that radiates to the groin. Diagnosis can be made with urinalysis or various imaging studies. Treat with pain management or lithotripsy.
  • Polycystic kidney disease – usually asymptomatic, but ultrasound reveals multiple large cystic spaces in each kidney. Can be autosomal dominant or autosomal recessive. Conservative management is most common.

References:

1.  Brochert, A. Crush Step 2, The Ultimate Step 2 Review. 2003. Hanley & Belfus, Philadelphia, PA.

2.  Marino, B. Blueprints Pediatrics: Fourth edition. 2007. Lippincott Williams & Wilkins. Philadelphia, PA.