Although all of the above answers can cause peripheral vertigo, the correct answer in the above vignette after eliminating the other choices is choice B, Meniere’s Disease. The classic presentation for this illness consists of episodic vertigo and hearing loss that tends to fluctuate (and often is low or high frequency loss), as well as tinnitus. Some data has also shown it can be more common in people who have a history of migraines.

Choice A (BPPV) would also cause episodic periods of vertigo, but it is not linked to any hearing loss. These periods of vertigo are also most commonly 10-20 seconds long, rarely as long as a minute. In addition, the provider performed a Dix-Hallpike Maneuver during the visit, which with BPPV would likely cause some fatigable nystagmus, of which the patient had none.
Choices C and D are diseases involving inflammation of the vestibular portion of eighth cranial nerve thought to be associated with viral illnesses. These would also cause dizziness, but in this case the symptoms of vertigo would be more constant instead of fluctuating. In addition, acoustic neuritis is not associated with hearing loss until the inflammation involves the bony labyrinth of the inner ear, when it becomes labyrinthitis.

Choice E is unlikely as well, since the patient underwent an MRI which did not show any sign of mass suggesting an acoustic neuroma. Also, the hearing loss associated with an acoustic neuroma is irreversible and thus would not be coming and going as the above patient described.

Discussion:
Meniere’s Disease is a frustrating and complicated diagnosis, and while it may lack life-threatening qualities it can absolutely have a devastating effect on the patient’s quality of life. The typical patient presents with Meniere’s Disease in the 3rd-5th decade of life but people of all ages can be affected.1 Children with Meniere’s Disease will often have congenital problems, specifically malformations of the cochlea and vestibular organs of the inner ear. It affects as many as 150 out of 100,000 people in the general population, although it is difficult to definitively measure due to nonstandard and obscure reporting of cases.

The inner ear is made up of not only the cochlea, which is responsible for interpreting air waves conducted through the external and middle ear and transmitting them to the brain, but also the vestibular organs which include the semicircular canals, the utricle, and the saccule. All of these together make up the bony labyrinth of the inner ear. These structures contain endolymph within them which facilitates the various vestibular and auditory functions in order to properly hear and balance. It has been demonstrated that patients who suffer from Meniere’s Disease display “endolymphatic hydrops,” or excess fluid build-up within these inner ear structures.1 Unfortunately the cause of this imbalance is not clearly understood. It is possible that there is some sort of blockage of the endolymphatic duct or narrowing of the vestibular aqueduct that causes the back-up, and other various immunologic, genetic, viral, and vascular etiologies hypotheses exist as well.1
The clinical triad associated with Meniere’s Disease is episodic vertigo, sensorineural hearing loss, and tinnitus.1 It is very important to distinguish true vertigo from other types of “dizziness” during a patient interview. When a patient reports dizziness, the true complaint can range from vertigo (a spinning sensation with central and peripheral causes), presyncope (associated with vascular causes), disequilibrium (musculoskeletal, neuropathies, or cerebellar causes), or even vague/nonspecific causes (associated with psychiatric disorders/anxiety).2 While aural fullness, nausea, and tinnitus may or may not be present with this condition, it is necessary for diagnosis to have episodic vertigo as well as hearing loss.1 This defines the condition from various differentials, such as BPPV which would have similar episodic vertigo without any hearing loss, and vestibular neuritis/labyrinthitis, which would have more continuous symptoms of vertigo. The hearing loss experienced usually comes and goes and is primarily a lower frequency loss that progresses over the course of the disease. The intensity of hearing loss and vertigo vary from patient to patient.

It is almost impossible to measure the amount of endolymph within the inner ear without risking permanent damage, and imaging leaves a lot to be desired. Often it can only be truly assessed post-mortem, which is little help to the patient. Therefore, the diagnosis of Meniere’s Disease is almost always a clinical one. Often the first diagnostic test that will be done is an audiogram to assess the patient’s level of hearing loss and differentiate between a sensorineural or conductive hearing loss. Again, this is commonly a low frequency loss, or occasionally high frequency with normal mid-frequency hearing.1 Additionally vestibular testing can be done, such as an electronystagmogram. This test measures inner ear response to caloric stimulation and various movements which can provide insight towards the source of the vertigo. The ear is irrigated with warm air followed by cold while the patient lies down, and as the temperature change triggers movement of fluid in the semicircular canals, nystagmic movement of the eyes follows.3 A normal test would result in equal nystagmic response in each eye. With Meniere’s, often times the affected side will display a lesser response to testing, while in contrast some sort of inner ear lesion or irritation may result in an increased response.3 Labs and imaging studies such as an MRI for diagnosis of Meniere’s Disease are primarily used to rule out other possible causes, most importantly brain lesions that can cause similar symptoms of vertigo. Some controversial tests attempt to assess endolymphatic hydrops such as glycerine, urea, and sorbitol stress tests but are not widely used due to their low specificity and sensitivity.1

The treatment for Meniere’s usually doesn’t aim to cure the disease but rather to control the chronic symptoms associated with it. Hearing loss connected with this diagnosis does not have any treatment. However, the vertigo spells have several options to reduce severity and frequency. First line treatments for vertigo spells are anti-emetics (Zofran or Promethazine) to control nausea, and motion sickness medications (Valium or Antivert) to reduce spinning sensations. The most non-invasive option for long-term control is strict diet control. Often Meniere’s patients will be affected by certain dietary triggers, and it usually helps to restrict salt consumption as well as caffeine, alcohol, and nicotine, which reduce blood flow to the inner ear and also cause imbalances to fluid and electrolytes.1 Diuretics such as acetazolamide may also reduce the frequency of vertigo attacks.4 There are also several more “destructive” options to control refractory vertigo. These consist of injecting dexamethasone, a steroid, or gentamicin, an ototoxic antibiotic, into the inner ear. Gentamicin can be especially damaging to the cochlea and semicircular canals but may alleviate some chronic symptoms of Meniere’s. Most times it has the added complication of further reducing hearing ability. The most invasive options include surgical routes of endolymphatic sac procedures, vestibular nerve sections, or even a total labyrinthectomy, which would only be performed if the hearing loss in the affected ear was already completely lost.

References:

1. Moskowitz HS et al. Meniere Disease. UpToDate. https://www.uptodate.com/contents/meniere-disease?source=search_result&search=meniere%20disease&selectedTitle=1~29#H4. Updated 3/22/16. Accessed 4/22/17.
2. Branch WT et al. Approach to the patient with dizziness. UpToDate. https://www.uptodate.com/contents/approach-to-the-patient-with-dizziness?source=search_result&search=disequilibrium&selectedTitle=1~79#H7. Updated 10/20/14. Accessed 4/22/17.
3. Li JC. Meniere Disease (Idiopathic Endolymphatic Hydrops) Workup. UpToDate. http://emedicine.medscape.com/article/1159069-workup#c1. Updated 11/29/16. Accessed 4/22/17.
4. Mayo Clinic Staff. Meniere’s Disease – Treatment and drugs. Mayo Clinic. http://www.mayoclinic.org/diseases-conditions/menieres-disease/basics/treatment/con-20028251. Published 11/26/15. Accessed 4/22/17.

The answer is A. Exudative pleural effusions form due to an underlying disease. This patient presented with shortness of breath, which is one of the most common symptoms patients present with when they have a pleural effusion. This patient also has newly diagnosed breast cancer, which was indicated by her breast mass stated in the question and supported by her chest x-ray. Effusions can oftentimes occur in patients who have malignancies because of changes in the permeability of pleural membranes secondary to malignancy (10). A diagnosis of an exudative effusion can then be made confirmed if because the pleural fluid LDH is greater than two thirds of the upper limit of normal for serum LDH (8).

Choice B is incorrect because transudative pleural effusions are usually caused by disease processes such as congestive heart failure, cirrhosis or pneumonia renal failure (9). Evaluation of the pleural fluid is used to confirm the diagnosis.

Choice C is incorrect because patients with TB have a productive cough of bloody sputum and chest pain. Although she has a cough, it is non-productive and she denies chest pain. The classic chest x-ray finding of tuberculosis is an upper lobe cavitary opacification. Another common symptom is fever, but she is afebrile because her vitals show her temperature at 98°F (7).

Choice D is incorrect because, like TB, patients with bacterial pneumonia usually have a fever, productive cough, and chest pain. This patient denies these symptoms. Her chest x-ray showed blunting of the left costophrenic angle and a hyperdense area in the left apical lung. These findings suggest a cancerous mass and a pleural effusion in the base of the left lung, and not a lobar infiltrate commonly seen on a chest x-ray that is positive for bacterial pneumonia (6)

References
1. Pleural Effusion Clinical Presentation: History, Physical Examination. Emedicinemedscapecom. 2017. Available at: http://emedicine.medscape.com/article/299959-clinical#showall. Accessed April 24, 2017.
2. What Are Pleural Effusions?. WebMD. 2017. Available at: http://www.webmd.com/lung/pleural-effusion-symptoms-causes-treatments#1-4. Accessed April 24, 2017.
3. Management of the Patient With a Malignant Pleural Effusion. Medscape. 2017. Available at: http://www.medscape.com/viewarticle/736939_3. Accessed April 24, 2017.
4. Management of Malignant Pleural Effusions. Uptodatecom. 2017. Available at: https://www.uptodate.com/contents/management-of-malignant-pleural-effusions. Accessed April 24, 2017.
5. Pleural Effusion: Background, Anatomy, Etiology. Emedicinemedscapecom. 2017. Available at: http://emedicine.medscape.com/article/299959-overview#a6. Accessed April 24, 2017.
6. Pneumonia-Exams and Tests. WebMD. 2017. Available at: http://www.webmd.com/lung/tc/pneumonia-exams-and-tests. Accessed April 24, 2017.
7. CDC | TB | Basic TB Facts | Signs & Symptoms. Cdcgov. 2017. Available at: https://www.cdc.gov/tb/topic/basics/signsandsymptoms.htm. Accessed April 24, 2017.
8. Light J. Diagnostic Approach to Pleural Effusion in Adults – American Family Physician. Aafporg. 2017. Available at: http://www.aafp.org/afp/2006/0401/p1211.html. Accessed April 24, 2017.
9. Light’s Criteria: Light’s Criteria. Emedicinemedscapecom. 2017. Available at: http://emedicine.medscape.com/article/2172232-overview#a1. Accessed April 24, 2017.
10. Fluid Around the Lungs or Malignant Pleural Effusion. CancerNet. 2017. Available at: http://www.cancer.net/navigating-cancer-care/side-effects/fluid-around-lungs-or-malignant-pleural-effusion. Accessed April 24, 2017.

Answer is D. Psoriasis is a chronic, multisystem inflammatory, immune-mediated disorder. Plaque psoriasis of the skin is the most common type of psoriasis. It is caused by epidermal proliferation that results in a thickened stratum corneum layer of the skin. Research has shown that uncontrolled T-cell activation and cytokine release causes immature skin cells to mature rapidly- up to 7 times the normal rate resulting in epidermal thickening (James 2011). The etiology of psoriasis is still unknown, although many factors can increase a person’s risk of developing the disorder. Evidence has shown a genetic disposition in which 30-50% of patients with the disease have a positive family history of psoriasis. Many factors can trigger psoriasis including stress, infections, obesity, skin trauma (known as Koebner phenomenon), and certain medications, such as Lithium, NSAIDs, and beta blockers James 2011). Psoriasis can affect all ages, but most commonly it occurs in the 3rd decade of life. The onset can be gradual or sudden. The hallmark sign of psoriasis is a well-demarcated erythematous plaque with silvery scale. The psoriatic plaques most often affect the extensor surfaces of the body, and most commonly occur on the elbows, knees, and scalp. Symptoms include pruritus, pain, and arthralgia (Papadakis 2016).

There are many types of psoriasis including psoriatic arthritis, in which 30% of people suffering from psoriasis develop joint pain and deformation. Nail psoriasis affects the nail bed causing nail pitting and discoloration. Guttate psoriasis usually follows a strep infection and is characterized by multiple small plaques peppered throughout the body. Pustular psoriasis is characterized by small pustules on the hands and feet (Williams 2014). Palmar/ Plantar psoriasis symptoms are confined to the hands and feet. Inverse psoriasis symptoms occur mainly in skin folds and are often mistaken for a tinea infection (James 2011).

Treatment for Psoriasis varies depending on the severity, location, symptoms, and patient preference. There is no cure for psoriasis. The goal of treatment is to control the symptoms to a manageable level for the patient. Treatments range from topical to systemic (James 2011). Topical treatment includes topic steroids, which decrease inflammation. Calcipotriene (Dovonex) is a vitamin D analog that binds to keratinocyte receptors, which alters keratinocyte proliferation. Tazarotene (Tazorac) is a topical retinoid that alters epidermal proliferation and decreases scale. Systemic therapy includes Methotrexate, which is an immunosuppressive drug that inhibits cellular proliferation. Hepatotoxicity is a common side effect, along with GI symptoms. Newer medications such as biologics, like Enbrel and Humira are weekly injectables that suppress inflammation through T cell interference. Increased risk of infection and lymphoma are adverse effects to be considered with these drugs (James 2011).

In question 1 the patient is 29-years old (psoriasis onset is usually in the 3rd decade of life) with a recent history of bipolar disorder. Lithium is a common medication for bipolar disorder and has been a known trigger of psoriasis. Although it is not stated in the vignette, the provider should ask what medications the patient is currently taking for bipolar disorder. The patient’s physical exam shows erythematous plaques with silvery scale, which is the hallmark sign of psoriasis. The plaques are located on the patient’s scalp and extensor surfaces, which is also a classic finding of psoriasis.
Lichen Planus is an idiopathic cell-mediated immune response commonly associated Hepatitis C. It is characterized by pruritic flat-topped violaceous papules (James 2011). Fine white streaks, called Wickman’s striae, are commonly found within the lesions. Lichen Planus can affect the scalp, nails, genitals, and mucous membranes. It most commonly occurs in the flexor creases, unlike psoriasis, which normally affects the extensor surfaces. The oral lesions associated with Lichen Planus are described as lacy white patches found on the buccal mucosa. Treatment includes topical steroids, systemic steroids for severe cases, and phototherapy. The rash can resolve within 8-12 months with treatment (Williams 2014).

Atopic dermatitis, or eczema, is an altered immune reaction (increased IgE production) that usually has a childhood onset, unlike psoriasis. Patients with atopic dermatitis usually display the atopic triad of symptoms including eczema, allergies, and asthma. It is characterized by chronic tiny erythematous, edematous, pruritic, ill-defined blisters, that can produce scale (similar to psoriasis) from the “itch-scratch cycle” (Williams 2014). The symptoms usually occur in the flexor creases, unlike psoriasis. Treatment usually consists of moisturizers, topical steroids, systemic steroids for severe acute flares, and Calcineurin Inhibitors (Protopic), which can trigger an immune response to potentially clear up the eczema. Antihistamines can be utilized for pruritus (Papadakis 2016).
Lichen Simplex Chronicus is characterized by skin thickening in patients secondary to repetitive rubbing and/ or scratching. It is caused by the chronic itch scratch cycle suffered by patients with conditions such as atopic dermatitis. The affected areas are described as scaly, well-demarcated, rough papules, with exaggerated skin lines. Treatment usually consists of potent topical steroids to decrease inflammation, antihistamines for pruritus relief, and behavior modification (Papadakis 2016).

References:
1. James W, Elston D, Berger T, Andrews G. Andrews’ Diseases Of The Skin. [London]: Saunders/ Elsevier; 2011.
2. Papadakis MA, McPhee SJ. Current medical diagnosis and treatment 2016. New York: McGraw-Hill Education; 2016.
3. Williams D. PANCE Prep Pearls. Lexington, KY: CreateSpace; 2014.

Answer B. This patient’s urine calcium and creatinine levels should be measured. His laboratory values are consistent with hypercalcemia, and her parathyroid hormone level is toward the upper end of the normal range. In his age group and with a family member with a suspicious history, it is important to distinguish between primary hyperparathyroidism and familial Hypocalciuric hypercalcemia (FHH). The distinction between primary hyperparathyroidism and FHH can be made by a 24-hour urine collection for calcium and creatinine, which will establish the amount of kidney calcium excretion and will allow evaluation of the calcium-creatinine ratio. Total urine calcium of less than 200 mg/24 h and a calcium-creatinine ratio less than 0.01 are highly suggestive of FHH. Bone densitometry is not indicated in this age group in the absence of fragility fractures or other risk factors such as long-term high-dose glucocorticoid use or primary hyperparathyroidism. A parathyroid sestamibi scan is a very useful nuclear imaging study for localization of adenomas in patients with primary hyperparathyroidism or parathyroid cancer. However, primary hyperparathyroidism has not been confirmed in this patient with suspicion for FHH, making this study premature. The need for surgical treatment in this patient has also not been established. Therefore, surgical referral for parathyroidectomy would not be appropriate.

References:
1. Mcmurtry CT, Schranck FW, Walkenhorst DA, et al. Significant developmental elevation in serum parathyroid hormone levels in a large kindred with familial benign (hypocalciuric) hypercalcemia. The American Journal of Medicine. 1992;93(3):247-258. doi:10.1016/0002-9343(92)90229-5.
2. Marx SJ, Attie MF, Levine MA, Spiegel AM, Downs RW, Lasker RD. The Hypocalciuric or Benign Variant of Familial Hypercalcemia: Clinical and Biochemical Features in Fifteen Kindreds. Medicine. 1981;60(6):397-412. doi:10.1097/00005792-198111000-00002.
3. Shinall M, Dahir K, Broome J. Differentiating Familial Hypocalciuric Hypercalcemia from Primary Hyperparathyroidism. Endocrine Practice. 2013;19(4):697-702. doi:10.4158/ep12284.ra.
4. Law WM. Familial Benign Hypercalcemia (Hypocalciuric Hypercalcemia). Annals of Internal Medicine. 1985;102(4):511. doi:10.7326/0003-4819-102-4-511.
5. Marx SJ. Familial Hypocalciuric Hypercalcemia: Recognition Among Patients Referred After Unsuccessful Parathyroid Exploration. Annals of Internal Medicine. 1980;92(3):351. doi:10.7326/0003-4819-92-3-351.

Correct Answer: B – subdural hematoma. A is incorrect because epidural hematomas do not cross suture lines and moreover epidural hematomas are “convex” (lens) in shape. C is incorrect because intraparenchymal hematomas do not follow suture lines, as IPHs occur in the brain tissue. Finally, answer D is incorrect since the patient did not complain of sudden onset of headache and subarachnoid hemorrhages normally present with sudden onset of “thunder-clap”, “worst headache of my life”. B is the most likely diagnosis because the CT scan showed a hematoma crossing suture lines and the hematoma was “crescent”-shaped, which is indicative of a subdural hematoma. However, in chronic SDH, the shape can change to biconvex.

Subdural hematoma

The brain is enclosed within a closed and fixed space and is surrounded by cerebrospinal fluid (CSF), which acts as a shock absorbent. The brain is surrounded by 3 layers: the pia is the innermost layer, the subarachnoid is the middle layer, and the dura is the outermost fibrous membrane – the extremely tough layer of the three meningeal layers. The skull encompasses all of these layers. Brains have fixed volume, in which 80% is brain tissue, 10% is CSF, and 10% is blood (Kaye et al). Increases in intracranial pressure (ICP) is fatal for brain function. Brain hemorrhage is the most likely cause of increased intracranial pressure (Kaye et al). There are two type of brain hemorrhage: intracranial, which includes intraventricular and intraparenchymal hemorrhages, and extracranial, which includes subarachnoid, subdural, and epidural hemorrhages.

In subdural hematomas (SDH), bleeding occurs in-between the dura and subarachnoid membrane. SDH is further divided into subtypes based on time of injury. Acute is 1 week from injury. SDHs can also be mixed in nature, as acute injuries can turn into chronic SDHs. Acute SDHs are the most common type of traumatic intracranial hemorrhage. Acute SDHs can also present with other brain injuries such as subarachnoid hemorrhage, diffuse axonal injury, and so on. 72% of SDH occur following fall or assaults and 24% are associated with MVA. Chronic SDHs more commonly occur in the elderly population and are the most common type of treatable cause of dementia. Chronic SDHs are more common in males and the incidence increases with age. SDHs can also present in children. Bilateral presentation of SDHs in children is associated with underlying physiology, while interhemispheric presentation is associated with child abuse, also known as shaken baby syndrome (Meagher et al).

Subacute
As the clot ages and protein degradation occurs, the density starts to drop. At some point between 3 and 21 days (typically 10-14 days), the density will drop to ~ 30 HU and become isodense to the adjacent cortex, making identification potentially tricky, especially if subdural collections are bilateral 4. Contrast-enhanced CT is often useful in this instance if MRI is unavailable. The key to identification is visualising a number of indirect signs, including:
• CSF filled sulci do not reach the skull but rather fade out into the subdural
• mass effect including sulcal effacement (distortion) and midline shift
• apparent thickening of the cortex

Chronic
By definition it is at least 3 weeks old,
The subdural collection becomes hypodense and can reach ~0HU and be isodense to CSF, and mimic subdural hygromas.
Shape from crescentic may change to biconvex.

Acute on chronic
Acute on chronic subdural hematomas refers to a second episode of acute haemorrhage into a pre-existing chronic subdural hematoma. It typically appears as a hypodense collection with a haematocrit level (located posteriorly). A similar appearance can be seen in patients with clotting disorders or on anticoagulants 4.

While trauma is the most common cause of SDH, atrophy, ruptured aneurysms, tumors, alcoholism, anticoagulants, seizure disorders, intracranial hypotension, CSF shunts, and intravenous drug use are also other etiologies. Many of these etiologies can lead to either acute or chronic SDHs. Though, atrophy of the brain is more commonly associated with chronic SDH, which is also associated with alcoholism.

The prognosis of acute SDHs is variable with mortality ranging between 36-79%of cases. Only 40% of acute SDHs results in favorable outcomes. The reason for this fatal prognosis is due to its anatomy and pathophysiology. As veins exit the pia matter, they bridge into the dura membrane. Those bridging veins drain into the cerebral sinus and then drain into jugular vein. SDHs occur when those bridging veins tear. In the setting of acute trauma, the space between the dura and arachnoid fills up with blood very rapidly, which causes increased ICP and compression of the cortex.

The rapid increase in ICP is the most common reason for mortality. It has been shown that acceleration injuries from assaults and falls cause more damage than energy absorption trauma as seen in dashboard injuries from MVAs. When initial insult leads to increases in ICP, the compression of arteries causes infarct in various parts of the brain. It also results in other brain injuries, like cerebral edema, which further increases ICP. If it is not treated, it can cause the brain to herniate downward. Downward herniation of the brain causes compression of major blood supplies, such as the Circle of Willis. Herniation of the brain cuts off blood supply to the brainstem, which results in death. Acute SDHs can also change the brain’s metabolism and cause secondary brain injury, according to Meagher. Tissue under the SDH does not respond to oxygen metabolism and switches to anaerobic metabolism, which increases the levels of lactate, which is toxic for the brain.

In the setting of chronic SDHs, cerebral atrophy increases the tension on bridging veins and even with minor trauma those veins can rupture. Sometimes acute small SDHs fail to dissolve and form membranes surrounding it, which can turn into chronic expansion. An imbalance in the osmotic gradient can also cause fluid to shift into the subdural space. However, often, the cause of chronic SDHs is idiopathic.

Most of the patients, about 50%, with acute SDHs are comatose due to other brain injuries. Neurologically intact will progressively deteriorate with time. Patients with chronic SDHs present with various neurological problems, such as insidious onset of headaches, light-headedness, apathy, dementia, hemiparesis, and ataxia, like in the case of NM. Symptoms related to increased ICP like nausea, vomiting, and changes in vision can also be present. Seizures can also be seen in patients with SDHs (McBride et al).

Due to the high fatality rates, patients who present following traumatic injuries, with sudden onset of symptoms described above, or status post falls warrant a head CT scan. Head CT scans of acute SDHs show hyperdensed crescent lesions that cross the suture lines. Due to the nature of injuries, acute SDH may also present with IPHs and SAHs. Midline shifts can also be seen on head CT. Alternatively, head CTs of chronic SDHs is hypodense due to degraded blood and the liquefaction effect. But the shape of chronic SDHs is also crescent, as seen in acute. Brain MRIs are more sensitive in picking up small SDHs, however the availability and time-consuming process limit its use in the evaluation of traumatic SDHs (McBride et al).

Acute (symptomatic) SDHs are medical emergencies, hence it requires surgical innervations. Such injuries need to be evaluated by neurosurgeons. According to McBride et al, surgical decision is made based on the GCS score, head CT, clot thickness, midline shift, neurologic exam, and comorbidities. If the patient is stable and the head CT shows a bleeding area

References
1. Kaye AH. Brain Tumors: An Encyclopedic Approach, 2nd, Churchill Livingstone, New York 2001. p.205
2. McBride W, Biller J. Subdural hematoma in adults: Prognosis and management. Uptodate. https://www.uptodate.com/contents/subdural-hematoma-in-adults-prognosis-and-management?source=search_result&search=subdural%20hematoma&selectedTitle=1~150#H1
3. Meagher RJ, Young VM. Subdural Hematoma. Subdural Hematoma. http://emedicine.medscape.com/article/1137207-overview#a3. Published January 6, 2017. Accessed May 21, 2017.
4. Victor M, Ropper A. Craniocerebral trauma. In: Adams and Victor’s Principles of Neurology, 7th ed, Victor M, Ropper A. (Eds), McGraw-Hill, New York 2001. p.925

Anemia, defined by decreased hemoglobin or red blood cells, can occur due to many etiologies. G6PD deficiency anemia is caused by a genetic mutation leading to quantitative and qualitative changes in the enzyme, which has a protective function against oxidation. This disorder may be asymptomatic with incidentally found intermittent anemia. If a patient presents clinically it is most commonly with jaundice in a newborn and episodes of hemolytic anemia later in life due to illness or exposure to foods and medications that increase oxidative stress. Most notably are fava beans and sulfa drugs (Bactrim).2 Peripheral smear is a helpful diagnostic tool that can be used in determining the cause of anemia. G6PD deficiency anemia is caused by acute hemolysis when red blood cells are exposed to oxidative stress which appear as bite cells with Heinz bodies (B) on peripheral smear. Microcytic hypochromic red blood cells (A) are characteristic of iron deficiency anemia which would not present with intermittent decrease in hemoglobin. All children born in the United States are screened for sickle cell anemia at birth, suggested by thin, elongated sickle shaped cells and Howell-Jolly Bodies (C & D) on peripheral smear. It is also unlikely that a peripheral smear and CBC would be normal at any point in a one year old patient. Megaloblastic RBCs and hyper-segmented neutrophils (E) are present in macrocytic anemias commonly caused by B12 deficiency and is associated with an insidious onset of gastrointestinal and neurologic symptoms.

References
1. Luzzatto L. Glucose 6-phosphate dehydrogenase deficiency: from genotype to phenotype. Haematologica/the hematology journal. 2006; 91(10):1303-1306.
2. Luzzatto L, Nannelli C, & Notaro R. Glucose-6-phosphate dehydrogenase deficiency. Hematology/oncology clinics of North America. 2016;30(2):373-393.
3. Luzzatto L, Seneca E. G6PD deficiency: a classic example of pharmacogenetics with on-going clinical implications. British Journal of Haematology. 2013;164(4):469-480. doi:10.1111/bjh.12665.

Popliteal artery aneurysm (PAA) is an abnormal dilation of the arterial wall that can cause life and limb threatening complications if the aneurysm burst or clots. Thromboembolic events are the most frequent complication (occurring in 42-77% of patients), which can lead to amputation in up to 20% of patients. PAA’s account for 70-80% of all peripheral aneurysms and occur bilaterally in 50% of patients. Although the exact etiology is unknown, the presences of arteriosclerosis is thought be the most significant contributor. Hypertension also adds mechanical stresses to the artery which can play a role in aneurysm formation. Popliteal aneurysms will naturally expand over time, on average about 10% a year. Large PAA’s expand faster than smaller ones. PAA’s are often asymptomatic but as they enlarge can cause pain, swelling, pulsation, and distal edema and venous thrombosis (if the aneurysm compresses the popliteal vein). The rate of complications is greatest with PAA’s greater than 2 cm and increases with time (24% rate in 1 year, 35% rate in 4 years, and 74% in at 5 years). PAA’s that are symptomatic and greater than 2 cm should be treated surgically. Anticoagulants have no effect on the growth of PAA’s and ischemia complications cannot be prevented by observation. Current surgical options include open vs. endovascular repair, with similar success rates between the two. 1, 2

References
1. Ghotbi R, Sotiriou A, Schönhofer S, Zikos D, Schips K, Westermeier W. Stent-Graft Placement in Popliteal Artery Aneurysms: Midterm Results. Vascular Disease Management. E-edition. 9/5/08
2. Dawson I, Brand R. Popliteal artery aneruysm. Longer term follow-up of aneurysmal disease and results of surgical treatment. Journal of Vascular Surgery 1991. Volume 13 (3). 398-407.

Accessory ossicles are boney structures (normal congenital variant) that separate from adjacent bone and are usually embedded within tendons. Over 40 different types of accessory ossicles have been known to occur in the foot. The most common types of ossicles in the foot include an os trigonum, os peroneum, and accessory navicular. It is important to have a general knowledge of the common accessory ossicles of the foot as they are often found incidentally on x-ray and can be confused with avulsion fractures. Accessory ossicles can also cause painful syndromes that are usually associated with tendinitis of the surrounding tendon. 1

Os peroneum is an ossicle located just lateral to the cuboid and is embedded within the peroneus brevis tendon. Several sources of os peroneum pathology can cause pain in the peroneus brevis tendon including fracture of the ossicle, rupture or tearing of the tendon around the ossicle, and stenosing tenosynovitis. Os peroneum syndrome generally causes symptoms of pain over the lateral cuboid and pain during palpation of the ossicle. Treatment of os peroneum syndrome is the same as for peroneal tendinitis, which includes a period of NSAIDS and immobilization. 1,2
Os trigonum is located posterior to the talus and may be a source of pain due to posterior ankle impingement. Os versalianum is located proximal to the base of the 5th metatarsal and is often confused with an avulsion fracture of the tuberosity. Os naviculare, or accessory navicular, is a large accessory ossicle adjacent to the medial side of the navicular. 1

References
1. Nwawka OK, Hayashi D, Diaz LE, Goud AR, Arndt WF, Roemer FW, Malguria N, Guermazi A. Sesamoids and accessory ossicles of the foot: anatomical variability and related pathology. Insights Imaging. 2013 Oct; 4(5): 581–593.
2. Heckman DS, Reddy S, Pedowitz D, Wapner KL, Parekh SG. Current Concepts Review: Operative Treatment for Peroneal Tendon Disorders. JBJS 2008; 90: 404-418