2nd-degree AV block

Symptoms include:

• an aching, painful, red eye
• blurred or cloudy vision,
• a small pupil,
• an iris that may have a slightly different color
• sensitivity to light (photophobia),
• floaters (dots that move across the field of vision), and
• headaches.

These symptoms may develop gradually over hours or days. They may be acute or chronic and are associated with a laundry list of syndromes and disorders, including:

• AIDS
• Ankylosing spondylitis
• Behcet syndrome
• CMV retinitis
• Herpes zoster infection
• Histoplasmosis
• Injury
• Kawasaki disease
• Psoriasis
• Reactive arthritis
• Rheumatoid arthritis
• Sarcoidosis
• Syphilis
• Toxoplasmosis
• Tuberculosis
• Ulcerative colitis

• Normal or decreased visual acuity
• Pain, photophobia, blurring of vision:
  • Usually acute
• Anterior uveitis (~80% of patients with uveitis):
  • Generally acute in onset
  • Deep eye pain
  • Photophobia (consensual)
• Intermediate and posterior uveitis:
  • Unresolving floaters
  • Generally insidious in onset
  • More commonly bilateral

Slit-lamp exam and indirect ophthalmoscopy are necessary for precise diagnosis:

• Anterior uveitis (~80% of patients with uveitis):
  • Conjunctival vessel dilation
  • Perilimbal (circumcorneal) dilation of episcleral and scleral vessels (ciliary flush)
  • Small pupillary size of affected eye
  • Hypopyon or hyphema (white or red blood cells pooled in the anterior chamber)
  • Frequently unilateral (95% of HLA-B27–associated cases)
  • Bilateral involvement and systemic symptoms (fever, fatigue, abdominal pain) may be associated with interstitial nephritis.
  • Systemic disease is most likely to be associated with anterior uveitis.

  Family history is important as well. Inquire if there is a family history of uveitis or other symptoms in family members that might suggest associated diseases, such as a spondyloarthropathy or other human leukocyte antigen (HLA)-B27 processes.

  Inquire in particular about the following symptoms:

  • Dull, aching eye pain occurs and may worsen when one touches the eye through the eyelid. Pain may be referred to the temple or periorbital region.
  • Redness with no mucopurulent discharge is seen.
  • Most cases are unilateral.

–However, cholecystectomy for asymptomatic gallstones may be indicated under certain circumstances:

1. Patients with large gallstones greater than 2 cm in diameter
2. Patients with nonfunctional or calcified (porcelain) gallbladder observed on imaging studies and who are at high risk of gallbladder carcinoma
3. Patients with spinal cord injuries or sensory neuropathies affecting the abdomen nPatients with sickle cell anemia in whom the distinction between painful crisis and cholecystitis may be difficult

Epididymitis

Epididymitisis the most common local complication of C. trachomatis infection in young males.

Signs and symptoms of epididymitis include:

• Fever
• Unilateral scrotal pain
• Swelling
• Tenderness
• Evidence of urethritis on Gram stain
• Epididymal tenderness or mass on exam

Up to 70% of sexually transmitted cases are due to Chlamydia trachomatis. Some sexually transmitted cases are due to gonorrhea. Some cases have both pathogens.

-

Bacterial etiology varies by sexual behavior and age.

• young heterosexuals (usually due to chlamydia or gonorrhea) 
• men who have sex with men (can also be caused by enteric organisms or gonorrhea) 
• non-sexually transmitted epididymitis in older men (more often due to E. coli or pseudomonas)

epididymitis

Fatigue is a common and bothersome symptoms as MS progresses. It is often worse in the late afternoon

Treatment

Acute treatment includes IV prednisolone for 4 – 6 days follwed by steroid taper (oral prednisone okay now, but NOT first!!).  Outpatient therapy usually includes Interferon beta-1a (Avonex, Rebif).

Grading of murmurs

Maneuvers

• Inhalation (I for rIght) will increase the amount of blood filling into the right ventricle, thereby prolonging ejection time. This will affect the closure of the pulmonary valve. This finding, also called Carvallo’s Maneuver, has been found by studies to have a sensitivity of 100% and a specificity of 80% to 88% in detecting murmurs originating in the right heart.   Specifically positive Carvallo’s sign describes the increase in intensity of a tricuspid regurgitation murmur with inspiration
• squatting
• valsalva maneuver. One study found the valsalva maneuver to have a sensitivity of 65%, specificity of 96% in detecting Hypertrophic obstructive cardiomyopathy (HOCM). Both standing and Valsalva maneuver will decrease venous return and subsequently decrease left ventricular filling, resulting in an increase in the loudness of the murmur of hypertrophic cardiomyopathy, since outflow obstruction is increased by decreasing preload. Alternatively squattingincreases venous return and thus decreases the murmur. Maximum handgrip exercise also results in a decreased loudness of the murmur
• hand grip
• positioning of the patient. ie. positioning patients in the left lateral positionwill allow a murmur in the mitral valve area to be more pronounced.

• Risk (R) – Increase in serum creatinine level X 1.5 or decrease in GFR by 25%, or urine output <0.5 mL/kg/h for 6 hours
• Injury (I) – Increase in serum creatinine level X 2.0 or decrease in GFR by 50%, or urine output <0.5 mL/kg/h for 12 hours
• Failure (F) – Increase in serum creatinine level X 3.0, decrease in GFR by 75%, or serum creatinine level >4 mg/dL with acute increase of >0.5 mg/dL; urine output <0.3 mL/kg/h for 24 hours, or anuria for 12 hours
• Loss (L) – Persistent renal failure, complete loss of kidney function >4 weeks
• End-stage kidney disease (E) – Loss of kidney function >3 months

Use of the Modification of Diet in Renal Disease (MDRD) equation to estimate the patients GFR/1.73 mm based upon: serum creatinine level, age, gender, and race, NOT weight!

Three Causes of Acute Renal Failure:

1. Prerenal failure is defined by conditions with normal tubular and glomerular function; GFR is depressed by compromised renal perfusion.
2. Intrinsic renal failure includes diseases of the kidney itself, predominantly affecting the glomerulus or tubule, which are associated with release of renal afferent vasoconstrictors. Ischemic renal injury is the most common cause of intrinsic renal failure. 
3. Post-obstructive renal failure initially causes an increase in tubular pressure, decreasing the filtration driving force (BPH, stones, etc.).

Urine output:

Changes in urine output generally are poorly correlated with changes in GFR. Approximately 50-60% of all causes of acute renal failure are nonoliguric. 

• Anuria (<100 mL/d) – Urinary tract or renal artery obstruction, rapidly progressive glomerulonephritis.
• Oliguria (100-400 mL/d) – Prerenal failure, hepatorenal syndrome
• Nonoliguria (>400 mL/d) – Acute interstitial nephritis, acute glomerulonephritis, partial obstructive nephropathy, nephrotoxic and ischemic tubular necrosis, radiocontrast-induced acute renal failure, and rhabdomyolysis.

Changes in serum creatinine level correlate with changes in GFR by the following relationships:

If creatinine 1 mg/dL is baseline for a given patient with normal GFR:

• Creatinine 2 mg/dL – 50% reduction in GFR
• Creatinine 4 mg/dL – 70–85% reduction in GFR
• Creatinine 8 mg/dL – 90–95% reduction in GFR

Renal ultrasonography is the test of choice for urologic imaging in the setting of acute renal failure.

The prevalence of chronic insomnia is 1.2-2.0 times greater in women than men.

Chronic insomnia increases in frequency with age and is more common in the elderly. This is presumed due to greater psychosocial stressors, losses, and medical illnesses. Recent epidemiologic data indicate that the prevalence of chronic insomnia increases form 25% in the adult population to 50% in the elderly population.

Sleep history

Determining the timing of insomnia, the patient’s sleep habits and symptoms of sleep disorders associated with insomnia is important.

• Timing of insomnia: Patients should be asked about any difficulty falling asleep, frequent or early morning awakening, problems in sleep onset, and whether they feel sleepy when getting into bed.
• Sleep schedule: Patients must be asked what time they go to bed and rise from bed in the morning. Determine whether the sleep schedule is consistent and if the schedule has changed recently.
• Sleep environment: Patients should be asked about temperature, bed comfort, noise, and light levels. Ask whether the patient sleeps better in his or her own bed or in a chair or a foreign environment (like a hotel).
• Sleep habits: Patients with insomnia often have poor sleep hygiene. They should be asked about activities prior to bedtime (ie, relaxation or work), whether they read or watch TV in bed, and whether the TV or light is kept on during the night. Also, ask patients what they do if unable to fall asleep and whether they fall asleep after waking up in the middle of the night. Ask patients about daytime naps and whether they exercise and the time of exercise.
• Patients should be asked about symptoms of other sleep disorders such as obstructive sleep apnea (eg, snoring, witnessed apneas, gasping) and restless legs syndrome/periodic limb movement disorder (ie, restless feeling in legs on lying down, which improves with movement; rhythmic kicking during the night; sheets in disarray in the morning).
• Daytime effects: Patients should experience daytime effects if they truly are not sleeping at night. In fact, if a patient is having no daytime effects, he or she is probably getting adequate sleep and the complaint of insomnia is truly subjective.

Primary sleep disorders causing insomnia

• Restless legs syndrome is a sleep disorder characterized by the following:
  • An urge to move the legs, usually accompanied by uncomfortable and unpleasant physical sensations in the legs.
  • The urge to move or the unpleasant sensations begin or worsen during periods of rest or inactivity such as lying or sitting.
  • The urge to move or the unpleasant sensations are partially or totally relieved by moving, such as walking or stretching, at least as long as the activity continues.
  • The urge to move or the unpleasant sensations are worse or only occur in the evening or the night.
• Obstructive sleep apnea/hypopnea syndrome:A minority of patients complain of insomnia rather than hypersomnolence. They frequently complain of multiple awakenings or sleep-maintenance difficulties. They may also have nocturia causing frequent nocturnal awakenings.
• Circadian rhythm disorders

Treatment 

The treatment of primary insomnia begins with education about the sleep problem and appropriate sleep hygiene measures.  Before instituting therapy, most patients are asked to maintain a sleep diary for 2-4 weeks.  This gives the physician a clearer picture of the degree of sleep disturbance and allows him or her to better tailor the treatment.

Use a gamma aminobutyric acid agonist (exp.: estazolam, temazepam, zolpidem) to treat an acute or short term pure insomnia.

Do NOT use antidepressants (amitrptyline) unless depressed.

Do NOT use antihitamines (benadryl) unless they have allergy symptoms.

Vegan's don't eat any of these!!

The main syndrome of vitamin B₁₂ deficiency is Biermer’s disease (pernicious anemia). It is characterized by a triad of symptoms:

1. Anemia (megaloblastic anemia)
2. Gastrointestinal symptoms
3. Neurological symptoms

Each of those symptoms can occur either alone or along with others. The neurological complex, defined as myelosis funicularis, consists of the following symptoms:

1. Impaired perception of deep touch, pressure and vibration, abolishment of sense of touch, very annoying and persistent paresthesias
2. Ataxia of dorsal cord type
3. Decrease or abolishment of deep muscle-tendon reflexes
4. Pathological reflexes — Babinski, Rossolimo and others, also severe paresis

Vitamin B₁₂ deficiency can potentially cause severe and irreversible damage, especially to the brain and nervous system. These symptoms of neuronal damage may not reverse after correction of hematological abnormalities, and the chance of complete reversal decreases with the length of time the neurological symptoms have been present.

Causes:

1. Inadequate dietary intake of vitamin B₁₂.
2. Intrinsic factor deficiency
3. Malabsorption or maldigestion syndrome
4. Achlorhydria (including that artificially induced by drugs such as proton pump inhibitors)
5. Short bowel syndrome
6. Celiac disease
7. Bariatric surgical procedures
8. Bacterial overgrowth
9. Metformin
10. Chronic alcohol abuse
11. Nitrous oxide abuse

Three of the following 10 criteria must be present to classify a vasculitis as Polyarteritis Nodosa:

• Weight loss of 4 kg or more
• Livedo reticularis
• Testicular pain/tenderness
• Myalgia or leg weakness/tenderness
• Mononeuropathy or polyneuropathy
• Diastolic blood pressure greater than 90 mm/Hg
• Elevated BUN and creatinine levels
• Infection with hepatitis B virus (HBV)
• Abnormality on arteriography
• Biopsy of small- or medium-sized artery containing polymorphonuclear neutrophils

Treatment

• Steroids (prednisone 60 mg/day) and/or Cyclophosphamide.
• If Hep B induced: Prednisone with Lamivudine and plasmapheresis.

Psoriatic arthritis can develop at any age, however on average it tends to appear about 10 years after the first signs of psoriasis. For the majority of people this is between the ages of 30 and 50, but it can also affect children. Men and women are equally affected by this condition. In about one in seven cases the arthritis symptoms may occur before any skin involvement.

The classic findings of Psoriatic Arthritis in the hands are soft tissue swelling, joint space loss, bilateral asymmetric distribution, bone proliferation, distal tuft resorption, and marginal erosions. The soft tissue swelling is very severe, giving fingers a “sausage-like” appearance. A classic feature of PA is the “pencil-in-cup” or “cup-in-saucer” appearance in which the erosions become so severe that the proximal bone has been narrowed and appears to be resting in the shallow depression of the distal bone.

Treatment:

The underlying process in psoriatic arthritis is inflammation, therefore treatments are directed at reducing and controlling inflammation. NSAIDs are usually the first line medication.  Second line treatments with immunosuppressants such as methotrexate or leflunomide. An advantage of immunosuppressive treatment is that it also treats the psoriasis in addition to the arthropathy.

The hands, arms and/or legs are the usual site(s) of innoculation.

Sporotrichosis is a subacute or chronic infection caused by the soil fungus Sporothrix schenckii.  The characteristic infection involves suppurating subcutaneous nodules that progress proximally along lymphatic channels (lymphocutaneous sporotrichosis).

• The primary lesion develops at the site of cutaneous inoculation, typically in the distal upper extremities. Patients with these forms are typically afebrile and not systemically ill. The lesions usually cause minimal pain. Many affected patients have received one or more courses of antibacterial therapy without benefit.
• Splinters, thorns, or woody fragments of plants usually provide the penetrating trauma that introduces the fungal conidia into the human host; however, contact with any plant or plant product (eg, sphagnum peat moss, mulch, hay, timber) that causes minor skin trauma may initiate infection.
• Activities associated with the acquisition of sporotrichosis include gardening, landscaping, farming, berry-picking, horticulture, and carpentry.
• Cutaneous and lymphocutaneous sporotrichosis have historically been treated with saturated solution of potassium iodide. Although relatively inexpensive, it is poorly tolerated by many patients because of frequent adverse effects.   Currently, they are treated with oral itraconazole 200 mg/d until 2-4 weeks after all lesions have resolved, usually for a total of 3-6 months!!

Conidiophores and Conidia of the fungus Sporothrix schenckii

The principal causes of splenic vein thrombosis include pancreatitis, pancreatic pseudocyst, neoplasm and trauma. In most patients, there is splenomegaly.

Diagnosis is made by selective splenic arteriography.

In the presence of varices only, the recommended treatment is by splenectomy. Otherwise, no therapy is required.

Stage I sarcoidosis

Sarcoidosis is a multisystem inflammatory disease of unknown etiology that predominantly affects the lungs and intrathoracic lymph nodes. Sarcoidosis is manifested by the presence of noncaseating granulomas in affected organ tissues.

The male-to-female ratio is approximately 2:1 while the incidence peaks in persons aged 25-35 years. A second peak occurs for women aged 45-65 years.

The presentation depends on the extent and severity of the organ involved.

• Approximately 5% of cases are asymptomatic and incidentally detected by CXR.
• Systemic complaints, fever, anorexia, and arthralgias occur in 45% of cases.
• Pulmonary, dyspnea on exertion, cough, chest pain, and hemoptysis (rare) occur in 50% of cases.
• Löfgren syndrome: Symptoms consist of fever, bilateral hilar lymphadenopathy (BHL), and polyarthralgias.

Chest X-ray changes are divided into four stages:

• Stage 1 bihilar lymphadenopathy
• Stage 2 bihilar lymphadenopathy and reticulonodular infiltrates
• Stage 3 bilateral pulmonary infiltrates
• Stage 4 fibrocystic sarcoidosis typically with upward hilar retraction, cystic & bullous changes

Sarcoidosis is a systemic disease that can affect any organ. Common symptoms are vague, such as fatigue unchanged by sleep, lack of energy, weight loss, aches and pains, arthritis, dry eyes, swelling of the knees, blurry vision, shortness of breath, a dry hacking cough or skin lesions. Sarcoidosis and cancer may mimic one another, making the distinction difficult. The cutaneous symptoms vary, and range from rashes and noduli (small bumps) to erythema nodosum or lupus pernio. It is often asymptomatic.

Most patients (>75%) require only symptomatic therapy (nonsteroidal anti-inflammatory drugs). Approximately 10% of patients need treatment for extrapulmonary disease, while 15% of patients require treatment for persistent pulmonary disease.

• Scarlet fever generally has a 1- to 4-day incubation period.
• Emergence of the illness tends to be abrupt, usually heralded by sudden onset of fever associated with sore throat, headache, nausea, vomiting, abdominal pain, myalgias, and malaise.
• The characteristic rash appears 12-48 hours after onset of fever.
• In the untreated patient, fever peaks by the second day (temperature as high as 103-104°F) and gradually returns to normal in 5-7 days.
• Fever abates within 12-24 hours after initiation of antibiotic therapy.
• Recent history of exposure to another individual with a “strep” infection may aid in the diagnosis.

Physical

• Exudative tonsillitis preceding scarlet fever often is accompanied by erythematous oral mucous membranes, along with petechiae and punctate red macules on the hard and soft palate and uvula (ie, Forchheimer spots).
• On day 1 or 2, a white coating covers the dorsum of the tongue with reddened papillae projecting through, giving rise to the white strawberry tongue.

Treatment

The mainstay of treatment includes penicillin and erythromycin.

Tetracyclines and sulfonamides should not be used.

Exercise-induced asthma is an asthma variant defined as a condition in which exercise or vigorous physical activity triggers acute bronchospasm in persons with heightened airway reactivity. It is observed primarily in persons who have asthma (exercise-induced bronchospasm in asthmatic persons) but can also be found in patients with normal resting spirometry findings with atopy, allergic rhinitis, or cystic fibrosis and even in healthy persons, many of whom are elite athletes (exercise-induced bronchospasm in athletes). Exercise-induced bronchospasm is often a neglected diagnosis, and the underlying asthma may be silent in as many as 50% of patients, except during exercise.

Asthma symptoms may include the following:

• Cough, worse particularly at night
• Wheezing
• Shortness of breath
• Chest tightness
• Sputum production
• Decreased exercise tolerance

Precipitating or aggravating factors for asthma include the following:

• Environmental allergen exposure (dust mites, pet dander, pollens)
• Occupation
• Medications
• Exercise
• Viral upper respiratory tract infections
• Strong emotional expression
• Menstrual cycles
• Airborne dusts or chemicals

General asthma physical findings

• Evidence of respiratory distress manifests as increased respiratory rate, increased heart rate, diaphoresis, and use of accessory muscles of respiration.
• Marked weight loss or severe wasting may indicate severe emphysema.

• Pulsus paradoxus: This is an exaggerated fall in systolic blood pressure during inspiration and may occur during an acute asthma exacerbation.
• Depressed sensorium: This finding suggests a more severe asthma exacerbation with impending respiratory failure.
• Chest examination
  • End-expiratory wheezing or a prolonged expiratory phase is found most commonly, although inspiratory wheezing can be heard.
  • Diminished breath sounds and chest hyperinflation (especially in children) may be observed during acute asthma exacerbations.
  • The presence of inspiratory wheezing or stridor may prompt an evaluation for an upper airway obstruction such as vocal cord dysfunction, vocal cord paralysis, thyroid enlargement, or a soft tissue mass (eg, malignant tumor).
• Upper airway
  • Look for evidence of erythematous or boggy turbinates or the presence of polyps from sinusitis, allergic rhinitis, or upper respiratory tract infection.
  • Any type of nasal obstruction may result in worsening of asthma or symptoms of exercise-induced bronchospasm.
• Skin: Observe for the presence of atopic dermatitis, eczema, or other manifestations of allergic skin conditions.

Classification of asthma severity and treatment options are as follows:

• Step 1 – Intermittent asthma
  • Intermittent symptoms occurring less than once a week
  • Brief exacerbations
  • Nocturnal symptoms occurring less than twice a month
  • Asymptomatic with normal lung function between exacerbations
  • No daily medication needed
  • FEV₁ or PEF rate greater than 80%, with less than 20% variability
• Step 2 – Mild persistent asthma
  • Symptoms occurring more than once a week but less than once a day
  • Exacerbations affect activity and sleep
  • Nocturnal symptoms occurring more than twice a month
  • FEV₁ or PEF rate greater than 80% predicted, with variability of 20-30%
• Step 3 – Moderate persistent asthma
  • Daily symptoms
  • Exacerbations affect activity and sleep
  • Nocturnal symptoms occurring more than once a week
  • FEV₁ or PEF rate 60-80% of predicted, with variability greater than 30%
• Step 4 – Severe persistent asthma
  • Continuous symptoms
  • Frequent exacerbations
  • Frequent nocturnal asthma symptoms
  • Physical activities limited by asthma symptoms
  • FEV₁ or PEF rate less than 60%, with variability greater than 30%

The most common symptoms include nosebleeds, skin bruises, and hematomas. Prolonged bleeding from trivial wounds, oral cavity bleeding, and excessive menstrual bleeding are common. Gastrointestinal bleeding is rare.

• A common but nonspecific symptom is easy bruising.
• Prolonged bleeding after minor trauma to skin or mucous membranes is characteristic.
• Severe hemorrhage after major surgery is less common, but delayed bleeding may occur up to several weeks after surgery.
• Heavy bleeding is common after tooth extraction or other oral surgery, such as tonsillectomy and adenoidectomy.
• Menorrhagia is a common presenting complaint in women.
• Bleeding symptoms are often exacerbated by the ingestion of aspirin and are ameliorated by the use of oral contraceptives.

The deficiency of von Willabrand factor leads to poor platelet adhesion which can be confirmed by a Ristocetin Aggregation Assay.  Normal platelets aggregate with ristocetin, in this disorder, they don’t.  PT is usually normal, and the PTT is mildly elevated.  Bleeding time is variable.

For mild bleeding problems use dDAVP (stimulates factor 8).  Platelet transfusions are also an option.  Avoid cryoprecipitate and fresh frozen plasma because of the potential transmission of viral disease.

Hyperparathyroidism is often incidentally discovered during routine laboratory testing when hypercalcemia is noted. In 80% of patients with hyperparathyroidism, the symptoms of hypercalcemia are mild or are not notable at the time of discovery. Management of these patients is not clear-cut because routine laboratory tests have not been shown to assist in predicting development of overt manifestations of the disease. Conversely, patients with overtly symptomatic hyperparathyroidism (eg, those with urinary tract stones, bone pain, cognitive abnormalities) and those with marked hypercalcemia (calcium levels >10.2 mg/dL) should be referred for consideration for parathyroidectomy.

Although some controversy surrounds indications for surgery, current National Institutes of Health guidelines for curative, surgical intervention indications are listed below (Approximately 20% of patients with hyperparathyroid disease meet the following criteria):

• Patients with overt clinical manifestations of disease
• Age younger than 50 years
• Serum calcium concentration more than 1 mg/dL above upper limit of reference range
• Urinary calcium excretion greater than 400 mg/d
• Low or declining bone mineral density
• Uncertain prospect for successful medical monitoring
• Patient requests surgery
• Poor or uncertain follow-up
• Coexistent disease that may confound or contribute to disease progression
• Reduction in creatinine clearance of 30% or more
• Reduction of bone mineral density greater than 2.5 standard deviations below the reference range for bone density in terms of age, gender, and race (T score <2.5)

Most patients tolerate mild hyperparathyroidism well without operative treatment. Roughly 75% of asymptomatic patients who present with mild hypercalcemia did well over a 10-year period without significant loss of cortical bone, progressive hypercalcemia, or excessive urinary calcium excretion.

• Sudden Severe Headache (occasionally there we be a sentinal headache at the initiation of the bleed)
• Nausea and/or vomiting
• Symptoms of meningeal irritation (ie: neck stiffness, low back pain, bilateral leg pain): These are seen in more than 75% of cases of subarachnoid hemorrhage
• Photophobia and visual changes
• Loss of consciousness: About half of patients experience this at the time of bleeding onset.

Laboratory studies include the following:

• Complete blood count
• PT, PTT
• Troponin I (cTnI): cTnI measurement is important in patients with subarachnoid hemorrhage even in those without underlying cardiac conditions.

Electrocardiogram

• About 20% of subarachnoid hemorrhage cases have myocardial ischemia from the increased circulation of catecholamines. Typical results are nonspecific ST-and T-wave changes, prolonged QRS segments, U waves, and increased QT intervals.
• ECG changes reflect myocardial ischemia or infarction and should be treated in the usual manner. Suspicion of subarachnoid hemorrhage is a contraindication to thrombolytic and anticoagulant therapy.

• Lumbar puncture (LP) is indicated if the patient has possible subarachnoid hemorrhage and negative CT scan findings.  Perform CT scan prior to LP to exclude any significant intracranial mass effect or obvious intracranial bleed.  LP may be negative less than 2 hours after the bleed; LP is most sensitive at 12 hours after symptom onset.   Red blood cells (RBCs) in the cerebrospinal fluid (CSF) remain consistently elevated in 2 sequential tubes or punctures in SAH, whereas the number of RBCs in technically traumatic punctures decreases over time.
• Xanthochromia (yellow-to-pink CSF supernatant) usually is seen by 12 hours after the onset of bleeding.

Treatment:

• Endotracheal intubation of obtunded patients protects from aspiration caused by depressed airway protective reflexes.
• Intubate to hyperventilate patients with signs of herniation.
• The goals of therapy are to reduce pain, edema, and severity of cerebral vasospasm, relieve nausea and vomiting, and prevent convulsions.

• Episodic spasms that can mimic cardiac pain due to disorganized peristalsis. 
• There is elevated lower esophageal sphincter (LES) pressure.
• There is dysfunctional LES relaxation.

The symptoms show difficulty swallowing solids and liquids with associated regurgutation while supine or asleep. The symptoms develop insidiously over months to years.

The "bird's beak" of Achalasia

Diagnosis: Barium swallow showing the classic “Bird’s Beak” distally.  An EGD may be done to rule out other etiologies, and esophageal manometry can confirm the abnormal peristalsis.

Treatment is with pneumatic dilation or myotomy.

• The classic clinical presentation of Boerhaave syndrome usually consists of repeated episodes of retching and vomiting, typically in a middle-aged man with recent excessive dietary and alcohol intake.
• These repeated episodes of retching and vomiting are followed by a sudden onset of severe chest pain in the lower thorax and the upper abdomen. The pain may radiate to the back or to the left shoulder. Swallowing often aggravates the pain.
• Typically, hematemesis is not seen after esophageal rupture, which helps distinguish it from the more common Mallory-Weiss tear.
• Swallowing may precipitate coughing because of communication between the esophagus and the pleural cavity.
• Atypical clinical features sometimes delay a prompt diagnosis and appropriate intervention. This may result in an increase in morbidity and mortality.
• Shortness of breath is a common complaint and is due to pleuritic pain or pleural effusion.

Many patients present with a pleural effusion.

• Thoracentesis with examination of the pleural fluid can aid in diagnosis.
• Undigested food particles and gastric juices usually are found.

An Esophagram helps confirm the diagnosis.

• It typically shows extravasation of contrast into the pleural cavity.
• It the length of the perforation and its location
• Initially, use Gastrografin, NOT Barium!!

Endoscopy is not commonly used in this diagnosis.

Treatment:

• Intravenous fluids.
• Antibiotics
• Nasogastric suction should be applied.
• Keep the patient NPO.
• A tube thoracostomy or formal thoracotomy is vital.

Symptoms and infection may resolve without therapy, although treatment can be provided with praziquantel (20 mg/kg PO q8h for 1 d).

(1) compression or distortion of the spinal fluid spaces,

(2) displacement of the brain stem,

(3) compression of vessels producing ischemia or infarction, or

(4) compression and/or attenuation of nerves.

Unilateral hearing loss is overwhelmingly the most common symptom present at the time of diagnosis and is generally the symptom that leads to diagnosis. Assume that any unilateral sensorineural hearing loss is caused by an acoustic neuroma until proven otherwise. The tumor can produce hearing loss through at least 2 mechanisms, direct injury to the cochlear nerve or interruption of cochlear blood supply. Progressive injury to cochlear fibers probably accounts for slow progressive neurosensory hearing loss observed in a significant number of patients with acoustic neuromas. Sudden and fluctuating hearing losses are more easily explained on the basis of disruption of cochlear blood supply.

Hearing loss associated with acoustic neuroma can be sudden or fluctuating in 5-15% of patients. Such hearing loss may improve spontaneously or in response to steroid therapy. Consequently, a gadolinium enhanced MRI should be ordered in anyone with a sudden or fluctuating loss even if hearing returns to normal.

Treatment depends on multiple factors including the age and medical status of the patient, tumor size and location, hearing status, and patient preference. In older patients with small tumors, careful observation may be elected consisting of serial MRIs. In older patients with a growing tumor, radiosurgery may be an appropriate option. Young patients, large tumors (greater than 2.5 to 3 cm) and patients with small tumors and intact hearing may choose surgery.

Acoustic neuromas are managed in one of the following 3 ways: (1) surgical excision of the tumor, (2) arresting tumor growth using stereotactic radiation therapy, or (3) careful serial observation.

The nerve damage involves loss of retinal ganglion cells in a characteristic pattern. There are many different sub-types of glaucoma but they can all be considered a type of optic neuropathy. Raised intraocular pressure is a significant risk factor for developing glaucoma (above 21 mmHg or 2.8 kPa).

One person may develop nerve damage at a relatively low pressure, while another person may have high eye pressure for years and yet never develop damage.

Untreated glaucoma leads to permanent damage of the optic nerve and resultant vision loss, which can progress to blindness.

Glaucoma can be divided roughly into two main categories, “open angle” and “closed angle” glaucoma. Closed angle glaucoma can appear suddenly and is often painful; visual loss can progress quickly but the discomfort often leads patients to seek medical attention before permanent damage occurs. Open angle, chronic glaucoma tends to progress at a slower rate and the patient may not notice that they have lost vision until the disease has progressed significantly.

Acute Closed angle glaucoma is an ocular emergency!!

The patient presents as an African American or Oriental with:

1. Severe eye pain (which could be mistaken for severe headache)
2. Nausea
3. Halos around lights

Cherry Red Spot

Painless loss of monocular vision is the usual presenting symptom of retinal artery occlusion. Ocular stroke commonly is caused by embolism of the retinal artery.

Retinal artery occlusion represents an ophthalmologic emergency, and delay in treatment may result in permanent loss of vision.

Immediate intervention improves chances of visual recovery, but, even then, prognosis is poor, with only 21-35% of eyes retaining useful vision.

An embolism, atherosclerotic changes, inflammatory endarteritis, angiospasm, or hydrostatic arterial occlusion may occlude the retinal artery.

The most common presenting complaint is an acute persistent painless loss of vision. In central artery occlusions, visual loss is central and dense. In branch artery occlusions, visual loss may go unnoticed if only a section of the peripheral visual field space is affected.

A history of hypertension or diabetes mellitus is elicited in 67% and 25% of patients with CRAO, respectively.

Query about any medical problems that could predispose patients to embolus formation (eg, atrial fibrillation, endocarditis, coagulopathies, atherosclerotic disease).

Prolonged direct pressure to the globe during drug-induced stupor or improper positioning during surgery also may lead to CRAO.

The cherry red spot and a ground-glass retina are the classic findings but may take hours to develop. The funduscopic findings typically resolve within days to weeks of the acute event, sometimes leaving a pale optic disc as the only physical finding.

Start timolol early, as this is readily available in most emergency departments. Acetazolamide and mannitol should also be used when CRAO is suspected because there are few downsides to starting these medications early.

In carbogen therapy (5% carbon dioxide, 95% oxygen), carbon dioxide dilates retinal arterioles, and oxygen increases oxygen delivery to ischemic tissues.

Thrombolytics may be useful if initiated within 4-6 hours of visual loss, but they may not be much help if the embolus is cholesterol, talc, or calcific.

Thrombolytics are introduced via the proximal ophthalmic artery, delivering increased concentrations directly to the retinal artery and minimizing systemic complications.

Hyperbaric oxygen (HBO) therapy may be beneficial if initiated within 2-12 hours of onset of symptoms. Institute treatment with other interventions first; transport to a chamber may usurp precious time. Results from noncontrolled studies have been mixed. A 2001 controlled study in Israel showed a benefit in the treatment group.  In this study, all patients were treated within 8 hours of symptom onset.

Treatment with IV thrombolytics as with cerebral infarction has been discussed but currently is not the standard of care.

It is therefore important that healthcare professionals remain current on commonly occurring organisms, vehicles, and symptoms associated with foodborne illness, given that the few cases they see may serve as sentinel signals for more widespread infection. Healthcare professionals also should be aware of unusual presentations, pathogens, and vehicles, especially against the backdrop of potential intentional contamination and adulteration. Healthcare professionals also should be aware of the effects of global commerce and the national and international movement of goods and people on old and new foodborne threats.

Recognizing and Diagnosing Foodborne Illness

The typical presentations associated with foodborne illness are usually gastrointestinal, such as vomiting, diarrhea, and abdominal pain. Upon suspicion of a foodborne illness, the following are important questions for a physician or other healthcare professional to ask the patient:

• What symptoms have you been experiencing?
• How long have you been experiencing these symptoms?
• Do any of your close friends or family members have similar symptoms?
• What is your occupation? Do any of your coworkers have similar symptoms?
• Have you recently been hospitalized? If so, what was the reason for your hospitalization?
• Are you currently using any medication?
• Are you sexually active?
• Have you ever resided in a nursing home residence?
• Are you in contact with children on a regular basis?
• Have you ingested any raw or poorly cooked food, unpasteurized milk or juices, home-canned goods, fresh produce, or soft cheeses made from unpasteurized milk?
• Have you recently traveled or taken a camping trip? Do you live on or have you visited a farm? Have you had contact with an animal or pet?
• Before you began experiencing your current symptoms, when was the last time you were sick? What was the associated or preceding illness? What medication did you use?

It is not recommended that the healthcare practitioner attempt to identify the source of the illness. This should be left to appropriate public health authorities. It is therefore essential that a good history is elicited and recorded to assist public health authorities if the need arises.

Gastrointestinal symptoms are the most common presentation for foodborne illness. Other symptoms that may be present in combination with gastrointestinal symptoms include fever, rash, myalgia, arthralgias, neurologic symptoms (paresthesias, weakness, and paralysis), and malaise. Strong clinical suspicion is needed because many of these symptoms resemble viral illness. Timing of symptoms, as well as specificity of symptoms, must be elicited from the patient to assist in differentiating one from the other. Clinicians should pay particular attention to known immunocompromised individuals as well as the very young and the elderly. Bloody diarrhea; weight loss; diarrhea leading to dehydration; fever; prolonged diarrhea (3 or more unformed stools per day, persisting for several days); neurologic involvement, such as paresthesias, motor weakness, or cranial nerve palsies; sudden onset of nausea, vomiting, or diarrhea; and severe abdominal pain are signs and symptoms occurring alone or in combination that require laboratory testing to provide important diagnostic clues.

The preceding signs and symptoms may also be associated with non-foodborne diseases, such as irritable bowel syndrome and inflammatory bowel disease. As such, a history and physical examination should be completed to elicit signs and symptoms that would support these diagnoses. In most cases, chronicity of signs and symptoms is enough to provide the needed clues, but laboratory testing may give further proof. Other diagnoses that should be considered include malabsorption, malignancy, gastrointestinal tract surgery or radiation, structural or functional gastrointestinal blockage for various reasons (eg, worm infestation), and genetic or diet-related metabolic deficiencies.

Healthcare providers should also pay special attention to patients with neurologic symptoms because this may raise suspicion for potential life-threatening diagnoses, such as ingestion of contaminated seafood, mushroom poisoning, chemical poisoning, and ingestion of certain toxins (eg, botulinum toxin, tetrodotoxin) and chemicals (eg, organophosphates).

Laboratory Tests and Etiologic Agents

The most important laboratory test is a specimen collection. This should be done as soon as possible, and the specimen should be properly preserved. The specimen or the results should be reported to the appropriate public health authorities in the jurisdiction because all cases seen should be considered as possible index cases of a potential outbreak.

Healthcare professionals are encouraged to understand routine specimen collection and testing procedures, as well as circumstances and procedures for making special test requests. Healthcare professionals are also advised to be aware of the limitations of the laboratories they use in the event that more complex or special tests are indicated. Again, early communication with public health authorities is required in such situations.

Microscopy is recommended on all collected samples. The presence of leucocytes on microscopy suggests diffuse colonic inflammation and invasive bacterial infection. Stool culture is recommended in this instance. Stool cultures are indicated in such circumstances as an immunocompromised patient, a febrile patient, or a patient with bloody diarrhea or persistent illness.

Most laboratories limit routine stool cultures to screening for Salmonella and Shigella species and Campylobacter jejuni or E coli. Because cultures for Vibrio and Yersinia species, E coli O157:H7, and Campylobacter species other than C jejuni or C coli require additional media or incubation conditions, advanced notification or communication with laboratory and infectious disease personnel is needed in these cases.

Stool examination for parasites is indicated for immunocompromised patients, patients with suggestive travel history, and patients with persistent illness or illness unresponsive to treatment. Stool examination for infection with Cryptosporidium species and Cyclospora cayetanensis will require special laboratory procedures, and this must be considered when specimens are being submitted in suspected cases.

Table. Etiologic Agents to Consider for Various Manifestations of Foodborne Illness

Non-inflammatory diarrhea is characterized by mucosal hypersecretion or decreased absorption without destruction and generally involves the small intestine. Some affected patients may be dehydrated because of severe watery diarrhea and may appear seriously ill. This is more common in the young and the elderly. Most patients experience minimal dehydration and appear mildly ill with scant physical findings. Illness typically occurs with abrupt onset and brief duration. Fever and systemic symptoms usually are absent (except for symptoms related directly to intestinal fluid loss).

Inflammatory diarrhea is characterized by mucosal invasion with resulting inflammation and is caused by invasive or cytotoxigenic microbial pathogens. The diarrheal illness usually involves the large intestine and may be associated with fever, abdominal pain and tenderness, headache, nausea, vomiting, malaise, and myalgia. Stools may be bloody and may contain many fecal leukocytes.

Treatment of Foodborne Illness

Most episodes of foodborne illness are characterized by gastrointestinal symptoms of acute gastritis. These episodes are typically self-limiting and require only fluid replacement and supportive care, such as medications to control symptoms. This is the management of choice in most instances after careful history, examination, and tests if needed. However, it is important to note that antidiarrheal agents are not recommended in children because they could lead to potential adverse health effects. Oral rehydration is indicated and appropriate for patients who can tolerate it, and the report provides information on drinking when thirsty and after episodes of fluid loss (diarrhea or vomiting). It is also important to drink appropriate liquids, avoiding fluids that may worsen symptoms, such as sodas, fruit juices, alcohol, and coffee. Intravenous therapy is indicated in more severe cases. When indicated, choice of antimicrobial use should be made on the basis of:

• Clinical signs and symptoms;
• Organism detected in clinical specimens;
• Antimicrobial susceptibility tests; and
• Appropriateness of treating with an antibiotic (some enteric bacterial infections are best not treated).

Antimicrobial use should be judicious in order to avoid development of microbial drug resistance. Therefore, healthcare professionals should be aware of the antimicrobial resistance patterns in the patient’s presenting community. Additionally, adequate follow-up with the patient must take place to confirm treatment effectiveness. Botulinum antitoxin can prevent progression of neurologic symptoms in early phase of illness; it is therefore indicated in such cases.

It is more commonly called adult-onset Still’s disease (AOSD).

Fewer than 1 out of 100,000 people develop adult Still’s disease each year. It affects women more often than men.

Still’s disease that occurs in children is called systemic juvenile idiopathic arthritis.

The cause of adult Still’s disease is unknown. No risk factors for the disease have been identified.

Almost all patients will have fever, joint pain, sore throat, and a rash.

• Joint pain, warmth, and swelling are common. Usually, several joints are involved at the same time. Often, patients have morning stiffness of joints that lasts for several hours.
• The fever usually comes on quickly once per day, most commonly in the afternoon or evening.
• The skin rash is typically salmon-pink colored and comes and goes with the fever.

NOTE: The rash and fever are always simultaneous in coming and going.

High serum FERRITIN levels (10 x normal) signify poor prognosis

Treatment is same as for Rheumatoid Arthritis.

Diagnosis of Antiphospholipid antibody syndrome requires the presence of at least 1 of the clinical criteria and laboratory criteria:

• Clinical criteria
  • Vascular thrombosis
  • Pregnancy morbidity
    • 3 or more unexplained consecutive miscarriages with anatomic, genetic, and hormonal causes excluded
    • 1 or more unexplained death(s) of a morphologically normal fetus at or after the 10 weeks’ gestation
    • 1 or more premature birth(s) of a morphologically normal neonate at or before 34 weeks’ gestation, associated with severe preeclampsia or severe placental insufficiency
• Laboratory criteria
  •  
    • Positive aPL (lupus anticoagulant test, moderate-to-high titer anticardiolipin antibodies, or moderate-to-high titer β₂-glycoprotein-I antibodies).

The presence of the antibodies alone in the absence of other clinical symptoms does not define the syndrome.

Antiphospholipid antibodies are found in fewer than 2% of apparently healthy pregnant women, in fewer than 20% of apparently healthy women with recurrent fetal loss, and in more than 33% of women with systemic lupus erythematosus.

A history of any of the following should raise the examiner’s suspicion for Antiphospholipid Syndrome:

• Thrombosis (eg, DVT/PE, MI, transient ischemic attack [TIA], or CVA, especially if recurrent, at an earlier age, or in the absence of other known risk factors)
• Miscarriage (especially late trimester or recurrent) or premature birth
• History of heart murmur or cardiac valvular vegetations
• History of hematologic abnormalities, such as thrombocytopenia or hemolytic anemia
• History of nephropathy
• Nonthrombotic neurologic symptoms, such as migraine headaches, chorea, seizures, transverse myelitis, Guillain-Barré syndrome, or dementia (rare)
• Unexplained adrenal insufficiency
• Avascular necrosis of bone in the absence of other risk factors
• Pulmonary hypertension

On exam, the following should raise suspicion:

• Livedo reticularis (see image below) 

  • Antiphospholipid syndrome. Livedo reticularis.

    

• Superficial thrombophlebitis
• Leg ulcers
• Painful purpura
• Splinter hemorrhages

On labs you should see:

• Normal to prolonged PT
• prolonged plasma clotting time
• prolonged PTT (that is not corrected by adding1:1 mix of normal plasma, which does work when theres a clotting factor deficency)
• Positive VDRL

Treat with life-long anticoagulation

Muscle strength and electromyographic findings are normal. 

It is closely linked to giant cell arteritis (temporal arteritis), but this is believed to be a separate disease process.

Females over 50 predominate this process.

The patient’s history may include the following features:

• Pain and stiffness in the proximal muscle groups that usually is symmetrical and worse in the morning
• Gel phenomenon (stiffness after prolonged inactivity)
• Fever (low grade)
• Weight loss
• Fatigue
• Depression
• No weakness
• Abrupt onset of symptoms

The signs and symptoms of polymyalgia rheumatica are nonspecific, and objective findings on physical examination often are lacking. If present, findings may include the following:

• No muscle atrophy
• Muscle tenderness
• Decreased active range of motion of joints secondary to pain

The goal of therapy is to suppress autoimmune activity with prednisone.

Remission of polymyalgia rheumatica seemed to be achieved with a 15 mg/d dose of prednisone for most patients. A slow tapering of the prednisone, less than 1 mg/month, was associated with fewer relapses.

Limited systemic sclerosis/scleroderma

Diffuse systemic sclerosis/scleroderma is rapidly progressing and affects a large area of the skin and one or more internal organs, frequently the kidneys, esophagus, heart and lungs.

Typical scleroderma is classically defined as symmetrical skin thickening, with about 90% of cases also presenting with Raynaud’s phenomenon, nail-fold capillary changes, and anti-nuclear antibodies.

Laboratory testing can show anti-topoisomerase antibodies (causing a diffuse systemic form), or anti-centromere antibodies (causing a limited systemic form, and the CREST syndrome). Other autoantibodies can be seen, such as anti-U3 or anti-RNA polymerase.

Severe complications from scleroderma include:

• Heart: Untreated high blood pressure strains the heart; irregular heart rhythm and enlargement of the heart lead to heart failure.
• Kidney: scleroderma renal crisis in which malignant hypertension develops and causes acute renal failure. This was once a common cause of death, but now is easy to treat with ACE inhibitors.
• Lung: Two-thirds of all patients suffer from respiratory problems such as shortness of breath, coughing, difficulty breathing, alveolitis, pneumonia, and cancer.
• Digestive: Esophagus damage can make it difficult to swallow food, and GERD is common. A sluggish intestine may cause pain & bloating; undigested food can result in diarrhea, weight loss and anemia.
• Skin and joints: Carpal tunnel syndrome is common, as are muscle weakness, joint pain, and stiffness.

Treatment: Because scleroderma is an autoimmune disease, one of the major pillars of treatment involves the use of immunosuppressive agents. Symptomatic relief also plays an importmant part.

Other symptoms include severe fatigue, insomnia, and joint problems. Some patients may also report difficulty with swallowing, bowel and bladder abnormalities, numbness and tingling, and cognitive dysfunction.

Fibromyalgia frequently co-exists with psychiatric conditions such as depression and anxiety, and stress-related disorders such as posttraumatic stress disorder.

Not all people with fibromyalgia experience all associated symptoms.

Fibromyalgia is estimated to affect 2–4% of the population, with a female to male incidence ratio of approximately 9:1.

On physical exam, LOOK FOR TRIGGER POINTS !!!!!!  There are 18 symmetrical locations. 

Treatment consistes of tricyclic antidepressants, exercise, sleep hygiene, and stress reduction.

Some cases of dermatomyositis actually “overlap” other autoimmune diseases such as: Sjögren’s syndrome, lupus, scleroderma, or vasculitis. Because of the link between dermatomyositis and autoimmune disease, run an ANA test.

Skin findings occur in dermatomyositis but not polymyositis and are generally present at diagnosis. Gottron’s sign is an erythematous, scaly eruption occurring in symmetric fashion over the MCP and interphalangeal joints and can mimic psoriasis.

The heliotrope or “lilac” rash is a violaceous eruption on the upper eyelids and in rare cases on the lower eyelids as well, often with itching and swelling.

Treatment: High dose prednisone (60 – 80mg/day).  80% respond within 6 weeks!!

Invariably the presentation is with WEAKNESS, not pain (pain should suggest PMR).

Polymyositis, like dermatomyositis, strikes females with greater frequency than males. (Remember: Inclusion Body Myositis effects men more !!)

1.) Look for elevated CPK !!! (Presence of Anti Jo antibodies in >65% of patients.)

2.) Abnormal EMG showing decreased  amplitude with increased spikes

3.) Abnormal muscle biopsy showing myonecrosis with cytotoxic T cell infiltrates.

Treatment is high dose prednisone (60mg to 80mg /day)

Remember to evaluate for occult neoplasm!!!!!

Prominent weakness can occur elsewhere, but look for dysphagia as a co-symptom.

Drug exposure is the cause, with special attention to cocaine, alcohol, statins, steroids, and colchicine.

Labs don’t help with the CPK (marker for polymyositis) only mildly elevated.

Diagnosis is made with muscle biopsy (always biopsy a muscle!!) that shows vacuoles and muscle fiber inclusion bodies.

Prognosis is poor, high dose steroids can be tried (if it wasn’t the cause), but generally remove the offending toxin and wish for the best.

Notice the distal muscle atrophy in forearm and hands.

Pure Vegans (or vegetarians that avoid dairy) can only get B-12 deficiency related problems. (See below. . .)

Rhinoviral infections are chiefly limited to the upper respiratory tract but may cause otitis media and sinusitis. Rhinoviral infections may exacerbate asthma, cystic fibrosis, chronic bronchitis, and serious lower respiratory tract illness in infants, elderly persons, and immunocompromised persons. Although infections occur year-round, the greatest incidence occurs in the fall and spring. Of persons exposed to the virus, 70-80% have symptomatic disease.

Rhinoviruses are transmitted to susceptible individuals by direct contact or by aerosol particles infecting both ciliated areas of the nose and nonciliated areas of the nasopharynx. Few cells are actually infected by the virus, and the infection involves only a small portion of the epithelium. Symptoms develop 1-2 days after viral infection, peaking 2-4 days after inoculation, although reports have described symptoms as early as 2 hours after inoculation with primary symptoms 8-16 hours later.

The virus grows in a limited temperature range (33-35°C) and cannot tolerate an acidic environment. Thus, finding the virus outside of the nasopharynx is unlikely because of the acidic environment of the stomach and the increased temperature in both the lower respiratory and gastrointestinal tracts.

Individual patients exhibit a wide variety of signs and symptoms:

• The incubation period is 12-72 hours, averaging 8-16 hours after viral inoculation of the nose. Symptomatic complaints 2 hours after viral inoculation have been described.
• Illness initially begins with a sore throat, which is frequently the most bothersome of the early symptoms. This is followed by nasal discharge, nasal congestion, and sneezing, which intensify over the next 2-3 days.
• Other associated complaints include headache, facial and ear pressure, and loss of smell and taste.
• Thirty percent of infected individuals develop a cough, and 20% develop hoarseness, both of which may persist up to a week, although they seldom become bothersome until nasal symptoms improve.
• Systemic signs and symptoms, such as fever and malaise, are unusual. If they are present, consider an alternative diagnosis.
• Symptoms generally last 7-11 days, although they persist up to 2 weeks in a quarter of patients. Rarely, patients complain of lingering symptoms that last more than 30 days.
• Infants and toddlers may display only nasal discharge. However, Calvo et al recently reported that, among infants younger than 2 years with viral respiratory tract infection requiring hospitalization in Spain, rhinoviral infections are second only to respiratory syncytial virus infections in terms of frequency.  
• School-aged children usually complain of nasal congestion, cough, and runny nose. These symptoms persist for an average of at least 10 days.
• Most patients have obstruction and mucosal abnormalities of sinuses, eustachian tubes, and middle ear, which causes a predisposition to secondary bacterial infection in up to 2% of patients.
• Infection may exacerbate underlying asthma and chronic pulmonary disease.
• People who smoke do not appear to have more frequent rhinoviral infections; however, their infections are more severe and their symptoms of longer duration.

The physical examination findings are typically less severe than those reported by the patient.

• Red nose with dripping nasal discharge may be present.
• Nasal mucous membranes have a glistening glassy appearance without obvious erythema or edema. Yellow or green nasal discharge does not indicate bacterial infection because a large number of white blood cells migrate to the site of viral infection.
• If marked erythema, edema, exudates, or small vesicles are observed in the oropharynx or if conjunctivitis or polyps in the nasal mucosa occur, consider other etiologies, including infection with adenovirus, herpes simplex virus, mononucleosis, diphtheria, coxsackievirus A, or group A streptococci.
• Auscultation of the chest may reveal rhonchi, but the chest is usually clear.

Transmission

• Rhinoviral transmission occurs with close exposure to infected respiratory secretions, including hand-to-hand, self-inoculation of eyes or nose, and, possibly, large- and small-particle aerosolization. The virus has been cultured from the skin after up to 2 hours and after up to 4 days on inanimate objects in ideal conditions. Donors are typically symptomatic with a cold at the time of transmission, and virus is detected on their hands and nasal mucosa.
• One recent study assessed the transfer of virus to surfaces in 15 adults with rhinoviral infection. Each stayed overnight in a hotel room. Afterward, 10 commonly-touched sites in each room were tested for viral contaminants. They found that virus could be recovered from 35% of these sites. Furthermore, they found that virus could be transferred back from inanimate objects to fingertips in many cases. 
• Higher rates occur in humid, crowded conditions, as found in nurseries, daycare centers, and schools, especially during cooler months in temperate regions and the rainy season in tropical regions.
• The likelihood of transmission does not appear to be related to exposure to cold temperatures, fatigue, or sleep deprivation.

Treatment

Rhinoviral infections are predominately mild and self-limited; thus, treatment is generally focused on symptomatic relief and prevention of person-to-person spread and complications. The mainstays of therapy include rest, hydration, antihistamines, and nasal decongestants.

Antibacterial agents are not effective unless bacterial superinfection occurs. Development of effective antiviral medications has been hampered by the short course of these infections. Because peak symptom severity occurs at 24-36 hours after inoculation, antivirals have only a narrow window to positively affect a rhinoviral infection. In addition, the cause of the common cold is not always rhinoviral infection. Therefore, rapid and accurate diagnostic tests would be needed if a specific antiviral therapy were developed.

• Because of the large number of rhinovirus immunotypes and the inaccessibility of the conserved region of the viral capsid (the most likely effective site for targeting a vaccine), no rhinovirus vaccine is on the horizon.
• Because infection is spread by hand-to-hand contact, autoinoculation, and, possibly, aerosol particles, emphasize appropriate hand washing, avoidance of finger-to-eyes or finger-to-nose contact, and use of nasal tissue.
• Heated humidified air has been used for decades for the alleviation of symptoms due to rhinoviral infections but has never been shown to improve objective outcome measures.

Dietary supplements have been touted as possible therapeutic or preventive measures.

• Although large doses of vitamin C have been used for prevention and treatment of colds, controlled trials reveal minimal therapeutic benefit and no preventive qualities.
• Zinc has been found to inhibit rhinovirus replication in vitro, but no proven benefit has been shown in vivo on virus activity or immune modulation.

Drugs used in the symptomatic treatment include nonsteroidal anti-inflammatory drugs (NSAIDs), antihistamines, and anticholinergic nasal solutions. These agents have no preventive activity and appear to have no impact on complications. The combined effect of NSAIDs and antihistamines often relieves nasal obstruction; therefore, decongestion therapy is rarely needed. Oral (pseudoephedrine) and topical (oxymetazoline and phenylephrine) decongestants are commonly used for symptomatic relief.

First-generation antihistamines reduce rhinorrhea by 25-35%, as do topical anticholinergics and ipratropium bromide. Second-generation or nonsedating antihistamines appear to have no effect on common cold symptoms. Corticosteroids may actually increase viral replication and have no impact on cold symptoms.

Skin – Primary lesion of molluscum contagiosum

• Firm, smooth, umbilicated papules, usually 2-6 mm in diameter (range 1-15 mm), may be present in groups or may be widely disseminated on the skin and mucosal surfaces.
• The lesions can be flesh-colored, white, translucent, or even yellow in color.
• The number of lesions varies from 1-20 up to hundreds in some reports.
• Some lesions become confluent to form a plaque.
• Lesions generally are self-limited but can persist for several years.

The common goal of the different treatment methods is the destruction of the lesions. Once the lesion is gone, the infection is gone.  In immunocompetent people, no therapy is indicted with resolution in 6 to 12 months.  In the immunocompromised, aggressive therapy is needed to contain the disease with chemical, cryo, laser, or curettage. 

See the lesion at the arrow.

Hepatocellular carcinoma (HCC) is a primary malignancy of the liver. Hepatocellular carcinoma is now the third leading cause of cancer deaths worldwide, with over 500,000 people affected.  The incidence of hepatocellular carcinoma is highest in Asia and Africa, where the endemic high prevalence of hepatitis B and hepatitis C strongly predisposes to the development of chronic liver disease and subsequent development of hepatocellular carcinoma.

Hepatocellular carcinoma is a primary cancer of the liver and occurs predominantly in patients with underlying chronic liver disease and cirrhosis.

The cell of origin is believed to be the hepatic stem cells. 

Tumors progress with local expansion, intrahepatic spread, and distant metastases.

In general, the tumors are discovered either during routine screening or when symptomatic because of their size or location. Tumors may present as a single mass lesion or as diffuse growth, which can be difficult to differentiate from the surrounding cirrhotic liver tissue and the regenerating liver nodules on imaging studies.

The presentation may be caused in part by mass effect that can lead to obstruction of the biliary system or anywhere affecting the liver vasculature.

Without aggressive surgical resection, ablative therapy, or liver transplantation, hepatocellular carcinoma results in liver failure and death.

In the United States, the risk factors have historically included alcoholic cirrhosis, hepatitis B (HBV) infection, hemochromatosis, and now hepatitis C (HCV) infection. However, the obesity epidemic has resulted in a growing population of patients with nonalcoholic fatty liver disease, also referred to as nonalcoholic steatohepatitis. Patients with nonalcoholic fatty liver disease can progress to fibrosis, cirrhosis, and now hepatocellular carcinoma.

Among patients with cirrhosis, current recommendations include cross-sectional imaging studies every 6-12 months and serum alpha-fetoprotein (AFP) measurements.

Liver transplant is still the best treatment!!

Surgical treatment of porcelain gallbladder is based on results from studies performed in 1931 and 1962, which revealed an association between porcelain gallbladder and gallbladder carcinoma.

Porcelain gallbladder is an uncommon condition; recognizing the clinical and imaging characteristics of the disease is important because of the high frequency (22%) of adenocarcinoma in porcelain gallbladder.  

Surgery should not be delayed even if the patient is asymptomatic, because the occurrence of carcinoma in porcelain gallbladder is remarkably high.

Remember. . . a calcified gallbladder on routine x-ray in an asymptomatic patient NEEDS SURGERY!!