Approach to Rash & Basics of Skin Descriptions

Lecture Video: Click here!

Note: Please be sure to download the video.  For some reason only the first 14 minutes play if you stream it.

Layers of skin include epidermis, dermis and hypodermis

Skin appendages come from the epidermis and help maintain the body’s homeostasis (sebaceous glands, sweat glands, hair, nails, etc)

Approach to the Skin examination

  1. Use good lighting
  2. Vary distance of inspection
  3. Examine patient’s entire mucocutaneous surface
  4. Palpate lesion firmly and compare to normal skin
  5. Examine patient lying down and standing
  6. Look at patient again in 1 week

Rash Descriptors:

  • Blanching.
    • Erythema (blanching) connotes capillary dilation
    • Petechia or purpura (nonblanching) implies hemorrhage.
  • Skin phototype (varies by amount of melanin). Look for increased pigmentation or loss of pigmentation.
  • Look for dryness, sweating, oiliness, roughness/smoothness. Look at hair and nail closely as well.
  • Temperature- generalized or local warmth or coolness.
  • Distribution, especially if over sun-exposed surfaces.
  • Macule vs Patch (>1cm). Circumscribed area of change in skin color without elevation or depression.
  • Papule vs Plaque. Papule is a solid lesion < 0.5cm, while a plaque is > 0.5cm.
  • Nodule is a deeper, palpable, solid, round or ellipsoidal lesion.
  • Vesicle vs Bulla. A vesicle is a circumscribed, elevated, fluid containing cavity < 0.5cm and a bulla is > 0.5cm.
  • Pustule is a circumscribed, superficial cavity containing purulent exudate.
  • Cyst is a cavity containing liquid or semisolid materials and maybe superficial or deep.
  • Wheal is a rounded or flat-topped, pale red papule or plaque that disappears in 24-48 hours.
  • Crusts develop when serum, blood or purulent exudate dries on the skin surface.
  • Fissures result from marked drying, skin thickening and loss of elasticity
  • Erosion involves the loss of the epidermis and can heal without scar. An ulcer extends into the dermis or deeper.
  • Atrophy can be epidermal (wrinkling and shiny appearance) or dermal (leads to depression).
  • Lichenification has thickening of the epidermis and accentuation of natural skin lines.
  • Scar is the fibrous tissue replacement of the tissue by previous ulcer or a wound. Scan can keloid, hypertrophy or atrophy.

Acid-Base (made as simple as possible)

Lecture Video: Click on the Class Capture link on the Lecture Database page.

The revered Avi Gillespie gave his signature lecture.  Here’s one of the highlights.

Cases of Anion Gap Acidosis (goodbye MUDPILES, hello GOLDMARK!)

  • Glycols (ethylene and polyethylene)
  • Oxoproline deficiency (Tylenol)
  • L-lactic acidosis (shock, meds)
  • D-lactic acidosis (short bowel)
  • Methanol
  • Aspirin/Salicylates
  • Renal Failure/Uremia
  • Ketoacidosis

PFT’s and Oxygen Delivery

James Brown gave us an excellent talk on “PFT and Oxygen Delivery,” elucidating the various oxygen delivery modalities available to our hypoxemic patients.

PFT’s

  1. Look at the loop. Does it look obstructed or restricted?
  2. FEV1/FVC (post bronchodilator). If less than 70, they have obstruction. Then check FEV1 to determine the severity of obstruction.
  3. FVC: If FVC low, then be suspicious of restriction
  4. Check the volumes. TLC < 75 = restriction, TLC >110 = hyperinflation. RV > 120 = air trapping
  5. DLCO and DLCO/Va (corrected for volume) tells you the diffusion capacity

Oxygen Delivery in Hypoxemic Patients

Too much O2 can result in worsening V/Q matching in COPD patients (oxygenating areas that have difficulty with gas exchange)

Nasal Cannula: Your standard run-of-the-mill nasal cannula offers up to 6L/min of O2.  Anything flow above that is limited by the narrow tubing that feeds it.  So if your patient is still hypoxic on 6L NC, then seek another method of oxygenation.

Face mask: can go up to 10L.

Nasal Pendant: appears like a nasal cannula except it also has a disk chamber that fills during a patient’s expiratory phase. During inspiration, the patient breaths in the oxygen that has filled the chamber.  Unclear how much oxygen is actually delivered, and it varies depending on respiratory rate (ie – shorter expiratory phase for the disk chamber to fill with oxygen).  Typically can offer somewhere in the range of 6-12L/min of O2.

Venti-Mask: Like a face mask except that it has a dial to adjust the FiO2. One of the few oxygen delivery modalities in which you can definitely state the percent FiO2 the patient is receiving.

Non-Rebreather Mask (NRB): in theory a NRB offers 100% FiO2.  Since at least one of the tabs on the front of the mask is usually removed, it ends up providing about 80% FiO2.

A non-rebreather should only be used in an emergency.  Otherwise, use other oxygen delivery modality.

BIPAP: is used for work of breathing and hypercapnia. Top number is Inspiratory Positive Airway Pressure (IPAP) and bottom number is Expiratory Positive Airway Pressure (ie –  PEEP). Increasing the difference between the two numbers allows for better treatment if hypercapnia is an issue.

  • CPAP is just EPAP/PEEP, but no IPAP.  So there’s just one number listed (eg – 8cm H2O).  It is used for OSA/OHS and also helpful in pulmonary edema.
  • Note: for patients in respiratory distress, do not use CPAP.  It does not provide the offloading of respiratory muscles during inspiration that would help both alleviate their distress and decrease O2 consumption by the muscles.

High flow nasal cannula (at Temple the brand is Aquinox) can be used when flows greater than 10L are needed. They can go up to 60L and can also titrate the FiO2. The high flow also allows for a PEEP effect (but only if the mouth is closed) to keep the airway open in very mild OSA and to recruit more alveoli. Dead space can still be cleared if the mouth of the patient is open.

Ventilator: We’ll save this discussion for another lecture, but in essence it provides up to 100% FiO2, ability to add Heliox, offloads the patient’s respiratory muscles, multiple possible respiratory settings, etc.

Statins…the best thing since sliced bread?

Thank you to Dr Paul Williams for the many words of wisdom!

Check it out on Class Capture through our Lecture Database.

“Lipids. What are they good for? Absolutely nothin’. Huh”

Hypercholesterolemia leads to LDL accumulation in vessel intima, results in oxidative modification of lipoproteins, which triggers an inflammatory response. Monocytes invade the intima and become foam cells which also trigger smooth muscle cells to migrate from the media to intima.

Rupture of the plaque causes there to be contact of coagulation factors in the blood with the thrombogenic tissue factors.

Statin Drug Information

Statins lead to decreased cholesterol synthesis and hepatic cholesterol concentrations by inhibiting HMG-CoA reductase. They may also have anti-inflammatory effects by acting on Ras and Rho synthesis.

Statin intolerance can be manifested by myalgia, asymptomatic myopathy, myositis, and rhabdomyolysis. Risk factors include age >80, female sex, frailty, hypothyroidism, CKD, DM-2, EtOH abuse, infection, high doses of statins. If there is an elevated CK, statin should be avoided if CK >10 times upper limit of normal. ACC/AHA recommends niacin or cholestyramine if this occurs. Patients with normal CK and myalgias can stop the statin for two weeks and then restart to see if symptoms recur or reduce the dosage or change to fluvastatin or rosuvastatin.

Statins can also modestly increase the incidence of type 2 diabetes, in patients with risk factors for diabetes (metabolic syndrome, impaired fastin glucose, BMI >30, A1c >6%)

Guidelines

Current statin therapy are influenced by the 2013 ACC/AHA practice guidelines. Takeaway points include:

  • patients with clinical ASCVD should be on a high-intensity statin
  • those with an LDL >190 mg/dL should be on a high intensity statin
  • patients with diabetes with LDL between 70-190 should be on a moderate intensity statin (if 10 year ASCVD risk >7.5% should be on a high intensity statin)
  • patients with a 10 year ASCVD risk >7.5% should be on a moderate or high intensity statin.

Thyroid Emergencies

Lecture Video: head to the Lecture Database and click ‘Class Capture’.

Thank you Ajay Rao for giving us an amazing lecture.  Here are the highlights:

Thyroid Storm

  • Incidence of thyroid storm is less than 10% of patients hospitalized for thyrotoxicosis. Mortality rate can be as high as 20-30%.
  • Scoring system- Wartosky/Burch can be used to determine possibility of thyroid storm. Signs/symptoms of weight loss, generalized weakness/fatigue, diarrhea, palpitations, psychosis/confusion. A wide pulse pressure
  • Most common cause of thyroid storm is underlying Graves’ Disease.
    • Precipitating event like surgery, trauma, MI, VTE, DKA, infection, discontinuation of anti-thyroid drugs can lead to thyroid storm.
  • Management in the ICU:
    • Halt synthesis: give anti-thyroid drugs, i.e. methimazole or PTU
    • Halt release: give iodine therapy no sooner than 30-60 minutes AFTER anti-thyroid therapy
    • Halt peripheral effects: beta- blockade
    • Give steroids: inhibits peripheral conversion of T4 to T3

Myxedema Coma

  • Most patients with severe hypothyroidism present neither with myxedema or coma. Can present with progressive dysfunction of cardiovascular, respiratory and CNS systems.
  • Common precipitants include, sepsis, trauma, and surgery.
  • Findings include hypothermia, AMS, bradycardia, hypotension, and hyponatremia. Myxedema include swelling of the soft tissue associated with periorbital edema, ptosis, macroglossia or cool, dry skin.
  • Management:
    • Careful IV volume repletion
    • Hydrocortisone (if pituitary disease or adrenal insufficiency)
    • Give a SINGLE high dose of T4 (300-600mcg IV)
    • Daily T4 dosing (50-100mcg IV or PO)

Sepsis

Thank you Dr Erin Narewski for a shocking lecture!

  • Start antibiotics within one hour of recognition of severe sepsis or septic shock. Remove any lines or debride any tissue which may serve as a source.
  • Initial resuscitation efforts
    • CVP 8-12mmHg, MAP >65, Urine output >0.5 mL/kg/hr, Central venous or mixed venous oxygen sat 70 or 65%, respectively.
  • Patients with elevated lactate levels targeting resuscitation to normalize lactate
  • Transfusion goal of >7 g/dL in those without other circumstances (MI, severe hypoxemia, acute hemorrhage, ischemic heart disease).
  • Transfuse platelets with counts <10,000 in absence of bleeding. Prophylactic platelets when counts <20,000 with significant risk of bleeding. Counts greater than 50,000 when active bleeding is occurring, surgery or invasive procedure are planned.
  • Glucose goal <180 mg/dL. Be wary of point-of-care testing of capillary blood (maybe falsely low)
  • Do not use sodium bicarbonate in patients with hypoperfusion induced lactic academia with pH >7.15
  • Vasopressor therapy is to target a MAP of 65mmHg. Norepinephrine is the first choice, followed by epinerphine.
  • Discuss goals of care and prognosis with patients as early as is feasible.