Tumescent solution is also called “Klein’s Solution” after the physician who characterized the recipe and the use of it.
It’s called “tumescent” because it makes things tumescent, which is a fancy word for swollen. Tumescent is a dilute solution of lidocaine, epinephrine, and sodium bicarbonate that is injected in the subcutaneous tissue (fat). The epinephrine is the most important ingredient as it causes vasoconstriction, this means that the blood loss that could be a big problem for large procedures like burn surgery and liposuction becomes much less of a big deal.
The other interesting thing is that since fat is relatively avascular compared to other tissues, the “safe amount” of tumescent is much higher than what is normally stated for injections of lidocaine or epinephrine.
For example, it was reported by Klein that the toxic dose of lidocaine for tumescent solution is 35 mg/kg of body weight.
There are a few different recipes for tumescent anesthesia, the one presented in the doodle is the one first outlined by Klein, some use more or less lidocaine or epinephrine.
- Kucera IJ1, Lambert TJ, Klein JA, Watkins RG, Hoover JM, Kaye AD. Liposuction: contemporary issues for the anesthesiologist. J Clin Anesth. 2006, 18(5): 379-87.
- Klein JA. The tumescent technique. Anesthesia and modified liposuction technique. Dermatol Clin. 1990, 8(3): 425-37.
- Klein JA. Tumescent technique for local anesthesia improves safety in large-volume liposuction. Plast Reconstr Surg. 1993, 92: 1085-100.
Nevi (or moles) are very, very common. They are generally well-circumscribed dark spots (or “papules” to use the dermatological terminology) that can appear at any time in someone’s life.
Histologically they are composed of groups of melanocytic nevus cells and can be found in the epidermis, dermis or both.
The problem with nevi is that they are pigmented and people tend to get worried about pigmented things on the skin (for good reason as melanoma can be a pretty scary disease).
Common acquired nevi are grouped into three categories (I’ll leave out congenital and dysplastic nevi for now)
- Junctional: the nevus cells are completely in the epidermis, just above the dermal-epidermal junction. Clinically they are <1 cm, flat or minimally elevated and dark in colour.
- Compound: the nevus cells are in both the epidermis and the papillary dermis (top layer of the dermis), and cross the basement membrane. Clinically they are raised, and a medium-brown colour.
- Dermal: the nevus cells are completely in the dermis. Clinically they are raised and almost always pigment less as the cells lose their capacity for melanization when in the dermis. They usually have telangectasia and may or may not have hair. They don’t tend to appear until the 2nd or 3rd decades of life.
Burns are typically classified by their depth into (or through) the skin.
- 1st degree: just in the epidermis
- Pink, hot, no blisters
- Like a typical sunburn
- 2nd degree: into dermis, painful, wet
- Superficial: unruptured blisters, hair & glands spared, erythematous (red) but blanch with pressure
- Deep: ruptured blisters, hair often gone, can convert to a 3rd
- 3rd degree: through the dermis aka full thickness
- Lack vascularization, dry, leathery, no sensation
Zones of a Burn
A burn isn’t a homogenous spot on the skin; more heat means more damage (who knew!)
- 40 – 44 C: enzymes malfunction, protein denature
- >44 C: damage occurs faster than the cell can handle
- Damage keeps going after the heat source is removed
- Zone of Coagulation: The cells are dead and their proteins have denatured. Denatured proteins coagulate – think fried eggs. This is what forms the eschar of the burn.
- Zone of Stasis: The cells aren’t quite dead but the blood supply isn’t the best. If the circulation gets worse (usually due to vessel constriction and thrombosis) the cells in this area will die too. This is why it can take a couple days for a burn to “declare” itself.
- Zone of Hyperemia: “Hyperemia” means an increase in blood flow, in this case because of vasodilation. The cells in this area are alive and generally recover.
The image above shows a superficial 2nd degree burn.
BUY THIS AS A STUDY CARD
A kid without a rash just isn’t a kid.
- Incubation: 10-21d, infective until crusted over
- Rash: vesicles on macules (dewdrops on rosepetals),
- Very pruritic!
- Other symptoms: 1-3d prodrome of fever and respiratory symptoms
- Treatment: supportive, acyclovir for severe disease, VZIG for post-exposure prophylaxis
- Complications: 1st or 2nd trimester = congenital varicella syndrome
- Incubation: 5-15d
- Rash: pink macules and maculopapules, starts on neck.
- Other symptoms: HIGH FEVER, cough, respiratory symptoms, erythematous pharynx, tonsils & TMs
- Treatment: supportive
- Complications: febrile seizures
- * Generally affects kids <5 years old
- Incubation: 10-14d, dx with measles IgM
- Rash: maculopapular, starts on face.
- Other symptoms: the 3 Cs
- 1) Cough 2) Coryza (runny nose) 3) Conjunctivitis
- Koplik spots in mouth 1-2d before rash
- Treatment: supportive, prophylactic Ig
- Complications: secondary bacterial infection, encephalitis (1:1000), subacute sclerosing panencephalitis (1:100000)
Rubella aka German Measles
- Incubation: 14-21d, infective 5d before rash and 7d after
- Rash: pink maculopapular, starts on face.
- Other symptoms: non-specific
- Treatment: supportive
- Complications: congenital rubella syndrome (very bad*), first four months of pregnancy highest risk (this is why we check rubella immunity status in prenatal screening)
* Congenital Rubella Syndrome
“Blueberry muffin baby” (purpura). Cataracts/congenital glaucoma, congenital heart disease, hepatosplenomegaly, jaundice, microcephaly, developmental delay
Fifth Disease aka Erythema Infectiosum
- Incubation: 4-14d, infective prior to onset of rash
- Rash: slapped cheeks (raised uniform maculopapular lesions on cheeks), may appear on extensor surfaces
- Usually not pruritic
- Other symptoms: flu-like illness ~3d prior to rash
- Treatment: supportive, blood transfusions if aplastic crisis
- Complications: arthritis (10%), vasculitis
- Aplastic crisis: reticulocytopenia, not bad in normal people, very bad anemia if you already have chronic hemolytic anemia
- During pregnancy: fetal hydrops/fetal loss
* This is a good one to actually know the virus name! PARVOVIRUS B19
Other rash descriptors to think about
- Sandpaper rash: scarlet fever (Group A Strep), they also have strawberry tongue, fever and sore throat
- Pink macules with central clearing: erythema marginatum (one of the major Jones criteria for rheumatic fever)
- Palpable purpura: Henoch-Schonlein Purpura
- Non-blanching petechiae: BAD (meningococcal disease), could be other things too, but need to rule out meningitis
The epidermis is divided into five layers. From outside to inside (dermis). The stem cells are located in the stratum basale and migrate outwards in their differentiation process
- Stratum corneum: The outmost layer, made of dead keratinocytes with a layer of protein around them (they have undergone keratinization)
- Stratum lucidum: Also dead keratinocytes (there is no real distinction here other than that the poor keratinocytes have died but have not finished the keratinization process)
- Stratum granulosum: the keratinocytes are still on the move, by this point they have kertahyalin granules
- Stratum spinosum: the keratinocytes migrating up, they have nice oval nuclei
- Stratum basale: Single layer of proliferating columnar keratinocytes, melanocytes (pigmented cells) and Merkel cells (mechanoreceptors) also live here
Of note, Langerhans cells, which are specialized antigen-presenting cells are present in all layers of the epidermis but are mostly in the stratum spinosum.
Kawasaki Disease is one of the pediatric rashes that you always need to have in the back of your mind. Most of the time the disease is self-limiting, but the consequences of not catching it are pretty bad (turns out coronary artery aneurysms often lead to things like infarction and DEATH).
Warm CREAM is an unrelated (and somewhat unpleasant) mnemonic to help remember the signs and symptoms of Kawasaki. The “warm” is a fever (one lasting more than 5d) and then you need 4/5 of the other criteria (non-purulent conjunctivitis, rash, palmar erythema/swelling, cervical adenopathy, dry and red mucous membranes, the infamous strawberry tongue). The kid doesn’t need all 4 as he or she is sitting in front of you, but the presentation and the history combined should include those criteria.
Treatment is with high doses ASA and IVIG, you do this to prevent the sequelae of coronary artery aneurysms and myocarditis, and it’s best to get an echo to check up on things.
Hand, foot and mouth syndrome (or disease to all you lay people out there) is a common viral illness, most often caused by coxsackie virus. Generally it affects daycare-aged children (the 1-10ish age group), mostly under the age of 6. The big thing is the fever with a rash on, you guessed it, the palms, soles and in the mouth. Sometimes the rash can also present on the trunk or back as well. The worst part is that the vesicles in the mouth are VERY painful, so it’s not uncommon for kids to want to stop eating or drinking when they have it.
So a patient has skin cancer (duh duh duuuuh). How much of a margin should you give in your excision?
Like all things, this depends on the type of skin cancer
- Basal Cell Carcinoma (BCC)
- Squamous Cell Carcinoma (SCC)
Low-risk BCCs: 4 mm (high-risk: Mohs surgery)
Low-risk SCCs: 4 mm (high-risk: Mohs surgery)
Melanomas: depends on the tumour (T) stage, which is dependent on tumour thickness
- T1 (<1 mm): 1 cm margin (92% 10 year survival)
- T2 (1-2 mm): 2 cm margin (80% 10 year survival)
- T3 (2-4 mm): 2 cm margin (63% 10 year survival)
- T4 (>4 mm): 2 cm margin (50% 10 year survival)
- Though it might seem counterintuitive that once you’re past 1 mm thickness, you don’t have a bigger margin, but larger margins haven’t been shown to increase survival