Perianal Disease: Not Everything down there is a Hemorrhoid (Cortez, 11/20/2024)

 A recording of this presentation is available HERE. 

Many thanks to Dr. Allen Cortez for an excellent presentation on perianal disease. I learned a lot and was really impressed by how much Dr. Cortez, a long-time local general surgeon, knows and cares about a region of the body that many people are pretty uncomfortable talking about. I recommend you watch his presentation, the link above. 

My notes:

Hemorrhoids are extremely common -- 5-10% of the population, >2.2 million people per year with over 2 million prescriptions per year that add up to over $43 million in healthcare costs. But many patients are being treated for hemorrhoids when there may be other things going on down there, including: fissures, fistula, abscess, pruritis, and rectal prolapse. 

Dr. Cortez reminded us to go back to the basics: 1) listen to the patient (e.g. hemorrhoids generally don't hurt, so if the patient is complaining of pain, broaden your ddx) and 2) examine the patient.

Fiber

Encourage fiber! All our patients need more fiber. And fiber isn't good for just the perianal region. Fiber decreases risk of cardiovascular disease, decreases risk for colon cancer. "The best fiber out there is the one you'll take". Really, the only downside is increased flatulence.

Fiber options abound, including: psyllium husk, benefiber (can sprinkle on yogurt), fiber capsules or gummies (e.g. Kirkland brand, 2-4 gummies 2x per day, with LOTS of water).

Once you start a fiber supplement, don't make any changes for 5 days.

Miralax is good too, but it shouldn't replace fiber. Use miralax PRN for constipation. 

Dr. Cortez reminded us that the increased pressure of diarrhea can also contribute to hemorrhoids. The goal is ONE nice big healthy bowel movement per day, no more than 4-5 minutes sitting on the pot. It is better to return 3 or more times than sit for prolonged period of time on the toilet.

When you are going to examine a patient for perianal complaints: put them in L lateral decubitus (better to see than lithotomy). Look externally for tags, fissures/openings, thickened skin, ulcerations, masses. If you see a fissure stop there (you can make it worse). Use anoscopy and a digital exam to check for tone, masses, blood, etc. 

Dr. Cortez is not a fan of donuts for any perianal condition. In his eloquent words: "Gravity tries to push your liver right out your butt"

Hemorrhoid Treatment 

1) Banding (in office), no prep, effective, can be done several times, no downtime, no severe pain

2) Hemorrhoidectomy (surgical) is always a last resort, very pain ful but most effective. Stapled hemorrhoidectomies are not superior.

Thrombosed hemorrhoids, which present as big purple extremely painful lumps should be unroofed in first 2-3 days for pain control (in ED or office). If it has been > 5 days, healing is equivalent and intervention is not indicated.

Fissures

Perianal fissures, which are tears in the anoderm exposing the sphincter muscles, are extremely painful. Patients may describe symptoms as "crapping out glass" or "jamming a knife in my butt". 73% present midline posteriorly. If you visualize a lateral fissure, that patient needs a work-up, including testing for Crohn's, HIV, syphillis, TB and more. 

Acute fissures (< 6 months) can be treated with fiber, fiber and fiber, as well as hydration and sitz baths. This takes time! Topicals can sooth and manage symptoms, including topical nitroglycerine. Dr. Cortez's preferred topical is compounded diltiazem/nifedipine cream (locally can get compounded at Dollar Drug). Can be rx'd TID.

Chronic fissures (>6 months) require treatment with chemo-denervation, including Botox, which is effective and stops spasm. Some people need surgical intervention: with sphincterotomy or anocutaneous flap.

Perianal abscess

Perianal abscesses can also be extremely painful. 30-70% of abscesses have an accompanying fistula. 40-50% will develop a fistula over time.

 Treatment of perianal abscess is I&D, and usual management with packing is not effective because the skin often heals over before the abscess heals. Instead make a BIG incision (this may require sedation-- need to happen in ED?) and may need an initial packing but then should probably not be packed . Perianal abscesses can occur in several locations: ischiorectal, intersphincteric, perianal and supralevator. No antibiotics are indicated once drainage (i.e. source control) is achieved. Many fistulas will heal themselves and not all perianal abscesses need CT imaging. But if you are concerned, send to surgeon for further assessment. 

Malignancy

Finally, malignancies can present in the perianal region and the only way to diagnose them is to look for them. These can include squamous cell carcinomas and melanomas. See images below for some examples. 

Perioperative Evaluation (Schneider - 10/4/23)

Sorry, there is no recording available for this session. 

***

Thank you to our very own Dr. Dave Schneider for an excellent presentation on Perioperative Evaluation. Unfortunately, I forgot to hit "record" on the zoom meeting, so we do not have a recorded version of his presentation. Sorry about that!

My notes:

First off, "clearance for surgery" is not our job!  Our job is to assess each patient's perioperative risks and optimize and manage those risk factors as they head into surgery. Do note that there are gender and race disparities in those who receive surgical interventions (BIPOC patients receive fewer PCI interventions, fewer orthoplasties and have increased mortality when undergoing these procedures).

The new-ish term for perioperative cardiovascular complications is Myocardial Injury after Non-Cardiac Surgery (aka MINS). 5-19% of surgical patients will experience MINS, 84% will be asymptomatic. MINS is associated with increased morbidity and mortality.

The American College of Cardiology (ACC) last updated their Guidelines for Perioperative Cardiovascular Evaluation and Management for patients undergoing non-cardiac surgery in 2014. These old guidelines are available here. The flow diagram is a doozy and the recommendations are confusing: 

In classic Schneider-fashion, Dr. Schneider invented an acronym to summarize their 2014 recommendations. It is called E-A-R-L-I

E: Emergent: if a surgery is emergent--> take patient to the OR and deal with the negative outcomes later

A: ACS: if the patient has s/sx of ACS, manage per guidelines

R: Risk assess --> use any of several tools (e.g. RCRI, NSQUIP calculator, MICA calculator, see below for more info)

L: Limitation of function --> if patient unable to  perform at 4 METs using the Duke Activity Scale, optimize their functional status before proceeding to surgery

I: Impact on decision? --> Yes or No? If the cardiac stress test outcome will change how/when you will proceed with surgery, then go ahead with a stress test. If not, then proceed to the OR.

The European Society of Cardiology (ESC) updated their guidelines on perioperative management more recently in 2022. And their guidelines are much more simple than those of the ACC. They are summarized here by the ACC. In essence, they say: 

Is the surgery. . .

Emergent? -->  Proceed to surgery without delay, cardiac testing is not feasible

Urgent? --> Proceed to surgery without unnecessary delay (using a multidisciplinary team to determine about individualized cardiac testing)

Time-Sensitive? --> Do the surgery ASAP

Their guidelines are summarized in this lovely flow charts. Don't you just love flow charts?

***

Should you check a Hemoglobin and Renal function in all patients pre-operatively? The answer is no, but your should check in intermediate and high risk patients. 

Don't forget, for everyone, advise smoking cessation!

There are two risks to consider in evaluating patients: 1) the risk of the surgery itself (e.g. highest risk includes intra-thoracic, vascular) and 2) the risk of the patient

• If the surgery is low risk, no CV assessment needs to be made
• If the surgery is intermediate risk, and the patient is either >65 or with CV risk factors, get an EKG and check functional capacity
• If the surgery is HIGH risk, consider EKG and biomarkers** for patients older than 45, definitely get them for patients >65 or with CV risk factors. If the patient has known CVD, get a cardiology consultation and make a multidisciplinary decision. 

**Note: Biomarkers referred to above include BNP and/or Cardiac Troponin (also in table above). They have been shown to predict MI. Either one is predictive and do not change outcomes. 

There are several risk calculators to help you determine your patient's  risk level:

1) Revised Cardiac Risk Index (RCRI), which Dr. Schneider shortens to DRC4 (diabetes, risky surgery, CAD, CHF, CVD, Cr>2)

2) The NSQUIP calculator

3) Gupta's Perioperative MICA calculator

Each calculator is slightly different and variably useful depending on the patient in front of you. All three of these have been validated and you should get familiar with all of them.

Okay, now for a few pearls:

• There is NO benefit to coronary revascularization before surgery.
• Labs and other tests should only be done pre-operatively if you were going to do them anyway
• Coag testing is usually unnecessary unless patient is on warfarin. Family Hx and PMH are just as predictive of bleeding (e.g. if patient has history of prior bleed, or family member has bleeding problem, patient has higher risk of bleed)
• Only get a pre-op EKG if the patient has known CVD, CV risk factors >65 and they are having an intermediate/high risk surgery
• TTE only needed if patient has known valvular lesion and no TTE in the last year. You may consider if new onset dyspnea or change in status of their HF
• Pre-op CXR is NOT recommended (Choosing Wisely, ACR 2017)

What about medications?

Statins: if a patient is on a statin, continue it (okay to miss a few days due to NPO, etc.). Perioperative initiation is reasonable if someone is getting vascular surgery

Beta blockers: if patient is already on BB, continue them perioperatively (perioperative withdrawal has 4x increased mortality). You may consider decreasing BB dose due to risk of hypotension after surgery. You can consider starting a BB at least one week (up to 28 days) prior to cardiac surgery if high risk patient and high risk surgery. 

Other anti-hypertensives: post-op hypotension is a common problem. Consider holding all BP meds on day of surgery, add them back slowly post-op, ?one at a time

ASA: it is okay to go to the OR on aspirin. Also okay to stop ASA in high bleeding risk patients (e.g. those on DOAC or warfarin as well). Continuing ASA has been shown to be cardioprotective: decreased MI by 56% and decreased composite CV outcomes. There is a non-significant increased bleeding risk if you continue ASA.

What about patients with recent drug eluting stents (DES)? Delay elective surgery for up to 6 months if possible so as not to interrupt DAPT. 

Abnormal Liver Function in Obstetrical Patients (Ludwig, 6/1/2022)

Many thanks to Dr. Alec Ludwig for an excellent presentation about liver and biliary abnormalities in pregnancy. It was jam-packed with good information. 

A recording of his presentation is available HERE. 

My notes:

Remember that what we typically call "liver function tests"  is actually a misnomer. In fact, there is no test that reliably demonstrates the liver's function. Elevation of AST and ALT -- the liver enzymes-- indicates liver injury, not liver dysfunction. Albumin and prothrombin time are factors that are produced by the liver and may be better markers of function. 

In normal pregnancy, you can see elevated alkaline phosphatase (up to 3x normal), as well as elevated cholesterol, triglycerides, and fasting gallbladder volume. Note that many measures we use to evaluate the liver (AST/ALT, T Bili, PTT, liver size, bile acids) don't change in pregnancy.

Hepatocellular injury as measured by elevation in AST/ALT:

• acute viral/toxic hepatitis: AST/ALT 25x upper limit of normal
• ischemic hepatitis: AST/ALT 50x upper limit of normal
• chronic HCV/HBV: slight elevation of AST/ALT (2x normal), rarely greater than 10x normal

Gallstone disease in pregnancy

Gallstone disease is much more prevalent in pregnancy for several reasons. 1) Increased estrogen levels increase cholesterol, thereby supersaturating bile with cholesterol. 2) Progesterone slows contraction of gallbladder, disrupting the excretion of bile acids. AND 3) Increased fasting gallbladder volume.

• acute cholecystitis: blockage of the cystic duct causing inflammation in the gallbladder
• fever, WBC count, can have slightly elevated AST/ALT (if large stone)
• choledocholithiasis: stone in CBD or hepatic duct, causing backup into liver, injury to liver
• definite elevation AST/ALT
• acute cholangitis: can be emergency due to severity of illness
•  Charcot's triad (RUQ pain, jaundice, fever)

Generally treat GB disease in pregnancy with IV antibiotics, surgery if indicated. Laparoscopic cholecystectomy is safe in pregnancy, safest in the second trimester. Should occur within 24-48 hours conservative management. ERCP is also safe in pregnancy; minimize radiation by shielding, fetal monitoring.

Viral Hepatitis (A-E)

• HAV: most common acute hepatitis in general population, but infrequent in pregnancy. 
• Acute infection  (only care about IgM). 
• Generally mild (malaise, HA, fever, jaundice, RUQ pain), supportive treatment. 
• HAV vertical transmission rare but has been documented. Associated with preterm birth, neonatal cholestasis. 
• Breastfeeding okay, HAV vaccine safe in breastfeeding
• HBC: surface Ag used to screen everyone in pregnancy, core Ag, e Ag indicated infectivity/vertical transmission to 80-90% if occurring in the 3rd trimester. 
• Major causes IVDU, sexual intercourse with people w/HBV, vertical transmission. 
• can present with asymptomatic acute phase, can pick up infection even prior to symptoms
• if mom has chronic HBV in pregnancy: need to check viral load, 1 million to 100 million is elevated, may need treatment during pregnancy w/Tenofovir after 28-32 weeks (to prevent vertical transmission)
• Babies born to mothers with HBV needs HB IVIG and first dose of vaccine within 12 hours, don't determine delivery method
• Breastfeeding is safe as long as infant got IVIG and HBV vaccine
• HCV: can be acute and chronic 
• HCV on the rise in the last few years (2009-2019 2x increase of patients with HCV), likely due to IVDU
• vertical transmission 3-5%
• 75% HCV infections are asymptomatic
• ACOG does have some recommendations of Category B meds that could be used to treat HCV in pregnancy to decrease vertical transmission (Ribavirin is teratogenic)
• Vertical transmission increases if co-infection w/HIV, invasive surgical procedure, ROM >6 hours, conflicting data but discourage fetal scalp electrode
• Breastfeeding okay w/HCV
• HDV: coexists with HBV only, anyone with chronic HBV should be tested for HDV. Supportive treatment, monitor symptoms. If treat HBV, clears HDV.
• HEV: can be acute and chronic, based on genotype
• some areas in Mexico, Asia, Africa and South America endemic (travel recommendations not to travel to endemic areas in 2nd and 3rd trimester)
• believed to be water born
• pregnancy women are particularly susceptible to severe liver damage and liver failure, 20-30% mortality
• rare vertical transmission
• breastfeeding okay

Other viral hepatitis: HSV hepatitis (rare but high mortality), CMV hepatitis (also rare, more common in organ transplant pts): most common hearing loss

Cirrhosis in Pregnancy: it is more difficult to get pregnant if cirrhotic (due to secondary amenorrhea), but can still get pregnant. High risk for bleeds, aneurysms and acute on chronic liver failure. Need variceal screening DURING pregnancy. Increased mortality with pregnancy (should calculate MELD, do HCC screening even during pregnancy). Can use beta blockers (e.g. propranolol) but can cause some side effects to baby. Octreotide okay. Mode of delivery unclear, should be individualized.

Autoimmune hepatitis in pregnancy generally improve during the 2nd trimester BUT can flare post partum.

Hyperemesis Gravidarum: 50-60% of patients hospitalized with hyperemesis demonstrate some abnormal liver tests: hyper bilirubin, elevated AST/ALT. Generally don't get fever, jaundice. 

Cholestasis of Pregnancy (ICP) is the most common liver disorder unique to pregnancy. Generally presents as pruritis without a rash. Even though palms and soles are most common places, can be in other places as well. May see abnormalities in AST/ALT. Increased serum bile acids confirm a diagnosis (>10=cholestasis dx, >100=severe, should be induced after 36 weeks, earlier other indications).

• Elevated ALT 30x normal, elevated conjugated bilirubin
• generally not jaundiced
• start antenatal testing right away
• treatments (all grade C): ursodiol improved labs and symptoms but no data that improves still birth. Other treatments: Hydroxyzine, cholestyramine
• Some data on PO vitamin K (evolving evidence)
• Can progress: 2-5x risk of progression to preE, if bile acids >40

Pre-Eclampsia is diagnosed by blood pressure criteria: SBP >140, DBP >90, 2 x, 20 minutes apart after 20 weeks AND either proteinuria (>0.3 microalbumin/creatinine ratio) OR lab abnormalities (platelets <100K, SCr>1.1 or double baseline, impaired liver tests (2x normal). Symptoms-based diagnosis is NOT recommended. Antenatal testing twice weekly. Deliver at 37 weeks

Pre-E with severe features: 

• BP >160/110 (2x, 4 hours apart) OR
•  thrombocytopenia, elevated SCr or liver test abnormalities (regardless of BP)
• Antenatal testing daily, deliver at 34 weeks

HELLP syndrome is considered a complication of PreE even though 15% of patients don't have elevated BP or proteinuria. 10-20% of women with severe PreE progress to HELLP. Diagnosed with signs of hemolysis (LDH>600, platelets <100, AST/ALT 2x normal).  High mortality. Can lead to hepatic rupture/hematoma, placental abruption, acute renal failure, etc. Treatment is magnesium sulfate, treat BP and delivery. Hepatic hematoma and rupture (stretching of Gleason's capsule) -- pts often have severe RUQ pain. 

Acute Fatty Liver of Pregnancy has a lot of similarities with HELLP, Severe PreE and acute fatty liver. Originates from genetic defect in fetus and a susceptible mother. Presents with n/v, pain, jaundice, fever. Generally don't present with elevated BP. Swansea criteria to make diagnosis. Can add ammonia, uric acid to help classify. Imaging may demonstrate hypoechoic liver with lots of fatty deposits. 

Skin Cancer Reconstruction (Pourtaheri 4/13/2022)

Many thanks to Dr.  Navid Pourtaheri, new-to-our-community plastic surgeon, on Skin Cancer and Skin Cancer Reconstruction. This is a great summary of skin cancer findings and some specific indications and recommendations of when to involve plastic surgery. 

A recording is available HERE 

Skin cancer types: basal cell (BCC) squamous cell (SCC) keratoacanthoma, melanoma

Basal cell cancer (~4 million cases/year in US)

• variable in appearance, "can look like anything"-- don't know what it is until you remove it
• always slow growing (even high risk ones)
• primarily occur on sun-exposed areas (hand, ears, face)
• do sometimes spontaneous bleed or ulcerate
• can be locally invasive
• very rarely metastasize

Squamous cell cancer (SCC), 1.5 million cases/year in US

• variable appearance, but more commonly dry and scaly, also can be rough/thickened, wart-like, can ulcerate and form open sores
• more accelerated growth with local invasion than BCC (tend to progress more quickly)
• lower lips more common with SCC 
• can be locally invasive, can metastasize
• curable if treated early
• actinic keratoses (AK) is pre-squamous cell lesion

Keratoacanthoma, 275K cases/year in US

• once considered subset of SCC
• dome-shaped lesion with central keratin plug
• almost always in sun exposed areas (face, ears, nose, hands)
• quite rapidly growing (faster than SCC), can be locally destructive
• unpredictable, can spontaneously regress
• less likely to metastasize

Melanoma, 197K cases/year in US

• most costly type of skin cancer
• 25% found in existing moles, 75% spontaneously occur on normal looking skin
• 50% are melanoma in situ>> high cure rate (90-100%)
• can be found ANYWHERE
  
• most common form is superficial spreading
• when goes deeper, called lentigo maligna
• 10-15% of cases are nodular melanoma, most aggressive, tends to be found invading
• remember ABCDE (see below) with special attention to "E" (evolving-- that is a changing mole)
• Breslow thickness correlates with 5-year survival

Treatment options for skin cancer

• Moh's surgery 
• most commonly used in BCC and SCC (often contraindicated for melanoma)
• high risk areas (H zone)
• cosmetically sensitive areas, over joint surfaces
• decreases amount of tissue excised, maintaining the same cure rate
• Excision with margins and simple closure also acceptable
• Curettage (EDC)
• scrape the abnormal tissue, then burn it
• Cryotherapy more common in older patients, people who don't want a procedure, on blood thinners, large number (e.g. on face)
• Melanoma best excised w/margins, possible lymph node biopsy (plastic surgery, general surgery)
• sentinel node biopsy not indicated for melanoma in situ

When to refer to plastic surgeon?

• skin cancer not indicated for Mohs
• post dermatology resection, cannot close
• melanoma

Biopsy options

• shave: get full epidermis but only part of dermis (this is good because it won't form scar)
• always inappropriate for c/f melanoma because need full thickness
• punch: takes full thickness of skin
• incisional biopsy: get piece of abnormal with normal adjacent, done with scalpel
• excision: preferred for lesion is <1cm (cut the whole thing out with margin, 1mm of normal tissue is acceptable margin 
• FNA not used for skin, but for clinically positive nodes
• Sentinel lymph node biopsy (SLNB) after melanoma diagnosis, after lymphoscintigraphy (radioactive dye that drains to the lymph node)

Imaging

• Always needed in >Stage 3 melanoma, definitely NOT indicated in stage 1 (stage 2, use your judgement, may be indicated)
• Most common: PET CT for assessing for metastases
• Chest CT also good modality b/c melanoma so often goes to lungs (chest xray not sufficient)

Wound Care (Cardenas, Cortez, Daly, 3/16/2022)

Many thanks to wound care nurse Wendy Cardenas, general surgeon Allen Cortez, and wound vac rep Kevin Daly for an informative talk this week on Wounds and Wound Care. I learned so much!

For a recording of their presentation click HERE (starting 11 minutes into the recording)

My notes:

• There are all kinds of wounds: surgical/traumatic, pressure, vascular, diabetic, infectious
• 1.3-3 million Americans are treated for pressure wounds each year
• 60,000 deaths per year are attributed to pressure wounds
• $9.1-11.6 billion dollars spent in the US on pressure wound are alone
• You only need 33 mmHg of pressure to create a pressure wound--> equivalent to a "gentle handshake"

Physician role in wound management

• decrease pressure
• decrease friction/shear forces
• manage incontinence (urinary, fecal>> indwelling/suprapubic catheters, ostomy)
• nutrition! nutrition! nutrition! (protein-calorie, blood sugar control, obesity)
• pain management
• managing comorbidities (DM, tobacco, drug addiction, venous stasis, etc)
• education (patient, caregiver, nursing staff, family)>> "you can tell people what to do, but if you give them the reason why, there is much more acceptance and compliance"

Initial management of wounds

• Identify and treat the cause
• Clean the wound--> tap water is just as good as sterile saline or any other wash (okay to shower day after surgery, no baths). Pulse evacuation (in OR) with fluid and pressure has been shown to improve outcomes. A simple syringe can also help w/debridement
• Keep wounds MOIST to allow capillary ingrowth (not too wet/not too dry)
• Debridement (wet to dry, enzymatic, surgical at bedside or in OR)
• you want to see bleeding
• Optimize nutrition (glucose control, protein)
• Optimize comorbidities (stop smoking!)
• Antibiotics if appropriate--> only if s/sx infection, "use common sense"
• Adjuncts (e.g. iodine/betadine-- can cause tissue damage, which can disrupt healthy granulation tissue. No evidence that adjuncts improve healing). 

Q: What is the perfect wound dressing?  A: Skin

Wound Vacs

3M Rep, Kevin Daly, then took us through the history of wound vacs (in hospitals since 1995, outside the hospital since 2000) and the range of products that are available, including silver-impregnated foam, special non-adherent dressings (silicone-based) designed to lay between wound and the wound vac (to prevent foam from sticking to the wound), the evolution of the instill vac 

What does a wound vac do?

reduces edema around wound

heals wound 60% faster than standard dressing

stretches cells--> leads to degranulation tissue

Contraindications to using a wound vac

No active cancer in the wound
Dead/necrotic tissue in the wound
Untreated osteomyelitis (if osteo is being treated, it is fine)

Who qualifies for a wound vac at home?

if wound vac was started in the hospital, generally patients can go home with the vac, but a wound vac isn't always the best thing for a patient

wound vacs weigh 8-11 pounds, too heavy for some

need to have home health care (dressing change 3x/week, 1x/week has to be licensed person who measures the wound to demonstrate healing)

must be able to keep wound vac on 22 hours/day 

• Of note, patients should be off their wound vac no more than 2 hours/day
• When vac dressings are used in skin grafts, you must use non-adherent dressing between the graft and the foam
• Vac instill: instills fluid (e.g. normal saline) into the wound. Protocol: dwell time 10 minutes, 2 hour suction. Vac instill leads to 40% more granulation tissue than regular wound vac. Only available in acute care (hospital, some LTAC/some SNF
• Prevena vac is used along closed clean incisions, helps approximate the wound. Not for everyone, only place in patients who are high risk for dehiscence (morbid obese, redo). Put on in the OR. Entire product is disposable. When stops holding suction, battery makes noise, it shoudl all get thrown away. No wound care needed, no home health required.

• 

  Prevena vac

Our Wound Care Queen, Wendy Cardenas, finished off the presentation with these gems

Four stages of wound healing: hemostasis (immediate)>> inflammatory stage (6 days, WBCs/macrophages debride bioburden) >>proliferation (up to 3 weeks, this is where wounds get stuck, go from acute to chronic)>>maturation (can last up to a year, skin is never going to be exactly the same, always a place that can reopen, tensile strength permanently compromised)

How to approach a wound ala Wendy Cardenas

1) Figure out what happened

    chart review, look for all old notes pertaining to wound

    ask the patient, "How did this happen?"

    check for pressure points

2) Check for infection: is the surrounding tissue hot, red, indurated, painful?

    wound bed funky, milky, shiny, smell bad, creamy or copious fluid

3) Foot wounds: pressure, diabetic, venous vs. arterial ulcers

    venous: medial/lateral/posterior: irregularly shaped, shallow, yellow slough, not painful>> compress!

    arterial: medial/lateral: round, deep, pale bed, don't bleed easily, not much pulse>> no pressure!

4) Wound products you might use in the hospital

    foam dressings: prophylactic on sacrum or coccyx, heel + offloading boot

    plura-gel: adds hydration, cleans up wound

    silver-impregnated hydro-gel

    honey: better for superficial wounds

    zinc: moisture associated breakdown, good for venous stasis legs (use w/compression)

Additional pearls:

• do NOT ever do superficial cultures on wounds; superficial cultures will only reveal polymicrobial organisms and skin flora
• quantitative tissue cultures are gold standard
• silver is bacteriostatic 
• primary closure (clean wound), delayed primary closure (w/steristrips a day or two after), closure w/secondary intention
• skin graft wound vacs STINK when you first remove (5 days after a skin graft)
• if you have an abscess make a BIG BIG hole, making a tiny incision and packing will cause more pain. Big wounds are better

Diverticular Disease (Sawyer, 8/11/2021)

Diverticulitis is. . . 

• the 3rd most common cause of GI illness requiring hospitalization
• the leading cause of elective colon surgery
• a bit unpredictable but often managed medically
• 15% of cases ultimately require surgery 
• surgical indications: medical therapy failure (or not amenable)

Medical management

Medical/conservative treatment of uncomplicated diverticulitis generally involves antibiotics x 7-10 days

Note: there is NO high quality evidence regarding the ideal duration of antibiotics and which abx are superior

Good abx choices include: bactrim DS/flagyl (favorite of Dr. Sawyer), cipro/flagyl, levo/flagyl augmentin, and more

Diet

There is NO high quality evidence for specific dietary management of diverticulitis

Older surgeons prefer clear liquids x72 hours, advancing as tolerated after that (the rationale for this is really about possibility of surgery-- to be better prepared for a bowel prep if a surgery becomes necessary)

Of note, more recently trained surgeons will often let patients eat as tolerated (i.e. ad lib)

Of note, avoiding nuts, popcorn, seeds, corn, tomatoes, strawberries, etc is NOT evidence based and not necessary (JAMA 2008 paper). Do NOT tell patients to avoid these foods to prevent diverticulitis.

Known complications of diverticulitis:

• Perforation
• Fistula
• Obstruction

Perforations that are very small are characterized as microperforations: conservative treatment with abx (oral/IV) is appropriate for microperforations; of note,19% of microperforations go on to form abscesses. Random pearl: diverticulitis as seen on CT often looks "worse" than the patient. 

Classification of perforation

• Microperforation (not included in Hinchey classification system)
• Hinchey I pericolic or mesenteric
• Hinchey II walled off pelvic abscess
• Hinchey III purulent ascites
• Hinchey IV feculent ascites

Hinchey I and II can be managed non-operatively, III and IV should be managed with surgery

4cm abscess is used as the cutoff for IR drain placement

<4 cm diameter, abx alone usually sufficient 

>4cm diameter, IR drain + abx

if an abscess is exactly 4cm, it's at the discretion of the interventionalist/location of the abscess that determines best practice for management

What if it doesn't work?

If patients fail to improve after 48-72 hours of abx (usually repeat imaging is done), the next step is  a bowel preparation (if pt can tolerate it) and a surgical anastomosis. Of note, a "contaminated" peritoneum may require a diversion.

Surgical options:

colon resection w/primary anastomosis: one step, requires well-vascularized, non-edematous bowel, good nutritional status, good immune state (not immunocompromised)

colon resection w/proximal diversion

Hartman's procedure

open vs. minimally invasive: MIS preferred if feasible, shorter hospitalization/ileus and less pain. Long term, outcomes are about equal

Goal of surgical management of diverticulitis:

1. Source control: remove the perforated segment
2. Restore intestinal continuity-- depends on hemodynamics of the patient, degree of contamination, and surgeon preference/comfort

Free perforation (in an unstable patient) requires urgent damage control, which involves limited resection (if possible), peritoneal lavage, and usually a temporary abdominal closure. Alternative is a "Hartman's Procedure" with a limited resection, peritoneal lavage, end colostomy, and temporary closure.

• in a study of 58 patients with generalized peritonitis and perforated diverticulitis, 9% mortality (5 patients). OF the 53 survivors, 44 were stoma free at 2 years (pretty good!)

Stable patient with feculent peritonitis (Hinchey IV) generally requires Hartman's procedure.

• these can be difficult to close (only 50-60% have closure)
• need to wait 6 months to 1 year for all the inflammation to resolve before rehooking

Of note, BOTH require a second look (return to the OR) at 24-48 hours

Fistulas can occur:

colo-vesicular 65%

colo-vaginal 25%

colo-enteric 7%

colo-uterine 3%

Obstruction: if diverticulitis is leading to obstruction, you MUST rule out cancer. Stenting-- while can be helpful in cancer-- is not helpful in diverticulitis

And, finally, the SSRRH Diverticulitis PROTOCOL

• admit with IV abx
• re-image at day 2-3
• if improved on imaging--> abx management (7-14 days)
• if imaging stable OR worse--> 
• if drainable abscess, then IR drain, followed by surgery in 6-8 weeks,
• if abscess NOT drainable, then mechanical bowel prep with surgery in 1-3 days

Vomiting in Children (Mueller, 4/21/2021)

Many thanks to Dr. Claudia Mueller, Stanford and CPMC pediatric surgeon, for an excellent presentation on Vomiting in Children-- her lens, unsurprisingly, was on the surgical causes of vomiting in children. 

As a family medicine physician, I don't typically consider vomiting in children a "surgical" problem, but it was sure a good reminder that sometimes it is! It's a hearty crew of clinicians who want to assemble at 7:30am to talk about vomit-- but hey-I have to tell you-- her presentation was excellent!  AND the best part was that Dr. Mueller gave us a number to call if we ever run into problems. 

To watch Dr. Mueller's excellent presentation click HERE.

For the Cliff's notes version, here you go:

• Surgical causes of vomiting in children can rapidly progress to be life threatening
• Ask yourself How sick is this kid? Do they have fever, tachycardia, moist music membranes, lethargy? Can I get them to stand for the KUB?
• Presence of vomiting and ABSENCE of diarrhea is a concerning sign 
• This makes sense; most vomiting in kids is related to acute viral gastroenteritis or food poisoning, both of which should be accompanied by diarrhea. The absence of diarrhea is a sign that surgical causes of vomiting should be on your ddx
• The color of the vomit is key: color gives you some indication of the level the vomit is coming from (I know, I know, who wants to talk about the color of vomit) 
• this is particularly true in infants
• yellow/green (bilious) emesis in children <1 year is an "alarm bell that should be rung through the streets of any city" as it could be a surgical emergency (cardinal hallmark of a midgut volvulus that you do NOT want to miss)
• most children will vomit food and other particulate matter, if they vomit long enough, they will eventually vomit bile, so prolonged vomiting leading to bilious vomiting may be less concerning than it starting out bilious

• The intestine is a tube: in addition to the color of the vomit, what is coming out the bottom gives us a lot of information. If a child is having something out the bottom, they are much less likely to have true obstruction
• Passing gas is best indication (more even than bowel movements)

SBO

• Previous abdominal surgery is #1 cause of of adhesions causing SBO in children
• traumatic surgeries (e.g. trauma ex-lap) are more likely to lead to adhesions
• laparoscopic surgery maybe less risky (eg. laparoscopic appy) 
• Farting is a good sign-- air doesn't just hang out in the colon; a child that is passing gas, even if there is an obstruction, it is at least partial
• Be aware: not all kids with SBO get abdominal distention
• An UPRIGHT KUB is the imaging modality of choice to evaluate for SBO in a child
• want to be able to visualize: diaphragm, rectal gas
• UPRIGHT is super important: air goes to top, liquid down to the bottom
• air-fluid levels (straight lines) in SBO (can see in ileus, but more common in SBO)
• a sick child who cannot stand up for KUB is concerning
• CT scans can show more detail, e.g. the "point of the obstruction" but generally try to avoid CT scans in children <10 due to radiation
• if you do CT scan, should do IV contrast; used to always require oral contrast (and can be more helpful), but should be done carefully due to risk of aspiration 

Upright KUB showing SBO

• Initial treatment: NGT for decompression 
• NGT should be adequate size (if it's too small, won't work as well). An NGT an actually treat SBO by relieving the pressure
• Babies, size 10-12
• Toddlers, size 12-14
• age >7 years, size 14
• teenagers/adults, minimum size 14, better >16
• NGT has to be flushed, or it will get clogged
• If NGT is working, as evidenced by the amount coming out of NGT decreases, and child starts feeling better, you may be able to avoid surgery
• Another option after NGT: small bowel follow-through with gastrograffin (or ominpaque) can be diagnostic AND therapeutic
• 25-50cc, repeat KUB 6-12 hours after administration: decreases hospital stay either because quicker to OR vs. able to discharge home
• Hydration and serial abdominal exams are important in SBO

Midgut volvulus is the most urgent cause of bilious vomiting, usually in children <1 year old (85% before 6 months, 95% before 1 year)

• A true emergency is caused because mesenteric vein and artery get twisted, no blood flow to the entire small bowel (colon and first/second part of duodenum have their own blood supply)
• Can be life threatening in a few hours
• Perfectly healthy baby totally fine, suddenly starts throwing up yellow/green, call a surgeon!
• Imaging: UGI shows cutoff; x-ray may show just a stomach bubble (no other gas)
• Consequence so dire: lose entire small intestine, may never be able to survive not on TPN

Pyloric Stenosis typically thickening/hypertrophy of pyloric muscle fibers

• No one know why it happens
• Usually age 2 weeks to 2 months, classically first-born males
• Non-bilious (breastmilk or formula), progressive and persistent
• Imaging: ultrasound
• Surgery: cut open hypertrophic fibers, outer layer and spread it (pyloromyotomy)
• Typically does not recur

Appendicitis

• n/v, abdominal pain, umbilical down to RLQ
• renewed interest in conservative management with antibiotics only
• 95% of cases can be treated with antibiotics only, but 20% will recur in 1 year, 30% in 5 years
• fecolith has VERY high recurrence, should be operated lap appendectomy

Ileocolic intussusception

• generally age 6-36 months
• small part of small intestine gets stuck in large intestine
• usually due to laxity, lead point usually a lymph node, can be seen after enteritis OR after immunization (e.g. rotavirus vaccine)
• Imaging: ultrasound, "target sign"
• Reduction via radiology (air or contrast from anus into rectum, pushes the intussusception , reduces the small intestine), works large majority of time in kids without ischemia
• 10% recurrence rate-->  to OR
• Older kids need work up, lead point (e.g. lymphoma)

Hernias

• bilious vomiting, if incarcerated
• remember to take off vomiting baby's diaper to look for non-reduceable hernia

Hospital Care of the Patient with Super Obesity (Kirchner, 11/11/2020)

Thanks to Dr. Julia Kirchner for a great Grand Rounds presentation this week on Super Obesity. Dr. Kirchner walked us through the myriad of ways in morbid and super obesity add physiological complexities to patient care and can seriously affect patient outcomes. The list of acute and chronic health implications of obesity is long, and the physiology is dense but also very interesting! In addition, don't forget the role that our explicit and implicit biases play into our care of obese patients.

For clarity, definitions of obesity:

Overweight: BMI >25-29.0

Obesity: BMI >30

Morbid or Extreme Obesity:  BMI >40

Super Obesity: BMI >50

• 9.2% of US population is severely obese
• Super obese is the fastest growing subgroup (maybe up to 1% of the population)
• Morbidly obese patients have increased ICU length of stay, with particularly well documented increased morbidity and mortality in obese trauma patients 
• In obese trauma patients: OR 1.4 mortality OR 1.8 in hospital complications (pneumonia, ARDS, UTI)
• Having a pulmonary diagnosis on admission increases with increasing BMI, and there is an increased need for non-invasive mechanical ventilation (NIMV)

Transport and transfer issues:

• stretchers with higher weight limits
• bariatric wheelchairs
• lift team
• adequate O2 for transport
• staff capability and training

Hospital Capacity issues:

• bariatric beds
• room layouts (doorways, hallways)
• bedside commodes, walkers
• lift equipment
• larger BP cuff (see Table 3), gowns, larger NIMV masks, longer needles
• imaging capabilities
• staff training

Physical Exam of obese patients, can be challenging: including heart and lung auscultation, abdominal exam and skin survey

Labs: 

• Obese patient tend to have higher baseline CO2
• We should use a higher BNP cutoff >54 (for BMI >40)
• Be aware of possibly inaccurate SCr (consider using a GFR calculator)

Imaging capabilities are often limited: 500lb weight max on CT scanner (30 inch maximum circumference), also higher rates of uninterpretable CXR (see image), challenges with ultrasound (difficult FAST exam, may need TEE)

Medications may need dosing modifications based on several factors, including weight, type of medication distribution, and renal and hepatic metabolism. Here is a link to a calculator for body weight calculations: idea/actual body weight and this is a really great resource for medication dosing in obesity called ClinCalc.

Okay, now for some serious physiology and pathophysiology

Respiratory issues are a BIG deal in the care of morbidly obese patients. Predisposing factors that make obese patients at risk for respiratory distress include: underlying chronic respiratory failure (that is why that elevated baseline CO2), difficulty with airway maintenance, higher baseline oxygen consumption, impaired central response to hypercapnia and hypoxia, and disordered gas exchange. 

• 42% of morbidly obese patients will require NIMV regardless of reason for admission
• AVOID SUPINE position (exacerbates everything), consider HOB elevated vs. reverse trendelenberg
• high PEEP may be indicated (starting 10, up to 20-25)
• care with fluids

Obesity hypoventilation is super common and important in our care of morbidly obese patients!

• BMI>30
• daytime hypercapnea (pCO2>45)
• disordered breathing during sleep
• all other dx excluded

Cardiac complications and Renal complications are common. Often these are acute on chronic. Take home points:

• Care with IV Fluids
• Consider ADJUSTED weight based dosing of IV fluids
• Have high suspicion for underlying renal and cardiac disease that may be undiagnosed but is very likely present. 
• care with nephrotoxic drugs
• low threshold for telemetry monitoring

lCVD=cardiovascular disease, IAP=intra-abdominal pressure, RV=right ventricle, LV=Left ventricle,

AKI=acute kidney injury, CO=carbon dioxide, AKI=acute kidney injury

And finally, how we treat patients matters!

Bias and Obesity:

"Weight appears to be the last acceptable bias", Rita Rubin writes in JAMA, article available here. The general population AND physicians show very high anti-fat bias and there is clear evidence of bias and discrimination against obese patients. There is an intersectionality with race and racism in this country that we need to be aware of, as there are higher rates of obesity in Hispanic and Black populations.  

T"Weightake home

Small Bowel Obstruction (Sawyer 4/15/2020)

Big thanks to Dr. Russ Sawyer for an excellent presentation this week on Small Bowel Obstruction (SBO) during Grand Rounds. We are all getting better and better at this Zoom platform!

Cliff notes version of what primary care providers should know about SBO:

1. Lactate is highly sensitive for SBO (but not that specific)
2. The money is in the CT scan (CT is BOTH sensitive and specific)
• with IV+oral contrast is are ideal, but IV contrast only is probably okay
3. Many SBO patients don't need surgery (you actually can let the sun set on an SBO)
• In fact, all patients NOT acutely ill (w/fever, leukocytosis, tachycardia) deserve a trial of non-operative management
• SBO patients with a BM in last 24 hours likely will not need surgery
4. Gastrograffin challenge is an effective way to differentiate patients who may need surgery vs. those who definitely don't. 
• 90cc PO or via NGT x 8 hours in early/minimal symptom SBO (see below for details)

And now for the more robust version of my notes for those of you more in depth readers. . .

SBO is super common, >$1.5 billion per year in the US go to management of SBO

Classification of SBO

• functional (i.e. adynamic ileus)
• mechanical (acute vs. chronic, partial vs. complete) 
• adhesions (account for 80% of SBO)
• hernia (internal, groin, ventral)
• malignancy
• inflammatory disorders (IBD, ischemic bowel)

Pathophysiology of SBO

obstruction prevents people from passing food and air --> interluminal fermentation causes gas to accumulate--> bowel edema--> diminished absorption and decreased motility--> can gt transudative losses into the abdominal cavity (free fluid in the peritoneum)

Stats reminder from Dr. Sawyer, which is always helpful to review

Sensitivity: "positivity in disease" (how much you trust a positive result to mean the patient actually has that condition)

Specificity: "negativity in health" (how much you trust a negative result to mean that the patient actually does NOT have that condition).

(We are talking a fair bit about sensitivity and specificity this day with COVID testing. This is an excellent reminder!)

Clinical History

• Acute abdominal pain (92%), usually precedes the onset of nausea/emesis
• Nausea 
• Emesis (82%-- more common than nausea)
• Abdominal distention

Risk factors

• Prior abdominal or pelvic surgery (even a simple appendicitis many years ago)
• Abdominal wall or groin hernia (even internal hernia)
• IBD
• Prior irradiation of the abdomen

Physical exam

• Dehydration (even if not apparent on labs), often notable on physical exam (dry mucous membrane, decreased skin turgor)
• Abdominal distention (most important finding on exam)
• Surgical scars
• Tympanic abdomen
• High pitched bowel sounds or more commonly a rush of bowel sounds

Labs

• Leukocytosis is common
• Electrolyte abnormalities (hyperNa, hypoK)
• Lactate is helpful. It's extremely SENSITIVE 90-100%, Specificity 40-80%. This means that a positive lactate gives high likelihood of surgical SBO, but a normal lactate does not rule out an SBO

Imaging: "Everything in SBO comes down to imaging"

• Plain film (KUB): not very specific or sensitive (equivocal 20-30% of the time, misleading in 10-20%), consider skipping it and going straight to the CT
• CT with IV contrast (+oral contrast if possible-- oral contrast commits patient to 4 hours in the ER, often get get enough info with just IV contrast), 
• >90% sensitive, 95% specific. So you can pretty much trust the CT. 
• If the radiologist sees it, it's there. If the radiologist doesn't see it, it's not there.
• CT can usually tell grade, severity and even etiology (adhesion vs. malignancy)
• However, intra-operative location is only correct 60-70% of the time
• MRI (if CT contraindicated, e.g. pregnancy)

Surgical vs. Non-surgical Management:

Patients with SBO should be evaluated for surgical intervention WHEN/IF they are acutely ill with fever, leukocytosis, tachycardia, metabolic acidosis, ongoing pain.

HOWEVER, without the above findings (or with only a few of them) MOST patients should undergo initial non-operative management (this includes both partial AND complete SBO). How so?

Management of early/minimal symptom SBO (with Gastrograffin)
For patients who meet these criteria, Dr. Sawyer and team are working on a protocol to be started soon

If patient meets the following criteria:

1) SBO on CT, 2) distention w/o emesis (x8 hours, or at least minimal emesis, only need NGT if emesis), 3) BM in the last 24 hours, 4) minimal leukocytosis (<14), lactate (<4), THEN you can give them a gastrograffin challenge

How do I do a gastrograffin challenge for minimal symptom SBO?

1. Give patient 90cc of full strength gastrograffin (via NGT or PO);  order from pharmacy (not radiology)
2. Wait 6-8 hours for BM (up to 24 hours). If they have plenty of BMs, they passed! You don't even need to do KUB
3. If no stool in 8 hours, get KUB to look for gastrograffin. 
4. If it has made it to the colon, can pull NGT, start clear liquids and probably let them go home. 
5. If no contrast in cecum, repeat KUB next day. If in the colon, start clear liquids. If not, call surgery.

How does gastrograffin work? For this purpose, it is actually being used therapeutically (rather than diagnostically). Gastrograffin pulls fluid into the lumen and "flushes things through", decreasing the bowel wall edema and improving the SBO.

Who NOT to give gastrograffin challenge to? 

• infection (e.g. appendicitis, diverticulitis)
• cancer
• incarcerated hernia
• pregnancy
• abdominal surgery in last 6 weeks

Prevention of SBO:

There is not great data on any intervention or product done intraoperatively to prevent adhesions and prevent SBO. However, if a patient has had a first episode of SBO or recurrent SBO, Dr. Sawyer recommends:

• low fat diet (maintains intestinal transit time)
• clear liquids are tolerated well (4-6 days): patients with SBO do not need to go home on a regular diet, once a patient feels true hunger, it's time to eat

Recurrence

• 20% recurrence after first episode
• after 3 episodes, their risk of recurrence is greater than 80%, need to consider surgery to lyse adhesions (depending on interval between the recurrences)