An Epidemic of Loneliness (Naderi, 4/29/2020)

Such an important topic this week from Dr. Tahereh Naderi: An Epidemic of Loneliness. While she focused her talk on loneliness in elders, her presentation certainly has me pondering a loneliness in my own life-- especially in pandemic times.

What is loneliness? It's subjective: it's your own perception of the lack of interaction
What is social isolation? An objective lack of meaningful and sustaining communication and/or interaction.

Risk factors for loneliness include: older age (esp >80), poor subjective health and self-reported functioning, large number of chronic illnesses, impaired hearing, functional disability, lack of mobility or motor decline, hopelessness, depressed mood, psychiatric morbidity (e.g. depression), quality and quantity of social interactions, living arrangements, low SES, and race.

2 in 5 Americans report they sometimes or always feel their social relationships are not meaningful.
1 in 5 Americans feel lonely or socially isolated
In the past decade, average household size has decreased leading to 10% increase in people living alone, 28% of older adults live alone
Over the past 2-3 decades, the average size of our social networks has declined

The impact of loneliness is real:

• greater risk of cognitive decline and dementia
• lower self esteem and limited use of coping mechanisms
• increase in personality disorders, schizophrenia
• increase in risk for depression
• predictive of suicidal ideation and behavior
• increased substance use (especially alcoholism)

And what about quarantining?

Data following the SARS health crisis in China in 2003, found that quarantining had particular impact on healthcare workers even after restrictions were lifting including:

• low social contact
• avoiding enclosed public spaces
• not returning to work
• long term behavioral changes such as excessive hand washing

Isolation can exacerbate feelings of anxiety, anger, and pre-existing symptoms, can increase one's risk of developing PTSD, and interrupt treatment for substance use disorders. 

Dr. Naderi reminded us (we need to keep hearing this) that social distancing DOES NOT equal social isolation.

Also, guess what? There is an antidote to loneliness: social connection. Social connection actually makes people healthier!

• A meta-analysis including >300K people concluded that greater social connection is associated with a 50% reduced risk of early death
• In studies of the "blue zones" (regions in the world with the greatest concentration of centenarians), social connection is a component of 4 of the 9 of the power principles. The power principles are the 9 lifestyle habits that seem to be associated with longer, healthier, happier lives. 

Believe it our note, we can work on increasing or firming up our social connections in several different ways-- through mindfulness and acceptance, increased use of technology (yep, it's true, even for seniors) and intentionally reaching out to others to form community.

• A randomized controlled trial using mindfulness-based techniques was able to reduce loneliness by 22% and increased social interactions in daily life by 2 more interactions per day and one additional person per day!
• The use of technology-- even in seniors-- can effectively decrease loneliness (multiple modalities including email, video conferencing and computer training). 
• Shared activities were effective: gardening, physical activity, visual arts discssion, even animal therapy!!

Dr. Naderi introduced us to the concept of  Moais (模合, Mo-ai):social support groups that form in order to provide varying support from social, financial, health, or spiritual interests. Moai means "meeting for a common purpose" in Japanese and originated from the social support groups in Okinawa, Japan. These have been studies as part of the blue zone studies.

While Okinawan Moais are inherently built in to society, we may have to be more proactive about reaching out and creating ours. If you don't have one, consider taking steps toward forming a Moias. Or identify and strengthen the one you have. 

Dr. Naderi concluded with an quote by Vivek Murthy, internal medicine physician, 19th Surgeon General of the US, who took a particular interest in loneliness as surgeon general:

"The irony is that the antidote to loneliness, human connection, is also a universal condition. In fact, we are hardwired for connection-- as we demonstrate every time we come together around a common purpose or crisis- and even now as we face the global COVID-19 pandemic and resort to physical distancing to reduce the spread of the virus, we are recognizing that we cannot make it through fear, dager, and uncertainty of the current moment without supporting one another. "

Go ahead, close this browser, call that person you've been meaning to call. You won't regret it.

Cardiovascular Benefit of New Diabetes Medications (Magnotti, 4/22/2020)

One of the reasons I love Grand Rounds is that each week I know-- whatever the topic, whomever the speaker-- I will walk away wiser. My curiosity will have been piqued. I will have learned something. I will have been challenged.  I will be a better family physician. And I will have often have new (more educated) questions.

And as expected, this week, Dr. Mike Magnotti (SMGR Endocrinology) did not disappoint. He gave an excellent presentation on the cardiovascular benefits of two classes of "new" diabetic medications: GLP-1 analogs and SGLT-2 inhibitors. Definite practice changer for me.

Here are a few questions to start you off:

• Do you manage your diabetic patients with cardiovascular disease  (CVD) differently than those without CVD?
• Are you aware of the evidence that both the GLP-1 and SGLT2-inhibitors reduce stroke, MI and possibly even CV death in diabetics with CVD?
• Are you using GLP-1 agonists for cardiovascular benefit?  What about SGLT-2 inhibitors?
• How do you (and your patients) assess whether or not they should be on one of these new meds?

I don't know about you, but I have a hard time keeping these medications in my head-- the names are complicated, the abbreviations don't make it simpler, the mechanisms of action are new, and nothing sticks. Plus, until recently they have been unavailable to most of my patients due to cost and/or insurance restrictions.

In case you are in the same boat as me, here's a brief summary of the two classes of meds Dr. Magnotti presented evidence for in CV risk reduction:

GLP-1 agonists: glucagon-like peptide 1 agonists (aka incretin mimetics) are almost all INJECTABLE medications (except for one new oral version of semaglutide). They act on the gut: improve glucose-dependent insulin release, suppress glucagon, suppress hepatic glucose output, decrease the rate of gastric emptying, and suppress appetite.  

• Benefits of GLP-1 agonists include HbA1c reduction of 1.2-1.7%, weight loss, no risk of hypoglycemia (unless combined with insulin or sulfonylurea), and CV risk reduction  (non fatal heart attack and stroke-- see below for details)
• Side effects: mostly GI (nausea, vomiting, constipation, diarrhea), headache, injection site reaction, possibly pancreatitis, and a black box warning MEN2 or medullary thyroid cancer
• Currently available forms: short and long acting exenatide, liraglutide, dulaglutide, semaglutide (oral and sq)

SGLT-2 inhibitors: sodium-glucose co-transporter-2 inhibitors (aka gliflozins) are ORAL medications that inhibit resorption of glucose into the kidneys, thereby lowering blood sugar

• Benefits of SGLT-2 inhibitors include: Hba1c reduction 0.8-1.2%, systolic BP reduction (~5mm Hg), weight loss (2-4% of body weight), heart failure risk reduction, slowed progression of CKD, CV risk reduction (non fatal heart attack and stroke-- see below for details), and even CVD death reduction (empagliflozin only)
• Side effects:  yeast infections (women>>men), UTI/pyelo, polyuria, transient decrease in GFR, orthostasis (esp in elderly), small increase in LDL, hypoglycemia (if combined with sulfonylurea, insulin), DKA with minimal glucose elevation, increase in fractures, possible increase in amputation, fournier's gangrene
• Currently available forms: canagliflozin, empagliflozin, dapagliflozin, ertugliflozin

Is HbA1c lowering the only outcome that matters?
Standard diabetes management has focused on reduction of HbA1c, which we know prevents progression of microvascular disease but has little effect on macrovascular outcomes. HbA1c goals are the metric by which we have considered a patient "controlled" or "uncontrolled". You all know, our  goal is HbA1c<7 in most adults, <8 in elderly and those with significant comorbidity.  Secondary goals have been to prevent/avoid hypoglycemia and prevent weight gain/promote weight loss.

It may be time to rework our paradigm; start thinking diabetes meds in CV Risk Reduction
Yes, we know lowering HbA1c is important to prevent retinopathy, diabetic nephropathy, peripheral neuropathy. However, we also know that cardiovascular disease (CVD) is an important cause of morbidity and mortality in diabetic patients. What if there were medications that reduce HbA1c and also reduce the risk of MI, stroke, and CV death?

Guess what? There are! Both the GLP-1 agonists and the SGLT-2 inhibitors seem to have a positive effect on CV outcomes (ie they reduce heart attack, stroke, and maybe even CV death). To be right up front, no one is exactly sure why.

Since 2008-- due to concern about thiazolidinidiones (TZD) actually showing increased CV risk in diabetic patients-- the FDA has required that any new blood sugar lowering med be evaluated for cardiovascular safety ("a cardiovascular outcome trial" or CVOT). Most of these studies use a composite endpoint called a 3 point MACE (time to a Major Adverse Cardiac Event, including non-fatal MI, CVA or cardiovascular death). Initial studies found most novel diabetes meds to be neutral, but  more recently, they started to show some benefit.

Here are the studies Dr. Magnotti reviewed during Grand Rounds:

• EMPA-REG: (empagliflozin), NEJM 2015
• DM2, a1c range 7-10%, BMI<45, established CVD--> primary outcome 3P MACE 
• Relative risk reduction of 38%, 2.2% Absolute risk reduction
• NNT 46 patients for 3.1 years to prevent on CV death (for comparison sake, NNT is 31 patients for simvastatin x5.4 years, 49 patients with ramipril x 5 years)
• There were also significant reductions in all-cause mortality and heart failure hospitalizations
• FDA indication for empagliflozin: to reduce risk of CV death in diabetic patients with known CVD
• CANVAS/CANVAS R (canagliflozin), Circulation 2018
• Primary outcome: 3P MACE
• Relative risk reduction 14%, NNT=224
• LEADER: (liraglutide), NEJM 2016
• Primary outcome: 3P MACE
• Relative risk reduction, 13%, 3P MACE
• Reduction in all cause mortality 15%, CV death 22%
• SUSTAIN 6 (semaglutide injection), NEJM 2016
• 26% relative risk reduction 3P MACE

Dr. Magnotti's summary of the literature: 

• To date, 5 new diabetes agents have been shown to lead to a significant reduction in 3 point MACE. 
• This effect is INDEPENDENT of A1c and other risk factors. 
• These were all measured in addition to other standard of care therapies (such as ASA and statin)

In light of these studies, both the American Diabetes Association (in 2018, again in 2020) and the American COllege of Cardiologists (ACC, 2020) have updated their guidelines with regards to using SGLT-2 and GLP1 medications in diabetes. 

For patients with known ASCVD, these medications should now considered first line after metformin (see diagrams below from ADA and ACC).

ADA guidelines HERE in FULL text (snippet of image).

ACC guidelines HERE in FULL text (snippet of image). 

In Type 2 patients with Diabetes AND CVD (ie. known CAD, hx MI, hx CVA, PVD), regardless of A1c or current diabetes therapy, patient should be started on EITHER GLP-1 (liraglutide daily injection, dulaglutide weekly injection, semaglutide weekly injection) OR SGTL-2 (empagiflozin oral, canagliflozin oral)

Dr. Magnotti's Considerations when choosing an SGLT2 vs. GLP-1

• SGTlL-2 in patients with Heart Failure, CKD (GFR>30), those who might need improved BP control (or who you aren't worried to be on a diuretic), someone with history of pancreatitis, gastroparesis, significant nausea, or MEN2/MTC
• GLP-1 in patients who need MORE Hba1c reduction, CKD with GFR<30, recurrent yeast infections or UTI, concern for risk of DKA or other potential side effects from SGLT-2

Some practicalities:

You don't need to adjust a patient's other diabetes meds UNLESS they are on insulin or sulfonylurea (for risk of hypoglycemia)

• IF they are on a sulfonylurea:
• A1C<7 to 7.5, stop the sulfonylurea
• A1C 7.5-8.5, cut sulfonylurea dose in half
• A1c >8, no change
• IF on basal insulin
• a1c<7, cut insulin dose in half
• a1c7-8, reduce insulin dose by 20%
• IF on prandial insulin, consider getting endocrinology input OR cut prandial insulin at least in HALF. 
• IF patient on antihypertensive, for SGLT2, consider reducing dose, if diuretic cut dose or stop

What about insurance coverage?

Coverage has substantially improved for these medications with CV indications. (Even with Partnership Health Plan). There are NO other medications that can be used for "step therapy" for CV risk reduction, so be sure to prescribe these under CVD (rather than DM). 

What about patients who don't want to take an injection?

If the patient meets criteria for a GLP-1 but doesn't want an injection, remind them: 1) this isn't insulin 2) they will likely LOSE weight and improve their blood sugar control and 3) they will reduce their risk of heart attack and stroke. Then get them nursing and diabetic educator assistance with getting over the injection!

If you work in the hospital, you might at least consider discharging every diabetic patient with established CVD (MI, CVA, TIA, PVD) on a GLP-1 or SGLT-2 agent. 

******************
Another reason I love Grand Rounds is that I love sitting in the same room with engaged, big-brained, big hearted colleagues. (This is the part I miss during our shelter in place-- Zoom works-- but it sure isn't the same). Join us next week on Zoom. We will be back in that conference room eventually.

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)

Reflections on Inequity and Solidarity in the Pandemic Present (Holmes, 4/8/2020)

Many thanks to Dr. Seth Holmes, who jumped in late to present a terrific and timely Grand Rounds this week on Inequity and Solidarity in the Pandemic Present.

As a great thinker and scholar, Dr. Holmes took us through history, sociology, anthropology, philosophy, and breaking news to challenge the lens we use to view our current state of the COVID-19 Pandemic. And to insist that while we comply with physical distancing, we should simultaneously be striving toward social solidarity.

Some questions to start us off:

• How does the novel Coronavirus pandemic follow the fault lines that already existed in our society-- particularly the inequalities and the discrimination?  How does this pandemic force us to look anew at these fault lines?
• Is this an historic opportunity to think about what kind of society we want to be-- to remedy those inequalities so that our health system and our social system can be more healthy, more safe, more truly democratic, and more inclusive for all people? 
• While we undoubtedly need to adhere to physical distancing recommendations, how can social solidarity help us survive this and any future pandemics?

In his presentation Dr. Holmes invoked several scholars' work on the notion of SOLIDARITY:

• French sociologist Emil Durkheim, who studied societies and asked the question: How do societies hold together despite social differences and increasing division of labor? His answer: Social solidarity: the sentiment and practice or feeling and action of interdependence between individuals and groups in a society

• Physician and scholar from Martinique, Frantz Fanon: Solidarity can and must transpire in the midst of social difference, including solidarity across national lines (against colonial powers) and between people within the countries against colonization, as well as solidarity across racial lines (against racist social systems)

• Educator and theorist Paolo Freire: Solidarity is a collective project. .  capable of changing not only the ways in which society is structured but also has to change everyone who is involved (people with less and more power) . . .Liberation brings about transformation of the exploited and the exploiter.

• Combahee River Collective (Robin D. G. Kelley, Angela Davis): Solidarity as coalition building recognizes connections between different forms of inequity, different forces of exploitation, and highlights the need to stand together for the good of everyone. . .this is difficult to achieve in the US in which individualistic models of health are most common.

And as we ponder our place in this pandemic and many of us work on the front lines in hospitals, clinics, and facilities across Sonoma County and beyond, Dr. Holmes challenged us to ask ourselves the following.

How might we use social solidarity during this pandemic to. . .

• protect our mental health? 
• avoid social constructs of stigmatization?
• build systems that benefit the health of all?
• protect the health of everyone, including (and especially) those who have been most marginalized our society?

As former US Secretary of Labor Robert Reich pointed out in a recent opinion piece,  "In many senses, our country doesn't have a fully functional public health system. Instead we work in a for profit health care system that is disjointed and ill-prepared for this crises and future crises. . .If we want to survive this and future pandemics we must understand how critical our public systems are for everyone in our society.

Let us not overlook the effect of this pandemic our most vulnerable, those who are

• incarcerated
• detained
• homeless
• poor
• people of color
• Recent Atlantic article by Ibram X. Kendi: inordinate numbers of people of color dying at roughly twice the rate of white people in the US (histories of institutional and structural racism) (Ref: What the Racial Data Show: the pandemic seems to be hitting people of color the hardest)

We are all in this together. We must stay connected. We must confront racism, xenophobia, and stigmatization. We must fund our public health and social systems. We must support those most marginalized, stop incarcerating and detaining those on whom our system relies.

With social solidarity, we can change our system.

Evidence-Based Management of the Second Stage of Labor (Guerrero 4/1/2020)

Muchas Gracias to Dr. Kiana Guerrero, who delivered our second shelter-in-place zoom Grand Rounds at SSRRH. She did so with great grace and great thought-- as she does most things. The topic was Evidence-Based Management of the Second Stage of Labor.

Some definitions:

• Second stage of labor: full cervical dilation (10cm) to delivery
• Spontaneous vaginal delivery: delivery that occurs without the use of forceps, vacuum, or cesarean delivery
• Delayed pushing: delay after full cervical dilation to allow for spontaneous decent. Patient starts pushing on average 60 mins – 180 mins after complete dilation
• Immediate pushing: patient would start pushing on average 15 mins after complete dilation
• Spontaneous pushing/physiological pushing: pushing after full dilation without instructions; may push with an open glottis and vocalization or use an intermittent
• Directed pushing/Valsalva pushing: pushing after full dilation against a closed glottis

Question 1: Should we encourage patients with an epidural to "labor down"?
Answer: Probably not.

In a 2018 Randomized Control Trial of  2414 nulliparous women, >37 weeks, all with an epidural, randomized to immediate pushing vs. delayed pushing

• There was NO difference in normal spontaneous spontaneous delivery and NO difference in rates of c-section in the two groups
• However, there were differences in postpartum hemorrhage (PPH), chorio, newborn outcomes, and other potentially important secondary outcomes
• The immediate pushing group  had shorter total duration of second stage, lower risk of  PPH and lower risk of chorioamnionitis, as well as  a lower likelihood of neonatal acidemia and suspected neonatal sepsis
• The delayed pushing group had shorter mean duration of active pushing (by about 9 minutes) and a lower likelihood of third degree laceration

(Reference: Cahill, Alison G., et al. Effect of Immediate vs Delayed Pushing on Rates of Spontaneous Vaginal Delivery Among Nulliparous Women Receiving Neuraxial Analgesia.)

After reviewing this study, Dr. Guerrero was left with more questions: 

• Would even more time for laboring down (i.e. >60 minutes) be better?
• Would the outcomes be different for multiparous women?

Dr. Guerrero used a 2012 Systematic Review  Tuuli, et al, to answer these questions. This review featured 12 RCTs (~1500 patients in each group: immediate vs. delayed), with primary outcome spontaneous vaginal delivery. There was variable quality and mixed results, but here are Dr. Guerrero's take home points:

Answer 1a: Longer isn't better. Largest study showed that maternal fever was nearly two-fold higher among women who delayed pushing. Risk of maternal fever increased in a dose–response fashion

• RR 1.14, 95% CI 0.54–2.38 for delayed less than 1 hour
• RR 1.73, 95% CI 1.10 –2.72, for delay of 1–2 hours
• RR 2.33, 95% CI 1.54 –3.51 for delay greater than 2 hours

Answer 1b: There isn't enough data specifically for multiparous women; the studies that have been done with multips are of poor quality.

(Reference: Tuuli, et al, Immediate Compared with Delayed Pushing in the Second Stage of Labor: A Systematic Review and Meta-Analysis, Obstetrics and Gynecology, September 2012, Voume 120, Issue 3, 660-668)

Question 2: Should we control how a woman pushes during the second stage?
Answer: Probably not.

Dr. Guerrero cited a Cochrane Review (see reference) of 8 trials, including 884 women. The largest study in the meta-analysis found the following:

• NO clear difference in spontaneous vaginal delivery comparing spontaneous pushing and directed pushing groups
• Spontaneous pushing may decrease the duration of pushing by about 10 minutes
• No difference in rates of perineal tears (3rd and 4th degree), risk of episiotomy, admission to NICU or 5 minute APGAR <7

(Reference: Lemos, Andrea, et al. Pushing/Bearing down Methods for the Second Stage of Labour. Cochrane Database of Systematic Reviews, 2017)

Question 3: Is there a "best" position for women to be in during second stage?
Answer: We don't know.

Dr. Guerrero gave us a quick peek at two recent studies asking whether a woman's position affects the birth outcomes: a 2017 Cochrane meta-analysis and a 2017 BUMPES RCT (comparing upright vs lying down)

• A 2017 Cochrane Review found that for nulliparous women without an epidural, the upright position showed a reduction in rates of episiotomy, assisted vaginal delivery and a very small reduction of duration of second stage 
• BUT upright position was associated with an increase risk of 2nd degree tears and blood loss >500mL
• The 2017 BUMPES RCT concluded that for nulliparous women with low-does epidural, the lying down position results in more spontaneous vaginal delivery
• Hmmm. . . .

(References:  Gupta et al, Position in the second Stage of Labor for Women without Epidural Anesthesia, Cochrane Systematic Review, 25 May 2017 and  

Brocklehurst et al, Upright versus lying down position in second stage of labour in nulliparous women with low dose epidural: BUMPES randomized controlled trial, BMJ 2017). 

Grand Rounds often one leaves with more questions than answers. See you next time!