Medical Evaluation of Suspected Child Abuse (Tayama and Evans - 8/23/23)

 A recording of this presentation can be viewed HERE.

***

This week's Grand Rounds Presentation, by Kaiser physicians Drs. Tricia Tayama and Michele Evans, on Medical Evaluation of Suspected Child Abuse, was an excellent review of when to suspect physical abuse, how to systematically approach a patient and family, and a reminder to check your biases while doing so.

I highly recommend you take 45 minutes to watch this one.

They covered medical history taking, physical exam findings, sentinel injuries, and how to minimize bias and disparities in suspected abuse. 

My notes: 

History

• use open ended questions (e.g. "tell me how this injury happened")
• take separate histories from everyone caring for the child (e.g. father, mother, grandparent)
• don't interrupt the patient
• be specific with your word choices, particularly if working with an interpreter
• clarify the mechanism of injury AND scene evaluation (e.g. stairway, toy, bed height)
• be aware of specific developmental skills (e.g. some 3 month olds do not roll, others roll actively)
• clarify when the child was "last normal"
• use humble inquiry, particularly with regards to discipline, cultural practices, and checking your own biases

Physical Exam

• do a thorough, undressed medical exam in person 
• this is NOT the time for telephone or video visits
• missed areas to examine: behind the ears, inside the mouth, anything covered by diapers, clothes shoes
• measure head circumference for any child under 2 years old

Photo documentation

• photos are extremely important to document injuries, but you are not the investigator, you are the clinician. Photograph injuries that will be helpful for your medical management and decision-making
• multiple views, show location, consider using a ruler or standard object (e.g. coin) to show the size of the injury
• use modesty
• get permission
• 
  
  
  

Sentinel injuries

Sentinel injuries are not confirmation of physical abuse, but they are injuries that definitely merit further evaluation. There are two pneumonics to help you remember sentinel injuries. 

• TEN-4
• T is for torso ("spine is fine")
• E is for ear
• N is for neck
• any TEN location in a child younger than 4 years old, or ANY bruise in an infant younger than 4 months old
• 
  
  
  
• FACES-p
• F is for frenulum (mouth in an infant)
• A is for angle of the jaw and auricular area
• C is for cheek (soft part)
• E is for eyelid
• S is for sclera, subconjunctival hemorrhage (whites of the eyes, care with newborns who can have such hemorrhages with traumatic birth)
• P is for patterned bruising

Labs and Radiology

the less verbal the child, the more evaluation needed

• standard of care for any child <24 months is a skeletal survey to check for fractures
•  this must always be repeated 2-3 weeks later to evaluate for any missed or new fracture
• this is ideally read by a pediatric radiologist (locally, can be done at SRMH but not read by pedi radiology)
• takes up to an hour to complete, can be a lot of the child and the parents

AND

• head CT with 3D reconstruction

Medical Evaluation depends on age of child, cut-off is generally younger than two years old

For a child 0-23 months, 

• Screen for bleeding disorders and metabolic/genetic conditions (with blood work). 
• If there is any sign abdominal injury or trauma (pain, bruising), screen with AST/ALT/amylase and lipase. If these are abnormal (usually defined as AST/ALT > 80), get a CT scan of the abdomen.
• 2 skeletal surveys (2-3 weeks apart, the second one generally excludes skull, spine, and pelvic bones)
• Dilated eye exam by optho to r/o retinal hemorrhage
• CT for any head injury <1 year old
• Urine tox (if indicated)
• other medical care

For a child 2+ years of age,

• a thorough undressed physical exam with pictures of any findings
• IF there are any findings, then do additional evaluation
• e.g. labs/imaging for abdominal trauma
• Xrays are only done PRN, skeletal survey not usually done, only xray body parts that need to be imaged based on your exam and history
• Urine tox if indicated
• Other medical care

If there are household contacts (e.g. twins, siblings), they should receive age-appropriate evaluation. A twin under 2 should also undergo skeletal survey.

Resources for family: it is our job not to decide who is abusing a child or what is the extent of the abuse. We are mandated reporters, and our job is to assess the child medically and document any evidence of suspected abuse. We also need to over support and resiliency for families undergoing this evaluation because it can be extremely stressful. 

Of note, a question came up during Q&A about neglect and mandated reporting, and the speakers deferred the topic to a future talk. They did note, however, that there is a movement in California to remove "neglect" from mandated reporting because it is almost entirely related to poverty and very racially biased. 

More to come. . .in the meantime, here is an interested policy paper on the topic, titled Shifting from Mandated Reporting to Community Supporting and another from Human Rights Watch, If I wasn't poor, I wouldn't be unfit.

Rheumatoid Arthritis Update (Kremer - 8/16/23)

 A recording of this presentation can be viewed HERE.

***

Renoir's Jardin du peintre à Essoyes

Many many thanks to our veteran SMGR Rheumatologist, Dr. Lisa Kremer for a compelling, artsy, and moving Grand Rounds presentation this week on Rheumatoid Arthritis (RA). Immediately after Dr. Kremer's presentation, a fellow primary care physician remarked to me, "I am not sure I have ever heard a specialist say so loudly and so clearly how important the social determinants are on the health of our patients."

Truth. And gratitude. From a primary care perspective, even one who is practicing almost entirely in the hospital these days, so much of health comes down to our social support and our community. Thanks, Dr. Kremer, for highlighting that.

RA is an autoimmune condition that developed in industrial society. Rarely seen before the 1600s, RA has some genetic susceptibilities (e.g. HLA DR4) and is precipitated by infections, environmental toxins (smoking doubles the risk), social and physical stresses, and hormonal triggers. 

RA is characterized by symmetrical polyarticular swelling of the small and medium joints on more than one occasion, over more than six weeks, supported by lab and/or xray and absence of other diagnosis. The back is not a small joint and is not involved in RA. 

photo source: https://www.nyp.org/healthlibrary/multimedia/

Classic x-ray findings (seen in above image) include loss of alignment of our normally beautiful joints, ulnar deviation, erosion of the MCP and PIP joints, but sparing of the DIP joints.

Exact causes of RA are unknown. There are a myriad of triggers.

• 1% of the the adult world has RA (1.5 million people in the US)-- the most common chronic inflammatory arthritis
• 4:1 female to male
• Peak age onset 40-60 years (but anytime after puberty is possible)
• All races and geographic areas are affected
• Specific populations with higher incidence (Native Americans, particularly: up to 10% of Sioux, Algonquian, Pima, Yakima, and Inuit peoples)

• 

  Renoir's Young Girls at the Piano
  

While Dr. Kremer presented us with a ton of medical information, she also presented the case of artist Pierre Aguste-Renoir (1841-1919), a French painter in the impressionist movement. She described him as a joyous and radical young man, struck by RA around age 50. His RA seems to have been precipitated by a fall from a bicycle and a resulting arm fracture. A trauma from which he never really recovered. And yet Renoir continued to paint long into his illness-- even designing his own wheelchair and equipment to be able to reach up to his large canvas painting surface. 

We live in a modern environment of autoimmunity

• lung exposures: tobacco, silica, textile dust
• chronic gingivitis
• GI tract microbiome patterns, diet (processed foods, e.g. cheese whiz and bologna)
• extreme and prolonged social stressors: war, jail, victims of abuse

Laboratory testing in RA is helpful but pretest probability determines the benefit of the test. 

• Rheumatoid factor (RF) is not specific
• Anti-CCP is more specific (can actually be positive a few years prior to onset of symptoms, but not always)
• ANA can be positive
• ESR and CRP really convey inflammatory cascade



(these are used more for research than for clinical application)

Sometimes it can be surprisingly hard to distinguish RA from osteoarthritis (OA). 

RA vs. OA (from PPM here): 

Extra-articular complications of RA only occur only in seropositive patients (i.e. +RF, +CCP ):

• fever and weight loss (can look like cancer)
• nodules (can be anywhere: eyes, heart, etc)
• interstitial lung disease
• pleuro-pericarditis
• CAD
• malignancy (specifically lymphoma)
• infections (like pneumonia)
• a variety of hematologic abnormalities (anemia, thrombocytopenia)
• osteoporosis

Prognosis and Disability:
Untreated, RA shortens life by 5-10 years. Aggressive RA therapy decreased mortality due to CV disease, lung, alanto-axial subluxation, and drug toxicity (e.g. steroids, NSAIDs). Treatment reduces the need for joint replacements by 50%.

In 1975, 50% of people with RA were disabled within 3 years; current estimates that 33% of people will be disabled (i.e. leave the workforce) within 5 years. Fatigue and unpredictable joint symptoms are frequently the most disabling issues. We should feel comfortable and confident filling out paperwork for our patients with RA. Their symptoms will wax and wane unpredictably.

Auto Amplifying loops

RA, like many autoimmune disease, consists of auto amplifying loops. Destruction of cartilage--> thickened synovium--> unstable tendons--> immune complexes--> extreme fatigue

Source: https://www.sciencedirect.com/science/article/pii/S1074761317300419

Treatment

Our current therapeutics have been created in direct response to this immunology. Treatments for RA are named for their immune targets. Note that methotrexate is still mainstay treatment for RA and steroids should only ever be given for short-term management. The combination of methotrexate and TNF inhibitors can actually stop all disease progression!

• Antimetabolites: Methotrexate (worldwide, best treatment for RA), Leflunomide
• TNF: Adalimumab, Etanercept, Infliximab
• IL-6: Tocilizumab
• Co-stimulation (CD28-CD80/86): Abatacept
• B cell depletion (anti-CD20): Rituximab
• JAK inhibitors: Tofacitinib, Baricitinib
• IL-1: Anakinra

Lifestyle matters!

This was perhaps the most compelling part of Dr. Kremer's talk. It turns out that these wonderful, effective meds are less effective if not used in combination with attention to a patient's life. 

• diet, exercise weight management
• tobacco cessation and limited alcohol
• stress management
• community and social support are key

And finally, Dr. Kremer's pearls of wisdom:

• Deformity does not equal disability
• RA does NOT cause back pain
• Never order tests if you don't know what you are looking for
• Low SES is associated with onset and severity of RA
• Smoking DOUBLES the risk and worsens the progression
• RA is "soft and spongy" (not hard and bony like osteoarthritis)
• A positive RF is not diagnostic, it should prompt you to keep looking for a diagnosis
• DIP joints are almost always spared
• If after careful exam and lab testing, you suspect RA, refer early to rheum for treatment!

Understanding Methamphetamine Use Disorder (Freschl 8/9/23)

Many, many thanks to Dr. Guille Freschl, who gave Grand Rounds this week titled Understanding Methamphetamine Use Disorder: A Deep Dive.  This was our first R3 Grand Rounds Presentation of the academic year, and Dr. Freschl knocked it out of the park. The link to a video recording of her presentation is available here. Below find my notes.   

A recording of this presentation can be viewed HERE.

***

Dr. Freschl was motivated to present on this topic by a longstanding interest in substance use disorders coupled with curiosity and concern about the oft uttered "Oh, it's probably because of the meth" that she heard from the mouths of her teachers. She was left wondering where the science meets the bias.

Did you know that amphetamine-type stimulants are the most widely used drugs in the world after cannabis?  Did you know that  between 2011 and 2016, overdoses from methamphetamine TRIPLED and that 1/4 of all overdoses in 2021 in the US were due to meth?

Methamphetamine use disorder can be seen all over the nation, but prevalence varies per region. Rates are highest in the West Coast and South. For example, prevalence of reported meth use in the past year in CA is reported at 1.04% of all adults, almost twice as much as most states in  the Northeast (see map below).

 

In California, non-fatal ED visits and overdose deaths have both risen over the last decade. In fact 32% of those in court-mandated substance use disorder treatment programs were there due to methamphetamine use. While the bulk of media and political attention is currently focused on opiates, one wonders, why aren't we talking more publically about methamphetamine?

What is methamphetamine?

Methamphetamine is an amphetamine derivative, notable for its additional methyl group; it enhances dopamine and norepinephrine in the synaptic cleft. Meth has a very long half life (12 hours cmpared to 90 minutes for cocaine). 

Why is meth bad? So many reasons. . . keep reading to understand a few of the major adverse effects. 

Cardiovascular toxicity

CV toxicity is the #1 cause of death in patients using methamphetamines, and risk of sudden cardiac death is increased by 27% with active meth use. CV toxicity includes a range of end-organ issues, including:

1) Hemorrhagic and ischemic strokes, due to vasoconstrictive effects and cerebral hypoperfusion

2) Very high rates of coronary artery disease (CAD) -- half of patients with regular meth use have CAD, despite lower rates of obesity and diabetes in these patients. This is thought to be directly related to the pro-inflammatory effects of meth. 

3) Angina, which does not respond well to nitroglycerin, is common, due to vasospasm

4) Pulmonary hypertension, especially with IV meth use, due to damage to pulmonary endothelial cells

5) Severe systolic dysfunction with LV dysfunction is another sequalae of meth use

6) Ventricular arrhythmias are notable

Neurotoxicity

Neurotoxicity is the #2 cause of morbidity and mortality in patients using meth. It rapidly crosses the blood brain barrier. It does a doozy on the brain, including disrupting pleasure centers, creating episodic memory issues, damaging executive function (2/3 of people with regular meth use show cognitive impairment, worse with older age and longer duration and frequency of use), disrupting motor function (including fine motor and choreas), and can lead to psychosis similar to schizophrenia (delusions of persecution, auditory hallucinations, and formication in almost half of people using). 

There is also a direct relationship between meth use and Parkinson's disease.

Dental effects

Serious dental effects include caries, tooth loss, tooth fractures -- all due to decreased saliva production (xerostomia), teeth grinding and jaw clenching that occurs with meth use.

Medication Assisted Therapy (MAT)?

Unfortunately, there are no FDA approved treatments for methamphetamine use disorder. A large meta-analysis of 43 RCTs with over 4000 patients found no clear evidence-based effective treatment. 

These included trials with mirtazapine (conflicting results), methylphenidate, bupropion, naltrexone and modafinil (limited evidence of benefit, no support for routine use). In addition, anticonvulsants, antidepressants, antipsychotics all low strength and insufficient evidence. Bummer. 

There was a small study that suggests that methylphenidate may be associated with decreased use over time: no difference at 30 days, but decreased in self reported use days at 10 weeks. 

Also, a small study of combination therapy --  IM naltrexone (380mg q3 weeks) PLUS PO bupropion (450mg daily) small treatment effect of 11% reduction in meth use. 

Hopefully, people will continue to investigate different agents for MAT and treatment of meth use disorder!

In conclusion, Dr. Freschl recommended that we use shared decision-making with patients when talking about trialing non-FDA approved treatment options. She reminded us to screen for CV and neurological sequelae of methamphetamine use. 

Pulmonary Hypertension (Wang - 8/2/23)

 A recording of this presentation can be viewed HERE.

***

Dr. Helena Wang gave an excellent Grand Rounds this week on Pulmonary Hypertension. It is worth watching!

We currently have at least three patients on our adult medicine service that we are evaluating for this condition after getting a TTE to look at their heart failure status. Pulmonary hypertension is such an interesting intersection between the lungs and the heart and a good opportunity to review basic physiology too! Dr. Wang gave an earlier version of this presentation 2 1/2 years ago, and I felt then, as I did this week, that I could watch it over and over. You can! 

But for those who prefer the written word:

The definition of pulmonary hypertension (pHtn) is simple enough: a mean PAP of > 20mmHg at rest.

Dr. Wang likens the pulmonary artery to something like a six lane highway (think of the 101 going north from Novato into Petaluma). When the lanes decrease from six to two in northern Novato, there is suddenly a lot of congestion, and all the cardiac output has to move through that smaller space at higher pressures. Voila! Elevated PAP.

Pulmonary arterial hypertension is rare, but not that rare, 15-50 cases/million, and more common in people with HIV (regardless of CD4 count or duration), connective tissue disease, and portal hypertension. For patients with any of these diagnoses, should be screened annually for pHtn with an echocardiogram (TTE).

Symptoms of pHtn include dyspnea on exertion, fatigue, edema, bloating, and syncope (obviously pretty non-specific). 

On exam, you can see elevated JVP (check the neck veins!), hear a split S2, and see peripheral edema.

Chest imaging reveals often a dilated R pulmonary artery on CXR, and even sometimes a prominent L pulmonary artery. Also, look for the "banana and egg sign" on CT, in which the aortic arch and the pulmonary artery are a little too close in size for comfort. The aortic arch is the banana; the pulmnoary artery is the egg.

Banana and egg sign (photo credit: CHEST Journal)

Okay, what about the TTE??

Oh, reminds the pulmonologist and the family physician, don't forget to pay attention to the right side of the heart in the echocardiogram! Dr. Wang urged us to scroll down, skip the conclusion,  and look at the text (often the third paragraph). Is the RV big? What is the velocity of the regurgitant jet? What is the TAPSE?

A first hint of pulmonary hypertension on a TTE comes on apical 4 chamber view where the R ventricle shows turbulent flow back into the R atrium

RVSP (right ventricular systolic pressure) is an estimate reported on most echo reports and can be very challenging for the Echo tech to calculate. However, a calculated RVSP>25 is considered HIGH right sided pressure and increases your suspicion for pHtn.

The R ventricle is often very plump and dilated under high pressure (so. . .a big chubby RV on echo is another clue that you might have pulmonary hypertension)

Tricuspid Annular Plane Systolic Excursion (TAPSE): RV contracts in a twisting motion with each contraction as RV shortens. Normal excursion is 1.5cm. If RV is volume overloaded and dilated, cannot squeeze as well, not shortening, TAPSE drops <1.5cm on echo

And finally, right heart catheterization is still gold standard for measuring R sided pressures, but really this should be done after you have done a full evaluation (see below) once you are pretty certain you have primary pulmonary hypertension (WHO Group 1). And, due to changes in insurance, it is no longer required always for diagnosis.

WHO Classification of Pulmonary Hypertension

• WHO Class 1: Pulmonary ARTERIAL Hypertension (pressure goes up, fluid backs up)
• WHO Class 1 has the worst outcome: 5 year survival 61%
• only diagnosed once other causes of pulmonary hypertension are identified and treated
• Seen in patients with HIV (regardless of viral load, duration), connective tissue disease (e.g. scleroderma), and portal hypertension
• All other WHO classes are actually pulmonary VENOUS hypertension (something downstream to the lungs causing poor forward flow, back up of blood, then high pressure on R side of heart). These include
• WHO 2: L heart disease (LV systolic or diastolic dysfunction, valvular disease, s/p TAVR, myxomatous disease)
• WHO 3: bad lung disease or hypoxia (COPD, inadequately treated asthma, ILD, sleep disordered breathing (OSA), OHS, chronic exposure to high altitute, developmental lung disease. Consider high resolution CT (with very thin cuts with and without contrast), home sleep test, pulmonary function tests.
• WHO 4: chronic thromboembolic pulmonary hypertension (small, little tiny chronic). You cannot see this on typical PE protocol CT scan. You need a VQ scan to evaluate chronic thromboembolic disease.
• WHO 5: potpourri

Once Pulmonary Hypertension is identified, the next question is DOES the patient have pulmonary hypertension that is primary or secondary

Ddx pulmonary arterial hypertension (WHO Group 1)

• idiopathic
• heritable (no current gene therapies)
• drug and toxin induced (fen fen, methamphetamines including stimulant medications prescribed)
• connective tissue disease (scleroderma)
• HIV
• portal hypertension
• congenital heart disease
• Schistosomiasis (#1 cause of pulmonary hypertension outside the US)

A quick interruption to review the three types of CT chest you might consider to evaluate the lungs:

• CT angiogram (aka CTA) is a very quick scan from feet to head chasing the dye, itskips very low bases and apices of lungs and should never be used to assess for interstitial lung disease. Great for acute PE asessment.
• A High Resolution CT Chest: much thinner cuts (2mm) than a CTA starting at apices and going all the way to the bases. 
• Very high detail of parenchyma
• Ground glass opacities can be atelectasis vs. ILD--> flip when prone to see if atelectasis resolves while doing high res scan
• CT w/wo contrast (e.g. nodule) 
• can see 4 generations of branches of bronchial tree, but keep in mind that there are 17, so you cannot see filling defects in the small peripheral vessels

Treatment of Pulmonary Arterial Hypertension (PAP)

1. First identify if the patient has any WHO 2-5 diagnoses that may be influencing their pHtn and treat them maximally, then repeat TTE to check for PAP
2. If they still display pHtn on TTE, they now meet criteria for pulmonary arterial hypertension (PAP).
3. Consider pulmonary vasodilator therapy (obviously in conjunction with pulmonologist). These, while still very expensive, are coming down in price. The meds range currently between $40,000 to $100,000 per year.

When to treat Pulmonary Arterial Hypertension?

There is NO specific number for pressure goals. Look at patients functional class, 6 minute walk, and Echo

Treatment goals:

• Functional class: symptoms at rest (class IV), normal (class I): goal is 2 or less
• 6 minute walk test: goal is 400mg in 6 minutes ("please walk as far as you can in 6 minutes", not "as fast as you can walk")
• BNP: can be elevated in R heart strain, goal is normal
• Echo: goal is RV not fat and chubby, decompressed and slender, TAPSE moving nicely

Pulmonary Hypertension Therapy

• Endothelin pathway: block (bosentan (black box liver toxicity, no longer used), ambrisentan, macicentan: side effects: edema, check LFTs, watch for rare malignant facial edema
• Nitric oxide pathway: enhance (sildenafil TID, tadalafil QD, no lab monitoring, can get blue green colorblindness, rare complication anterior ischemic optic neuropathy (sudden blindness one eye, reversible when stop), riociguat (TID, more systemic hypotension)
• Prostacyclin pathway: enhance (potent, short half life and unstable)
• epoprostenol: IV infusion, tubing connected to a pump, best mortality data, very labor intensive
• treprostinil: IV vs. sq (like insulin pump) and inhaled QID (takes a lot of time, breathing treatment like nebulizer, 20-30 minutes per treatment
• iloprost: inhaled 6-9 times/day
• selexipag: oral BID, no labs but unrealistic uptitration protocol

Guidelines for treatment are based on functional class. The ultimate goal is minimal symptoms with regular activity

If functional class IV-->  needs prostacyclins right away

If functional class III-->  can start with orals (e.g. tadalafil and macicentan)

Any questions? Email or staff message Dr. Helena Wang at: helena.wang@sutterhealth.org