Mysterious Encephalopathy (Manjuck, 3/27/2024)

 A link to this presentation is available HERE.

***

Thanks to Dr. Janice Manjuck, our amazing ICU director, for an entertaining and information-packed Grand Rounds this week on Evaluation of Encephalopathy in Medical Patients. I learned so much, and cannot wait to have Dr. Manjuck back. She is funnier as a presenter than I am a writer, so please do listen to her talk if you have time! If you do not, here are my brief notes.

Key points:

• When evaluating an altered patients, make sure you know their baseline
• Don't forget to look at vitals: BP (normal for them?), temperature (core) and oxygen saturation
• Labs can be helpful to determine etiology
• Labs include glucose, LFTs, ammonia (increase in mortality regardless of cause), calcium, sodium, thyroid function tests (+/- cortisol), VBG/ABG, carbon monoxide, tox screen, alcohol and drug levels.
• Ask yourself if there is a primary neurological process
• CT (non-con) vs. CTA, vs CTV (if you are concerned about hypercoagulable state), MRI (if CT normal)
• Sometimes medication administration can be diagnostic: D50, naloxone (don't ever give naloxone without suction nearby), thiamine

Altered level of consciousness (ALOC) is a spectrum. Every time you evaluate and examine a patient, you should document their baseline level of consciousness. 

• Alert
• Lethargic ("patient looks like they are just waking up from a heavy sleep")
• Obtunded ("patient looks like they took a sleeping pill)
• Stupor ("patient not waking to shaking"
• Coma

Dr. Manjuck, used a this acronym (a model by a neuro-intensivist) to explain most common reasons for encephalopathies: DOTSS: Drugs, Osmotic demyelination, Thiamine, Structural disease, Seizures)

Drugs

50% of patients with AMS are altered due to a "drug problem" -- either a drug taken by the patient, rx'd to the patient, or not given to the patient. This makes MEDICATION RECONCILIATION a very very very important tool in understanding why a patient is altered. Common meds that are associated with AMS in hospitalized patients and are not immediately recognized include: levodopa, antidepressants, and baclofen. 

Don't forget the half-life and a patient's renal function!

Anti-depressant discontinuation syndrome: FINISH (flu-like syndromes, insomnia, nausea, imbalance, and sensory disturbances including hyperarousal).

Also don't forget meth detox in altered patients

So,  as per Dr. Manjuck's pearl of the talk: "Look at the med list every single day like flossing"

Osmotic demyelination syndrome 

This is a rare but serious cause of AMS in patients with hyponatremia that is corrected too quickly.  Unlike what you may think, this actually happens much LATER than I realized -- 4-7 days AFTER correction. Clinical manifestations include: short term memory loss, dysarthrias and ataxia, flaccid quardiparesis, locked-in syndromes, seizures, and coma. 

Neuroimaging can confirm the diagnosis: "snout" and "trident" sign

ODS occurs really when initial sodium is <120 and MORE likely when it was <110, and it can occur EVEN if it was corrected slowly. 

Goal is to correct 6-8mg max per 24 hours

Thiamine Deficiency

Patients with chronic alcohol use are at high risk for Wernicke's encephalopathy, which presents as change in mental status, oculomotor dysfunction and cerebella dysfunction. 

Structural Abnormalities

10-15% of patients in the ICU with AMS have an abnormal head CT, but that doesn't mean that the abnormal head CT explains the AMS. In order for a structural lesion to cause AMS, you need to have broad disruption of the reticular activating system! This must occur in the dorsolateral upper midpons, upper mid pons, bilateral thalamus, or diffuse bi-hemispheric.

That being said, some structural abnormalities DO cause AMS. These include:

• Posterior reversible encephalopathy syndrome (PRES
• Hydrocephalus
• Diffuse cerebral edema
• Subdural hematoma
• Subarachnoid hematoma
• Diffuse cardioembolic stroke

Seizures

Non-convulsive status epilepticus (NCSE) is largely unrecognized. 

Seizures are not a "binary" thing -- that is, it is not 

The longer it takes to control them, the longer it takes to get rid of them. 

Final take homes from Dr. Manjuck:

• Make sure you do a good neuro exam on Day #1 of admission and every day. And don't forget to document that!
• Your exam should include: level of arousal, speech content, orientation, eye opening, and gross motor exam
• Do a medication reconciliation every single day. Be aware of opiate creep (opiates you didn't even know the patient was taking)
• Toxic-metabolic encephalopathy is very much a diagnosis of EXCLUSION
• Be aware of taking patient OFF anti-coagulation (diffuse cardioembolic stroke is a definite risk)

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

Interventional Radiology for the Hospitalist/Primary Care (Page, 10/13/2021)

Many thanks to Dr. Alex Page (Redwood Radiology Group) for a great presentation this week titled Interventional Radiology for the PCP/Hospitalist. It seems IR docs can do just about anything these days-- certainly with all kinds of tricks up their sleeves. But what should I know as a primary care doc? Who can I refer? What can patients expect? And how should I manage common post-IR procedural issues?

A recording of his presentation is available here: https://youtu.be/9wmAL7s9KAQ

For clarification, interventional radiology is defined as minimally invasive image-guided treatment of medical conditions that once required surgery, like surgery only MAGIC. ☺

IR physicians work with practically every body system (minus brain, skin and heart. Their work can be broken into two broad categories:

• Endovascular procedures: including vascular access (vein, artery, lymphatics) and catheterization (stenting, embolization, angioplasty, venoplasty)

and 

• Percutaneous interventions: using CT/ultrasound to advance a needle to put in drain, biopsy lesions, ablate tumors/growths, etc

"We can almost get anywhere" (danger zones where your local IR doc may take a moment: mediastinum, around heart, deep abdomen)

For detailed ideas of possible IR procedures, see the image below from Society of Interventional Radiology for the wide scope of IR docs

www.sirweb.org

Vascular Access

IR can place a range of central lines, HD catheters, and ports

Central lines (for abx/meds, not the same as PICC; locally our PICC nurses place these)

**Central line Pearl: If you are concerned that patient is heading toward ESRD and possible HD, PICC lines can ruin peripheral veins and make it hard for vascular surgeons to make AV fistula, so consider opting for a central line in that circumstance

HD catheters (large bore, two lumens)

**Pearl: Right after being placed, bleeding from tunneled catheters can only be in two places: along the tract where catheter is tunneled, the vein around the catheter at the IJ site. If it has been placed for some time, pressure should be held at the neck only because bleeding only coming from the IJ site

**Pearl: Noe that the Cuff (made of dacron) is supposed to be inside tract, body scars down on it to prevent CLABSI. If the cuff is EVER visible, catheter needs to be exchanged

Ports: if you look closely can see the image of a C/T on the port. If it is right side up, you should see it on the x-ray. In addition, the tip should be right at the top of the  R atrium (approximately two vertebral bodies below the carina, one vertebral body below bronchus intermedius)

Of note, the tip of Catheter/port does move based on patient position (when breathing out, tip will be at lowest position). If too deep, can cause arrhythmia. If too shallow (way up in SVC), can cause stenosis and create access issue. Fine balance to have in right spot

Ports can be implanted for 1-2 years, should be able to remove without difficulty

Do not use HD tunneled catheter for vascular access unless emergent

Ports can be easily accessed (usually by RN protocol); has to be accessed with a Huber needle (slight curve with hole on the side to prevent coring the membrane from the port), use sterile technique, pin down with fingers (has 3 little bumps),

Veins used for port/cath: IJ (nicest easiest, safest)>> EJ>> subclavian (can be done with landmarks)>> femoral (higher infection incidence, less clean)>>IVC>> hepatic veins

Fistulas and Grafts

Fistula is an abnormal connection between artery and vein, created by surgeons, can use either a native vein (i.e. fistula), e.g. brachial artery connected to cephalic vein

Takes time for vein to mature (months), more durable, last longer

If fistula not an option, they use a graft: firm loop use PTFE to create a circuit, can be used much sooner, don't last as long (because foreign material), anastomosis

Can have venous outlet stenosis, can do angioplasty to save fistula

Should feel a "thrill" instead of a pulse

Possible complications:

• Patients with MAJOR  upper extremity swelling= central stenosis of the fistula, indication for IR referral to help open
• Prolonged bleeding can also be caused by central stenosis, indication for IR referral
• Infection; native fistula doesn't commonly get infected (except thrombophlebitis), graft infection is major issue (needs to be removed): erythema pain, fever
• Steal syndrome: claudication, painful hand, especially during HD

Abscess Drains

Diverticular abscess most common. Additional abscess include: appendiceal abscess, hepatic abscess, pancreatic pseudocyst, cholecystitis, percutaneous nephrostomy tubes, tubo-ovarian abscess

Normal sequence for drains

IR places drain--> Bulb suction (flush until minimal clear output)--> Abscessogram vs. CT vs. "just pull"

Major problem: fistula

Repeat abscessogram q2 weeks until fistula closes

Can work with GI if place a wire in fistula to clip diverticula

Fistula= surgery (colectomy in setting of diverticulitis)

How much to flush:  many IR docs use 10ml flush (can do less if small cavity)

Abscessogram: fluoroscopic (moving x-ray, live x-ray used to do procedure), inject with contrast--> look for pocket where abscess was (when contrast injected, if big and distended, means pocket is still there). Can also visualized presence of fistula. Repeat until  pocket/fistula disappears

Biopsies

lung, liver, bone, lymph notes

CT and/or ultrasound (if a hollow viscous containing air, cannot see through it on ultrasound)

Lung biopsy is the most dangerous (20% of small pneumothorax, 5% chance for chest tube due to air leak, hemoptysis, air embolism=death)

Solid organ biopsies are risky because of bleeding (kidney, liver): if sending a patient for liver/kidney, SBP must be <150

INR and platelets: varies by procedure (HIGH vs. Low risk bleeding procedure)

platelets >50, INR <1.5

High risk bleeding procedures

Low risk bleeding procedure (e.g. port, tunnelle lines paracentesis, bone marrow bx): platelets can be quite low, BM <20

There is a document from SIR which dictates INR/platelet counts based on procedure

Kyphoplasty

can lead to immediate pain relief

Indications: osteoporosis, acute/subacute vertebral body fracture (<30 days) with midline pain/tenderness, cannot do too high (high thoracic, cervical spine)

Advance needle into vertebral body (through pedicle, stay lateral of medial aspect of the pedicle to avoid the spinal canal), inflate a meeting, put in cement, fill the anterior aspect of the vertebral body and stops fracture fragments from moving and can signficiantly improve pain

Risks: fracture adjacent vertebral body (because cemented body is so much stronger than natural bodies), cement migration

And finally, information to have ready for IR consultation

1) Desired procedure

2)  Indication for procedure

2) urgency of procedure

3) anticoagulation/platelets

4) NPO status

Who to call?

SSSRH scheduler: 707-576-4278

SRMH scheduler: 707-525-5269

IR on call: 707-571-7007

Elimination of TB in the US: 2021 Updates (Toub, 8/4//2021)

Many thanks to Dr. Danny Toub, a family physician, teacher, and public health professional-- who so often bridges the impossible gaps that exist between individual patient care conundrums and public health. While this bridge may seem intuitive, it is often rickety and not always clear how to begin to build it-- look to Dr. Toub, though, he always shows us the way. 

A recording of his presentation is available HERE. 

This week's topic was Tuberculosis (TB), a global behemoth; the original and ever-present airborne illness that still kills 1.4 million people worldwide per year, more than HIV/AIDS While we sit in the middle of a harrowing COVID-19 Pandemic and the words N-95 have become every day jargon, TB is still global problem. And while we have made great progress in the US with TB eradication, TB still unnecessarily killed 542 Americans in 2018, 200 of which were right here in California.

TB, much like COVID, disproportionately affects people who are living in poverty, people of color, and those who have less access to stable housing and health care services.

What is our responsibility as primary care providers?

• Screen ALL patients for TB Risk
• Screen HIGH RISK patients with a Tuberculin Skin test (TST) or interferon gamma release assay (IGRA)
• Treat Latent TB infections (LTBI)
• Report to Public Health any active TB cases and/or any LTBI in children or recent converters (<2 years)
• Oh, and don't forget to have TB on your ddx for other acute/subacute illness presentations!

If we break that down,

1) Screen ALL patients for TB Risk using the California TB Risk Assessment Tool which can be found HERE and is pictured below as well. 

Remember to AVOID testing low risk folks for LTBI (this form alone counts as a screen!) and if you have limited resources, prioritize those who are most likely to convert from LTBI to active TB. Key risk factors include being foreign born/immigrant from certain regions, immunosuppression, and those who have been in close contact with someone with TB. 

Important additional risk factors include, recent conversion, substance use disorder, patients with DM, patients with CKD, those with autoimmune conditions, people who smoke, people with cancer, and more. 

The point of screening is to prevent a future conversion to active TB by treating people before they get sick. Low risk patients have ~10% lifetime risk of converting. Higher risk (e.g. people with diabetes) have ~ 30% lifetime risk, and highest risk folks (e.g. HIV + LTBI) have a 7-10% per year risk of converting. 

2) Screen HIGH risk patients with TST or IGRA. The best TB test depends on your pretest probability. Here is a good cheat sheet.

• Low risk patient--> do not screen
• Asymptomatic child--> use the California Pediatric TB Risk Assessment
• Asymptomatic adult--> use the CA Adult TB Risk assessment
• Volunteer for school without risk factors--> use the CA Schools TB Risk Tool
• College or University student--> use the CA College tool
• Health care worker--> use CDC guidelines#
• Pregnant woman--> pregnancy itself is not a risk factor
• 2 year old foreign-born patient--> TST*
• Foreign born >2 year old, hx BCG--> IGRA**
• Patient experiencing homelessness--> IGRA
• Patient to start TNF alpha blocker--> IGRA
• Patients with >4 weeks cough, 5 pound weight loss--> Chest Xray
• SE Asian smoker with RUL cavity, and a1c>9%--> sputum (x-pert MTB)+

#Note that the CDC no longer recommends annual TB testing for healthcare workers!! Official recommendations released in 2019 are available here and recommend a risk based technique. Maybe that means YOU don't need that annual TST!

*TST: tuberculin skin test, **IGRA: interferon gamma release assay (often referred to as quantiferon gold). There is limited data in IGRA in children <5. IGRA are more specific than TST in pts with a history of a BCG vaccine.

+Remember, a negative IGRA or TST does NOT rule out active TB (you need sputum!)

3) Treat LTBI infection. Treatment for LTBI has been shortened and simplified over the last decade. It does not involve routine lab work (except in high risk folks) or directly observed therapy (DOT). 

Dr. Toub recommends this handy LTBI pocket card to help simplify your decision-making and treatment regimen planning. The image below to too small to actually read, but follow the link for specifics on indications, completion criteria, considerations, etc. 

Briefly, prior to initiating LTBI treatment, you want to be sure to r/o pregnancy, check for pre-existing peripheral neuropathy (which can be a side effect of tx), screen for liver disease risk factors (e.g. alcohol use disorder, NASH, HCV). 

Baseline LFTs are only indicated for patients with HIV, known liver disease, regular alcohol use, pregnancy or < 3 months postpartum, and other risks for liver disease.

And, Dr. Toub reminded us to remind your patients that EVERYthing will be orange (sweat, tears, and urine). Also be sure to check for drug drug interactions on any tool that you use for this purpose, as there are many. 

4) Report to SoCo Public Health any active TB cases and/or any LTBI in children or recent converters (<2 years). 

5) Oh, and don't forget to have TB on your ddx for other acute/subacute illness presentations! Remember TB can show up just about anywhere. 

For local assistance, you can utilize the Sonoma County TB Control Guidelines, which you can find at the bottom of this webpage. And if you ever have any TB questions, reach out to our local TB Control program at 707-565-4567.

And, finally, a list of trusted resources from Dr. Toub:

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