VOTW: In the Thick of It

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HPI

A 40-year-old female with a PMH of polycystic kidney disease, HLD, and HTN presents with 1 month of episodic dizziness. She was referred to the ED by her cardiologist for an abnormal EKG, and had previously been told that she had an enlarged heart. 

Her vital signs are unremarkable. Physical exam is notable for a harsh, blowing systolic murmur. Chest X-ray shows cardiomegaly.

Ultrasound Findings

Point-of-care echocardiogram showed no pericardial effusion and was notable for septal thickening to 2.2 cm, concerning for hypertrophic obstructive cardiomyopathy (HOCM).

Echocardiography is the first-line imaging modality for the diagnosis of hypertrophic cardiomyopathy. 

Key findings are wall thickening and intraventricular obstruction. 

  • Wall thickening > 15 mm (or > 13 mm in patients with relatives diagnosed with HOCM). This can be measured in the parasternal long or short axis views. 

  • Interventricular septum to posterior wall thickness ratio of > 1.3 in normotensive patients or > 1.5 in patients with HTN

  • Thickening usually occurs on a focal region of the LV wall

Other associated findings include mitral valve abnormalities, systolic dysfunction, and diastolic dysfunction.

  • Systolic anterior motion of the mitral valve may occur in HOCM due to the Venturi effect. Septal hypertrophy narrows the LVOT, accelerating blood flow and creating a suction force that pulls the mitral valve leaflet into the LVOT. This causes outflow obstruction as well as mitral regurgitation. 

Case Conclusion

Based on these findings, the patient was placed in observation for cardiology evaluation. 

Comprehensive echocardiogram revealed findings consistent with HOCM, including severe asymmetric left ventricular hypertrophy, hyperdynamic LV systolic function (LVEF 76-80%), moderate (grade 2) LV diastolic dysfunction, LV outflow tract obstruction, moderate systolic anterior motion of the anterior leaflet of the mitral valve, and moderate mitral valve regurgitation.

The patient was newly diagnosed with and educated about HOCM. She was discharged with metoprolol 25 mg daily and is anticipated to undergo further treatment with mavacamten and possible septal reduction surgery. 

References & Further Reading

Happy scanning! 


POTD: Potpourri (LLFTP #9)

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Welcome to my final POTD of this block, and the 9th installment of “Lessons Learned from The Pitt”. Rather than focus on a singular case, I’ll end with a potpourri. 

Spoilers and anguish ahead.

It is now 3pm at this ED, and the ratio of “things happening” to “time elapsed” continues to steadily increase. When the episode begins with an interrupted debrief for poor drowned Amber, followed by shots of much of the cast going through their own trauma responses (Dr. Langdon calling home, so he can hear his son’s voice, just hits different), you know that things are probably going to keep going downhill. The purpose of a debrief is to give the team a little time and space to process and recontextualize the events, identify areas of improvement within a supportive learning environment, and assess the need for further support (such as a Team Lavender consult). The facilitator (usually the attending, or other designated staff member) will gather the team members, establish that the debrief is intended to be a safe space, establish the above objectives, and then step back and nudge the conversation as needed. One of the staff (usually the team leader) will summarize the events that occurred; the rest should hit upon three areas — the “plus”, the “delta”, and the “take home”; respectively, those are the things that were done well, opportunities to improve, and learning/action items. If an official Clinical Event Debriefing form is submitted, there is an ED leadership team that will discuss those points in a biweekly meeting and try to address said action items. 

Back to the episode. With 4 hours left in the shift officially (though we all know that there are 15 episodes, so something’s coming), people start to hit their breaking points. The first two are on the patient side, and both occur in the packed-like-sardines waiting room. Mr. Driscoll, the chest pain patient who has become progressively more frustrated, hostile, and racist with each episode he continues to remain in the waiting room, finally decides he’s had enough and starts leaving after a tirade. Dr. Langdon calls Driscoll out over the speaker to tell him that he would be departing “Against Medical Advice”, with risks including dropping dead from a heart attack.

The AMA conversation is important when it comes to patient safety, as well as one’s own medicolegal protection (patients who leave AMA are more likely to have a bad outcome and more likely to sue). Patient autonomy is one of the ethical cornerstones of modern medicine, and restricting an individual’s freedom of movement without justifiable cause constitutes the crime of false imprisonment — thus, (most) patients cannot be physically stopped from leaving unless they are obviously impaired/dangerous. Ideally, before that happens, the treating physician is able to have a conversation with the patient; the discussion should allow the physician to assess the patient’s capacity to make this decision (briefly, displays understanding of their current condition, demonstrates insight into the benefits of staying vs the risks of departing including specific risks incurred by the suspected disease processes, and is able to articulate an intact thought process i.e. intact judgment regarding how they came to their decision), and then take steps to mitigate harms (such as giving prescription antibiotics, outpatient follow-up, et al.). The AMA discussion also may be the last opportunity for “service recovery”, a concept from the Patient Experience world; this can be an acknowledgement of the patient’s concerns, followed by explanations of what has happened and what can be done to improve. In this case, Mr. Driscoll has actually received a workup despite being in the ED; he’s had an ECG and troponin (plus other basic labs), with repeat troponin pending — and I don’t think anyone’s had the headspace to have an actual discussion about the plan and address his concerns with an empathetic veneer. 

The second waiting-room blowup is a fight between two women, instigated by one of them taking offense at being offered a mask for her coughing child, which charge nurse Dana steps into and ends with a dressing-down worthy of a standing ovation. This isn’t the time or place for a deep dive into the politics of masking, I’ll just say that droplet precautions were definitely around before 2020. The medical lesson here comes from the “fight bite” from our anti-mask perpetrator, who now has a tooth fragment lodged in her knuckle. Evaluation of such an injury should include assessment of the integrity of the joint capsule, of tendon involvement, of potential fractures, and of signs of infection (especially if presentation is delayed). Lacerations over the dorsal MCP joint should prompt a specific question about fights, as patients can sometimes be reluctant to divulge (they don’t know about the risk of severe infection leading to amputation). Treatment for the uninfected-appearing acute “fight bite” with no joint/tendon/bone involvement is copious irrigation, prophylactic antibiotics (usually augmentin 875mg/125mg PO BID x 7 days), +/- TDAP, healing by secondary intention, and close follow-up. Hand surgery should be consulted (and IV antibiotics considered) for signs of infection (usually with delayed presentation) especially if there is reason to suspect joint/tendon compromise. 

Back to the resus bay, another critical patient from this episode has hyperthermia and altered mental status in the context of MDMA abuse at a music festival. Her core temperature is 107 degrees, prompting the team to begin active cooling with ice-water immersion (with goal temp of 102 to prevent overshot hypothermia), as well as high-dose benzodiazepines (to oppose the centrally-mediated MDMA-induced component of her hyperthermia, as well as to prevent shivering). Later, when the patient begins seizing, Dr. Santos suggests that the patient has hyponatremia secondary to dehydration, orders 100mL of 3% saline (would raise serum Na by 2-3, usually given x3 to achieve effect), and goes above Dr. Mohan’s head to push the saline (100ml should be given over 10-15 minutes, not a 3-second push) (can also consider 1 amp of 8.4% sodium bicarb, which is in code carts and more readily available). The seizure terminates, and it’s the first resus win for Dr. Santos until Dr. Langdon returns furious and demands to know why no one bothered to come tell him about the seizure. Dr. Mohan freezes like a deer in headlights, and Dr. Santos throws herself under the bus and gives Dr. Mohan the credit for the save — prompting Dr. Langdon to go off on her, full-on shouting at her and berating her until Dr. Robby interrupts him. This is not how one should approach giving feedback to a learner — not in public, and not with such vitriol. The goal should be to communicate areas of improvement and concrete changes that can be made. If the learner has demonstrated a problematic pattern of behavior, pull them aside and address it before it becomes such an issue that you feel the need to scream at them. And if problems persist, there are people (i.e. attendings, charge nurses) to whom one can escalate.

Though Dr. Robby's response with Dr. Langdon is also not totally appropriate, shouting at him to “shut the f*ck up” when Langdon rushes to explain himself, and dressing him down in full earshot of the rest of the ED.

The episode ends with a sucker punch, delivered by a departing Mr. Driscoll to charge nurse Dana while she's stepped outside for a break. Violence against healthcare workers is a serious problem that often goes unreported or unprosecuted. Healthcare and social services workers are at the highest risk of workplace violence compared to all other civilian industries, with over a quarter of all workers facing victimization during their career. Reasons include perceptions that this is “all part of the job”, or that patients/families should be given passes due to their stress, or that they'll face censure for speaking up. Solutions include building a culture of safety and developing institutional policies. In the acute setting, early retreat and involvement of security are the best ways to protect oneself.

That's all from me today. I hope you've enjoyed this series because I've certainly had a blast writing each one! 

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POTD: Heavy Metals (LLFTP #8)

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Today's POTD will be based on the continuation of one of the cases I mentioned in my previous email. 

Spoilers?

I originally wanted to talk about Latrodectus (Black Widow) envenomation (a patient with Crohn's disease presented with isolated severe abdominal cramping, without any fever or other GI symptoms), but Dr. Ervin already wrote a nice POTD about it back in August. 

Instead, we'll follow the conclusion of Dr. Mohan's case with the altered beauty influencer. The heavy metal panel comes back at the beginning of the episode (seriously impressive turnaround time), and the patient has a mercury level > 90 mcg/L. The ordered treatment is "chelation TID, 10 mL/kg of DMSO" (which is actually a small scripting error, as you'll see below). Done and done, and Dr. Robby gracefully takes his lumps and acknowledges that "Slo-Mo" had handled the case appropriately. 

Let's learn about mercury toxicity as well as some of the other heavy metals that love to appear in test questions! 

Mercury (Hg/Hydrargyrum)

  • 3 common forms — elemental mercury, mercury salts, and organic mercury

    • Elemental — found in devices such as thermometers; volatile and easily aerosolizes, inhalation --> pulmonary, CNS, and renal symptoms

    • Salts — found in batteries, skin cream, dental products; absorbed by GI tract and across skin --> GI and renal symptoms

    • Organic — found in paint, skin cream, fish; absorbed by GI tract and across skin --> neurological symptoms

  • Hg bonds to various functional groups on proteins, leading to widespread dysfunction

  • Hg can cause direct oxidative damage to lung/GI membranes and renal tubules

  • CNS deposition of mercury (more common in elemental and organic mercury exposure) leads to posterior encephalopathy/atrophy --> sensory neuropathies, vision changes/deficits, ataxia

  • Neurological deficits likely longstanding or permanent, especially if chronic/subacute

  • Above symptoms are fairly nonspecific, diagnosis relies on thorough history

  • Supportive care is key, chelation (compounds that bind heavy metal ions, allow excretion) can help lower Hg levels

    • Elemental/salts —  IM dimercaprol 5 mg/kg q4h x 48 hours, then 2.5 mg/kg q6h x 48 hours, then 2.5 mg/kg q12h x 7 days; PLUS PO succimer (DMSA) 10 mg/kg q8h x 5 days, then q12h x 14 days

    • Organic — only succimer (DMSA), as dimercaprol has been shown to increase neurotoxicity

    • For acute ingestions, consider GI decontamination

    • HD can be considered as part of supportive care regimen if there is significant renal impairment, but does not effectively lower Hg levels

    • Exchange transfusions trialed in past with no proven benefit

Lead (Pb/Plumbum)

  • Previously had widespread presence in paint, gasoline (and exhaust), pipes; paint and pipes in older homes continue to be a source today, despite being banned in 1978 and 1986, respectively

    • Leaded gasoline banned in the US in 1996, but fumes could still cause agricultural contamination in imports; worldwide ban achieved in 2021

    • Childhood exposure through exhaust fumes reduced the intelligence (and worsened the health) of many Americans born between the 60's and 90's; i.e. petrol company lobbying and obfuscation (lead toxicity has never been unexpected, it has an older historiography than some modern religions) robbed multiple generations

    • Other exposure sources include industrial occupations, contaminated pewter/ceramics, contaminated spices, contaminated cosmetics, alternative pseudomedical practices, lead bullets

    • Children are at higher risk — they absorb more Pb for their body weight in both ingestion and inhalation, store more Pb in metabolically-active tissue, and excrete less Pb in their urine 

  • Like mercury, lead binds many proteins and inhibits their function, especially calcium and zinc related proteins

    • High blood Pb levels can lead to acute syndrome of lead-induced encephalopathy from cerebral edema --> AMS, seizures, coma, death

    • Chronic toxicity harms neurocognitive development, inhibits RBC production and maintenance ("basophilic stippling" on smear), dysregulates proximal renal tubule function, and impairs sex, growth, and thyroid hormones

  •  Nonspecific multisystemic symptoms, usually at Pb > 10mcg/dL

    • "Asymptomatic" children at risk for IQ loss (highest rate of IQ decrease is at 1 to 10mcg/dL)

    • Children may display irritability, constipation, and/or anorexia 

    • Adults may also have cardiovascular disease, peripheral neuropathy, gout, infertility

    • Levels >70mcg/dL have high risk for lead encephalopathy

  • Careful history is once again key to the path to diagnosis

  • Care is centered around screening and decontamination

    • All children with Medicaid are screened at 12 and 24 months (5mcg/dL is threshold for further testing)

    • All children recommended to be screened by age 3-5 

    • Supportive care (including supplementation with iron, zinc, and calcium)

    • Chelation indicated for levels of >45mcg/dL in children, >70mcg/dL in adults, or any patient with encephalopathy

      • BAL (dimercaprol) + calcium disodium EDTA is most common regimen, +/- succimer

      • Chelation may increase release of Pb from bones, leading to temporary exacerbation of symptoms

    • Developmental deficits from chronic toxicity likely to remain permanent

    • Permanent neurological sequelae from lead encephalopathy also likely 

Iron (Fe/Ferrum)

  • Easily available as an OTC dietary supplement, ingestion of such is the primary exposure

    • 325mg ferrous sulfate contains 65mg elemental iron

    • 300mg ferrous gluconate contains 36mg elemental iron

    • 100mg ferrous fumarate contains 33mg elemental iron

    • For prenatal vitamins and children's vitamins, check label/manufacturer's site

    • Ingestion of >20 mg/kg associated with moderate toxicity

    • Ingestion of >60 mg/kg associated with severe toxicity

  • Less commonly, iron toxicity can result from multiple transfusions for leukemia, thalassemia, etc.

  • Toxicity divided into two mechanisms

    • Caustic/corrosive effect results in direct injury to GI mucosa, can lead to perforation, peritonitis --> hemorrhage, death

      • Typically occurs during the first 6 hours

      • Iron tablets are visible on XR

    • Cellular toxicity is due to disruption of oxidative phosphorylation in the mitochondria, free radical formation and oxidative damage

      • GI symptoms may resolve prior to appearance of systemic symptoms

      • Nephropathy, cardiomyopathy, hepatopathy, and coagulopathy follow

      • Serum Fe levels >350μg/dL associated with moderate symptoms, >500μg/dL associated with severe symptoms

  • Treatment indicated for those a) with symptoms, or b) who have ingested potentially toxic quantities

    • Patients with resolved GI symptoms should continue observation/care for emergence of systemic symptoms

    • Decontamination with WBI indicated if large amount of pills are visible on XR

    • Patients with severe symptoms (acidosis, hemodynamic compromise) or high serum Fe level should receive deferoxamine chelation at 15 mg/kg/hr (max 35 mg/kg/hr) for up to 24 hours (or up to 6g)

    • Can give VitK and FFP to treat coagulopathy

    • Otherwise, supportive care as appropriate

Copper (Cu/Cuprum)

  • Exposure is most commonly from copper-containing cookware, contaminated water, or copper-containing pesticides or creams

  • Wilson's disease is also associated with high bioaccumulation of copper

  • Ingestions, like with iron, cause a direct gastropathy resulting in abdominal pain, vomiting, GI bleeding, et al. w/ potential for blue-green emesis (think how copper-containing surfaces like the Statue of Liberty develop verdigris)

  • High serum levels of copper can lead to:

    • Neuro — cognitive changes, encephalopathy

    • Cardiac — cardiomyopathy

    • Hepatic — necrosis

    • Heme — coagulopathy, hemolysis, methemoglobinemia 

    • Renal — rhabdomyolysis, AKI

  • Treatment, again, is mostly supportive + decon/chelation

    • High-dose zinc can help lower GI absorption 

    • Classically, D-penicillamine is the chelating agent of choice, given at a starting dose of 750mg QID

    • Can also use "single pass albumin dialysis" vs other extracorporeal cupriuresis

    • Symptoms generally reversible with successful elimination of copper

Other little lessons from episode #8:

  • If you have a backyard pool, invest in locked rigid covers and alarms, because otherwise the kids will find a way to get in

  • You're not dead until you're warm and dead — unless you're in rigor mortis, have obvious traumatic injuries incompatible with life, have snow in your airway after being buried by snow, or have a K > 12

  • If you lose any part of your body, to maximize the chances of replantation, you or someone else (if you're unstable) should retrieve it, wrap it in a moist towel/napkin/cloth, place it in a plastic bag, then put that plastic bag on ice

  • Peter Safar, the University of Pittsburgh, and the Freedom House Ambulance Service are the progenitors of the modern EMS model — a public service staffed by trained personnel tthat can provide care en route to the hospital, as opposed to a taxi service

  • Have a high index of suspicion for human trafficking (and/or other forms of abuse) when the patient is accompanied by someone who answers questions for them and refuses to allow a private history/exam; do your best to finagle a private conversation and assess safety, and consult social work to help provide resources if needed

References:
https://www.ncbi.nlm.nih.gov/books/NBK560920/
https://www.ncbi.nlm.nih.gov/books/NBK499935/
https://www.ncbi.nlm.nih.gov/books/NBK541097/
https://www.ncbi.nlm.nih.gov/books/NBK459224/
https://www.ncbi.nlm.nih.gov/books/NBK557456/

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