Grand Rounds Recap - 3/11/15

Health Care Disparities with Dr. Ford

There is a well established distrust of the medical system by minorities, especially African Americans. The historic causes of this distrust are widespread and seen in nearly all stages of American Healthcare. A great resource is Medical Apartheid by Harriet Washington. Some key examples of the use of AA in medical advances: 

1800s: Slaves referred to as "clinical material" in medical schools and journal publications. Slave bought and used for experiments and experimental surgeries including the first successful vesicovaginal fistula repair (caused by forcep deliveries) which was done without anesthesia. 

1900-1930: "malaria therapy" with fatal falciparum used to try and treat syphilis. Tuskeegee experiments- subjects recruited under false pretense of "free testing and medical treatment" for syphilis experiment with no intention to treat despite PCN being widely available. "The future of the negro lies in the research laboratory..." Patients were offered a free burial when they died from the disease so that an autopsy may be performed. "as I see it, we have no further interest in these patients until they die..."

By James E. Westcott [Public domain], via Wikimedia Commons

1940s: era of the Manhattan project: African Americans and psych patients exposed to high levels of radiation and suffered 3rd degree radiation burns to compare protective/harmful effects of skin color on radiation. Some injected with IV plutonium and then underwent multiple surgical procedures to test radiation levels (bone biopsies, tooth extraction, etc).

1960-70s: "Mississippi appendectomy" was common practice where AA women received hysterectomies without their knowledge. Radiology techs noted to be using 25% higher radiation levels in diagnostic tests of AA patients due to "thicker skin and harder bones". 

1980-1990s: 6-10yo siblings of juvenille criminals recruited for fenfluramine injection to test effects on violent behavior. In Baltimore, kids from lead laden home recruited and promised "lead abatement" but randomized to control group with persistent lead exposure. 

"Those who cannot remember the past are doomed to repeat it" - George Santayana

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CPC with Dr. Betham and Dr. Zammit

28yo M with frequent falls (2-3/day), h/o alcohol abuse, alcohol withdrawal, seizure disorder, presents intoxicated c/o falls. Seen in ED day prior for fall with orbital blowout fracture. Disheveled, tachycardic, soaked in urine. Neuro exam shows past-pointing on finger-nose testing, severely dysarthric, very wide based unsteady gate. Normal CT head, EtOH 207, CK 891, lactate 4.2. 

DDx: Wenicke's, acute ischemic stroke, B12 deficiency, hypocalcemia, pancreatitis, hypoparathyroidism, hypothyroidism, syphilis, GBS, AED toxicity, toxic alcohol ingestion, encephalitis/meningitis, tumor, sarcoidosis, normal pressure hydrocephalous, MS, toluene abuse, prion disease, whipple disease, gluten ataxia, mitochondrial disorder, paraneoplastic. 

Diagnostic test: Phenytoin Level - 38.1mg/L

Phenytoin toxicity -  90% of drug is protein bound; it is excreted by the liver. In low concentration excretion follows first order kinetics, but at therapeutic level follows zero order kinetics (maximal amount is constantly being excreted regardless of serum levels). Etiology can be intentional or accidental overdose, altered physiology (ie low albumin). Levels: 10-20 (therapeutic) will have mild horizontal nystagmus. 20-30: spontaneous nystagmus. 30-40: vertical nystagmus, diplopia ataxia, slurred speech, tremor, hyperreflexia, n/v. 40-50: lethargy, confusion, disorientation, hyperactivity, clonus, asterixis. >50: coma. Treatment: supportive care. GI decontamination not recommended b/c of airway compromise which can lead to aspiration. Dialysis of little utility due to protein binding. 

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EBM: Stopping Trials Early with Dr. Mann

Reasons that a trial gets stopped early: stopping for benefit, stopping for harm, stopping for futility, stopping for reasons independent of findings.

Studies are powered to look for a certain treatment difference. If you stop early, you may not reach this. Stopping early limits the utility of subgroup analysis. It also increases your incidence of Type I error (false positive) and will miss secondary harms/benefits. Unfortunately, studies stopped early can be seen as "remarkably good" and get implemented into guidelines based on incomplete data. 

Check out http://mdaware.blogspot.com/2013/06/this-is-not-gambling-advice.html for some more reading on the subject.

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Case Follow-ups

Dr. Boyer: 18yo G1 @ 37wk 1d with h/o sickle cell trait presents with decreased fetal movement, abd pain, SOB, fatigue. Reports SOB with minimal exertion - walking to bathroom. Cardiomegaly on CXR, EKG with deep S-waves in precordial leads consistent with LVH. Diagnosed with peripartum cardiomyopathy (EF 10-15%). Ultimately underwent C-section without complication and discharged on captopril, carvedilol, coumadin, and life vest. Visit #2: febrile with large infected pelvic hematoma, admitted and pelvic drain placed. Sent home on antibiotics. Visit #3: febrile, in acute hypotensive heart failure (EF 5%). No improvement despite maximal medical therapy (milranone, dobutamine, lasix, nitric, flolan) and had IABP placed and VA ECMO was bridge to LVAD.

Peripartum Cardiomyopathy: Most commonly seen in the last month of pregnancy up to 5 months post-partum. Usually present in NYHA class 3-4.

• 50% will recover over 3-6 months 
• 10% will require transplant
• 10% will die
• Acute treatment: Nitro, NIPPV, cardioversion is okay in pregnancy, digoxin is okay.
• In pregnancy, the natural physiology involves increased tidal volume (about 200cc/breath), decreased pCO2, HR increases cardiac output (increases 30-35%).
• Respiratory rate should not change, tachypnea is abnormal. Pregnancy shouldn't cause limitation in daily activity. 

Dr. Thomas: 34yo F French speaking (from Gabon, Africa) complaining of dental pain and has mass on neck. Mass has been there for 2-3 months but doesn't bother her, although it is getting bigger. CT neck shows loculated neck mass read as lymphadenopathy with necrosis concerning for metastatic disease of TB. Negative CXR, positive PPD, positive quantiferon gold [note: PPD can be positive with BCG vaccine, but not quantiferon gold]. AFB culture from biopsy returned positive for TB 4 weeks later. 

By Dr.J.S.Bhandari, India (Own work) [CC BY-SA 3.0 (http://creativecommons.org/licenses/by-sa/3.0) or GFDL (http://www.gnu.org/copyleft/fdl.html)], via Wikimedia Commons

Extra-pulmonary TB: 

• 80% of TB has some pulmonary finding.
• TB lymphadenitis is the most common extrapulmonary finding.
• Pleural TB is common, but usually develops into pulmonary TB.
• Skeletal TB "Potts Diseases" is not common in the US. 

Dr. Strong: 16 yo M with 5 days of headache, photophobia, phonophobia, emesis x2. Seen in outside ED 2 days prior with neg head CT except for sinusitis (placed on azithro). Initially treated with IVF, toradol, reglan without improvement. Then given more IVF, solumedrol (1g) without improvement. LP then performed with opening pressure 23cmH2O, 20cc removed, closing pressure 14cmH20 with much improved headache. CSF with high protein, 80 WBC with 10 lymphocytes. Admitted on ceftriaxone and MRI/MRV performed which showed epidural abscess that worsened in size despite antibiotic therapy and ultimately required craniotomy. 

Intracranial epidural abscess: 

• Etiologies include acute or chronic sinusitis, osteomyelitis of the skull, extension from middle ear infections, trauma, iatrogenesis from craniotomies, hematologic spread.
• Common signs/symptoms: headache, fever, vomiting, AMS, seizure, hemiparesis, cranial nerve findings, cellulitis or frontal swelling. 

Extra-pulmonary TB: 

• 80% of TB has some pulmonary finding.
• TB lymphadenitis is the most common extrapulmonary finding.
• Pleural TB is common, but usually develops into pulmonary TB.
• Skeletal TB "Potts Diseases" is not common in the US. 

Dr. Strong: 16 yo M with 5 days of headache, photophobia, phonophobia, emesis x2. Seen in outside ED 2 days prior with neg head CT except for sinusitis (placed on azithro). Initially treated with IVF, toradol, reglan without improvement. Then given more IVF, solumedrol (1g) without improvement. LP then performed with opening pressure 23cmH2O, 20cc removed, closing pressure 14cmH20 with much improved headache. CSF with high protein, 80 WBC with 10 lymphocytes. Admitted on ceftriaxone and MRI/MRV performed which showed epidural abscess that worsened in size despite antibiotic therapy and ultimately required craniotomy. 

Intracranial epidural abscess: 

• Etiologies include acute or chronic sinusitis, osteomyelitis of the skull, extension from middle ear infections, trauma, iatrogenesis from craniotomies, hematologic spread.
• Common signs/symptoms: headache, fever, vomiting, AMS, seizure, hemiparesis, cranial nerve findings, cellulitis or frontal swelling. 

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PEM Sim Session 

Sim case: 15yo M unrestrained passenger, GCS 5 on scene, ? seizure on scene followed by cardiac arrest x1-2 minures with ROSC. Intubated prior to arrival. Arrives bradycardic, hypotensive, with chest and abdomen ecchymosis and evidence of pulmonary contusion on CXR. FAST negative. Despite fluids, blood pressure did not improve. Ultimately diagnosed with cardiac contusion resulting in cardiogenic shock. 

Question to ponder: when do you reach for pressors in trauma? If so, which pressor do you choose?

Oral Boards Case: 8 mo M not feeding well x4 days. Seems disinterested in feeding and has decreased urine output x1 day. Is ill appearing, cool to touch, HR 160 and RR 60 with retractions. DDx: congenital cardiac abnormality, myocarditis, pulmonary infection, dehydration, pyloric stenosis, intussusception, tox, non-accidental trauma, sepsis, metabolic (acid/base status, glucose, adrenal suppression). 

• EKG with sinus tach with large p-waves and diffuse ST changes. CXR with cardiomegaly. Positive troponin. Echo with severe LV disfunction, OA hypertension, depressed RV function. 
• Myocarditis: 30% of cases of undiagnosed sudden pediatric cardiac death test positive for myocarditis on autopsy. Cause is most commonly infectious (enterovirus, adenovirus, parvovirus, EBV, CMV, influenza). Treatment is support with cardiovascular stabilization (antiarrhythmics, vasodilators, inotropes, diuretics), antimicrobial treatment as indicated, prevent further cardiac stress (restrict activity, may need mechanical ventilation), possibly a role for IVIG and LVAD/ECMO as bridge to resolution or transplant. 

Defib/Cardioversion in Pediatrics

• Very rare to shock a kid, so generally we are uncomfortable with it. 
• Stable SVT: first try vagal maneuvers (ice to face) or adenosine.
• Unstable SVT: Dose is 1J/kg synchronized cardioversion. Consider nasal versed prior to procedure. 
• VF/VT arrest: Dose is 4J/kg unsynchronized defibrillation