Grand Rounds Recap 11.10.21
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MED-MAL: THE DEPOSITION OF DR. WALSH WITH DR. HASSANI
Four elements in medical malpractice:
Duty - doctor-patient relationship established, treating per standard of care
Breach of duty - failed to meet standard of care
Proximate case - care had to be THE cause of the patient’s injury (definition varies by state)
Damage - economic (lost wages, hospital bills) and non-economic (pain, suffering)
The Deposition is the first element before the trial. It is a sworn testimony of a witness taken before trial, and during which, everything that is said can be referenced in the trial. You can’t win, but you can lose big in the course of a deposition. You have access to the medical record and are provided documents to review 180 days in advance.
Recommendations for individuals preparing for a deposition:
Less is better - think of the deposition as a document that is going to be used against you. The less there is, the less harm there can be
Be confident but not arrogant
Don’t guess
Don’t interrupt
Don’t say how busy the ED was
Use medical terminology sparingly
Assume everything is on the record
Be aware of common traps:
Rule out questions - For example, “Did you rule out a calcaneal fracture?” Make them explain what they mean by rule out.
Compound questions - two questions asked back to back. Always attempt to answer one question at a time so you know exactly what question you are answering.
Questions preceded by statements - “Looking back at his imaging, it appears he had two abnormal findings. How did you explain those findings?” You don’t know what they are referring to, which causes you to answer blindly.
Double negatives.
Hypothetical questions - what I was doing at the end?
Recommended reading:
R2 CPC: CBD DILATION AND LEMMEL SYNDROME WITH DR. STEVENS AND GENSIC
The case: Middle aged patient with PMH of GERD, esophago-tracheal fistula s/p repair remotely, cholecystectomy, IBS, right sided nephrolithiasis s/p lithotripsy and stenting, thyroid disease, appendicitis s/p appendectomy who presents with RUQ pain that is sharp and stabbing x 3 days, similar to previous nephrolithiasis pain, no other symptoms. Vitals unremarkable. Exam with RUQ and right CVA TTP, no rebound or guarding. Work up notable for negative UA and urine pregnancy, mild leukocytosis with WBC of 12, stable hemoglobin, renal US without hydronephrosis.
The proposed, narrowed differential and diagnostic test:
Liver - acute hepatitis (alcoholic, viral), hepatic abscess, hepatic malignancy
Gallbladder - choledocholithiasis
Pancreas - pancreatitis, pancreatic cyst, pancreatic pseudocyst
Diagnostic test of choice for intraductal biliary stone in post-cholecystectomy patient: CT abdomen/pelvis
The (actual) test: CT abdomen/pelvis, which demonstrated primary pancreatic neoplasm based on biliary and pancreatic ductal dilation with a lesion in the pancreatic head.
The plot thickens: later upper endoscopy with no pancreatic abnormality, smooth tapering of the distal bile duct. Recent MRI with small duodenal diverticulum which changes configuration with peristalsis and causes intermittent compression of the common duct with variations in upstream caliber consistent with Lemmel Syndrome.
Causes of CBD dilation:
Biliary calculi
Benign biliary strictures (congenital, post infectious, inflammatory)
Lemmel syndrome
Mirizzi syndrome
Sump syndrome
Lemmel Syndrome is a difficult and rare diagnosis, which refers to periampullary duodenal diverticulum causing extrinsic compression, dilation of the common bile duct, and potentially obstructive jaundice.
There are several proposed mechanisms for Lemmel Syndrome including the following:
Diverticulitis or direct mechanical irritation causing chronic inflammation of ampulla and chronic fibrosis of papilla
Dysfunction in sphincter of Oddi
Distal CBD or ampulla direct compression
Treatment hinges on whether an individual is symptomatic or not.
Asymptomatic: conservative
Symptomatic: endoscopic extraction, extracorporeal shock wave lithotripsy, surgery, sphincterotomy
Diagnosing cancer in the ED:
Those diagnosed with cancer during an ED visit are more likely to have the following according to a study by Sikka & Ornato:
To have 3 or more comorbidities
Be female
>85 years old
Be African- American (lung)
Diagnosed at a later stage
As compared to another study by Weithorn et al:
>80 years old
Medicare or Medicaid
Stage 4 cancer
Symptomatic
R1 CLINICAL DIAGNOSTICS: HYPERGLYCEMIA IN THE ED WITH DR. SHAW
See more via Dr. Shaw’s full post here
Epidemiology:
16 million ED visits with diabetes listed as one of the diagnoses
224,000 ED visits for hyperglycemic crisis
Key differences between DKA and HHS related to underlying pathophysiology. Specifically, DKA is due to an absolute insulin deficiency leading to decreased glucose use, hyperglycemia, fatty acid oxidation, and ketogenesis whereas HHS is due to insufficient insulin to control blood sugar but sufficient enough to suppress lipolysis and ketogenesis.
Precipitants for DKA/HHS: Infection, infarction, infant, indiscretion (dietary non-adherence), insulin deficiency
Diagnostics: Renal, VBG, serum ketones. Additional +/- labs: CBC, troponin, UA, pregnancy test, blood cultures.
Remember absence of urine ketones (which tests for acetoacetate) does not rule out DKA, so must secure serum ketones (beta-hydroxybutyrate, BHB).
The diagnostic criteria for HHS are profound hyperglycemia, hyperosmolarity, absence of DKA with a neurologic deficit (ie, altered mental status, focal weakness, sensory deficit, seizures, coma)
DKA and HHS Treatment:
Check out our Taming the SRU protocol
In short, fluid resuscitation for profound hypovolemia - up to 6 L in DKA and up to 9 L in HHS, though should be adjusted to the patient and response to initial resuscitation.
Check potassium before initiating insulin and add potassium to fluids depending on initial level.
Once there BG < 250 in DKA and < 300 in HHS, can consider adjusting insulin infusion rate and starting dextrose-containing IV fluids.
Insulin dosing:
Expected rate of decrease in serum glucose concentration is 50-75 mg/dL/hr.
There is no utility of initial regular insulin bolus based on several studies examining its effects on anion gap resolution, rate of change in hyperglycemia, or IV fluid management
However, if you do not bolus, then you should start at a higher rate ~ 0.14 U/kg/hr, which is not the default in most EHR right now. Otherwise, rate may be too low to suppress hepatic gluconeogenesis and facilitate glucose uptake.
You could consider manually changing this, but with increased boarding as well as comorbidities such as CKD, concern for frequent BG checks needed and risk of hypoglycemia and delayed clearance in the latter.
Asymptomatic moderate to severe hyperglycemia
2016 Driver et al study in Annals of Emergency Medicine - single center retrospective cohort sought to determine if there was an associated between discharge glucose and 7-day adverse outcomes, including DKA, HHS, repeat ED visits, hospitalization for any cause
Low rates in general. Of 566 hyperglycemia ED encounters included: DKA (0.4%), HHS (0%), Return visits (13%), hospitalization (7%), death (0%)
Annals of Emergency Medicine 2016: Hyperglycemia is incredibly common. Long-term glucose control does matter, but this is out of our realm.
Key points:
Fluid resuscitation is the most important initial step in treating DKA. Patients with DKA or HHS have significant total body water deficits. Care must be taken not to give fluid too rapidly.
A bolus of insulin has not been shown to have any benefit in treating DKA/HHS. If insulin bolus is not given, the continuous infusion rate should be started at 0.14 units/kg/hr to ensure adequate plasma concentrations of glucose.
You don’t have to ”treat the number” for an incidental finding of elevated glucose. What is most important is assuring home insulin and helping arrange close outpatient follow up to prevent long term complications of diabetes
R4 CASE FOLLOW-UP: HIV, AMS, AND TRIAGE BIAS IN PSYCHIATRIC PATIENTS WITH DR. LAURENCE
Paradigm 1: We should work to provide the best HIV care we can in the ED
Patients with HIV visit the ED three times more frequently than patients without HIV.
We must keep a broad differential and recognize known sequelae of specific pathogens.
Cultivate an understanding of the diseases that specific patients are at risk for, their barriers to care, and work to advance them to the next step.
Viruses do weird things; expect the unexpected.
Altered mental status in HIV should prompt consideration of a much broader differential diagnosis, particularly if the patient is significantly immunosuppressed. Some considerations include:
Opportunistic infections: neurosyphilis, TB, amebiasis, CMV encephalitis, toxoplasmosis, HTLV-1
Secondary HIV effects: progressive multifocal leukoencephalopathy, immune reconstitution inflammatory syndrome (IRIS), primary CNS lymphoma, AIDS dementia complex, HIV associated neurocognitive disorders (HAND), Kaposi sarcoma.
Neurotoxic effects of antiretrovirals (efavirenz can cause visual hallucinations)
HIV neurotropism: HIV affects microglia in the brain causing direct effects
HAART has poor CNS penetration, leading to viral haven
Key elements of the history in HIV: temporal progression, associated symptoms, focal symptoms, trauma, substance use, recent CD4 count and viral load, HAART regimen
Paradigm 2: Multiple forms of bias can influence our ED triage of patients with psychiatric complaints and our approach to medical clearance. While patients with HIV have a higher prevalence of psychiatric disorders, this should be weighted against other possible diagnosis.
4-10 times the rate of mental health problems among people vulnerable for acquiring HIV and people living with HIV compared to the general population.
21-71% prevalence of substance use disorder among people living with HIV compared to general population
Forms of bias that might influence ED triage or physician approach to psychiatric patients
Availability bias: we tend to judge the likelihood of disease by the ease with which relevant examples come to mind - keep an open mind and broad differential
Ascertainment bias: our thinking is shaped by prior expectations; you see what you expect to see.
Triage cueing: “geography is destiny;” where and how a patient is triaged can affect the perceived severity of illness
Diagnostic momentum: prior or recent diagnosis prevents broadening of the differential
Zebra retreat: less experienced providers hesitate to suggest a rarer diagnosis for fear of seeming illogical or using too many resources
Use of the Initial Triage Assessment (a 10-question prompt) may improve our triage and assessment of patients with psychiatric complaints, rather than using the current ESI criteria, though still imperfect
According to one other study by Olshaker et al of patients with behavioral emergencies, reliance of physician-elicited history had a sensitivity of 94% for detecting medical problems.
Paradigm 3: Preserve and integrate love for what drove you into medicine into your day-to-day patient care. Sometimes, this may mean looking for zebras, and there is value in this hunt with respect to type 2 thinking.
