Grand Rounds Recap 12.20.17

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Morbidity and Mortality with Dr. Gorder

Case 1 - Aortic Dissection

Stanford Classification of Aortic Dissection

  • Type A: involves the aortic arch, commonly starting in the right lateral ascending aorta which is where the RCA takes off of the aortic root
  • Type B: occurs distal to the left subclavian and does not involve the aortic arch

Epidemiology. Often presents in men between ages 50-70 years old. It is thought that 25% of aortic dissections occur between 8AM-noon due to daily swings in blood pressure.

Studies have shown that mortality increases by 1-2% per hour after initial dissection occurs. 

Risk Factors

  • Hypertension
  • Structural abnormalities such as aortic valve replacement, bicuspid aortic valve
  • Genetic abnormalities such as mixed connective tissue disorders
  • Drug induced most commonly from cocaine
  • Vasculitis like syphilis that cause dilation of the aortic root
Figure 1. 2014 ESC Guidelines on management of Aortic Diseases common presenting symptoms for dissections

Figure 1. 2014 ESC Guidelines on management of Aortic Diseases common presenting symptoms for dissections

Common presenting symptoms as described from the IRAD (International Registry of Acute Aortic Dissection) are sudden, acute onset of sharp, stabbing severe pain.  The 2014 ESC Guidelines on Management of Aortic Diseases comments on common presenting symptoms for type A and B dissections. (Figure 1).

Diagnostics

  • Blood pressure. Patients with type A dissections are often normotensive. Patients with type B dissection are commonly hypertensive. Patients are hypotensive due to either hemorrhage from extravasation or due to tamponade physiology. 
  • Abnormal pulses and unequal blood pressures occur in <30% of patients. 
  • D-dimer in aortic dissection. A study in Circulation in 2009 describes a 95% NPV at 500 ng/mL cut off for patients presenting in the first 24 hours. The American Heart Association does not recommend routine use of D-dimer in the diagnosis of aortic dissection. 
  • Chest x-ray. Mediastinal widening is seen in 63% of patients with type A dissections and 56% of patients with type B dissection, and terrifyingly chest x-rays are read as normal in 13% of patients. The AHA recommends that CXRs should not be used to rule in or out dissection but as part of the work up of aortic dissection. Pleural effusions are seen in 19% of patients and is likely due to extravasation from the dissection flap.

EKG Changes

  • Demand ischemia from hypotension, aortic regurgitation, or shock. These will often be non specific EKG changes.
  • Direct involvement of the right or left coronary arteries from the dissection flap. This is only seen in type A dissection.
  • Electrical alternans can be seen if cardiac tamponade is present. 
  • A study of patients with type A dissections found that 49% of patients present with new EKG changes. Of these patients, 8% of patients with type A dissections present with ST elevation, most commonly RCA STEMIs. ST depressions are seen in 34% of patients,

Most common ED working diagnosis in missed dissection is ACS. 

It is important to consider aortic dissection in intermittent to high risk chest pain patients with out a diagnostic EKG. 

Ultrasound

  • EM performed bedside TTE is 77-80% sensitive, 93-96% specific. Cardiac ultrasound is better for identifying type A dissection. 

Case 2 - Adrenal Insufficiency

Hypothalamus secrets hormones to the pituitary which secretes hormones to end organs. 

Diabetes Insipidus

  • Symptoms are commonly excessive urination and extreme thirst. 
  • Central DI implies that there is a problem with the hypothalamus or pituitary due to a lack of ADH. 
  • Diagnosed with a water deprivation test.
  • Treated with ddAVP, a synthetic analogue of ADH.

Adrenal Insufficiency

  • Primary - Problem with the adrenals themselves, a lack of production of hormones by the adrenal glans. Most commonly due to Addison's Disease, an autoimmune disorder. These patients lack glucocorticoids (cortisol) and mineralocorticoids (aldosterone). 
  • Secondary - Due to impairment of the hypothalamus or pituitary gland resulting in a lack of ACTH. Commonly due to pituitary adenomas.
  • Tertiary - Due to lack of corticotropin releasing hormone. Commonly due to abrupt cessation of chronic steroid use. 
  • Electrolyte abnormalities - Most commonly patients have no electrolyte abnormalities. However, some electrolyte abnormalities are classically described in the literature and often seen in primary adrenal insufficiency. Hyperkalemia is due to a lack of aldosterone which normally regulates the secretion of urinary potassium. Hyponatremia is due to a lack of aldosterone and also the lack of cortisol.
  • Treatment of adrenal insufficiency is individualized for each patient. Most patients need glucocorticoid (hydrocortisone) replacement and some patients may also require mineralocorticoids (fludrocortisone).

Adrenal crisis is the feared complication of adrenal insufficiency. Can be due to acute-on-chronic adrenal insufficiency or de novo. Most commonly, adrenal crisis is caused by acute steroid withdrawal or acute critical illness. Symptoms include nausea, vomiting, and weakness. In a worst case scenario these patients present with refraction hypotension and shock. Gold standard for diagnosis is an ACTH stimulation test which is time intensive and not feasible in the ED. 2017 ESICM and SCCM guidelines recommend treatment of adrenal insufficiency with steroids, 100mg IV hydrocortisone. This is because at doses of >50mg IV hydrocortisone has significant mineralocorticoid activity in addition to glucocorticoid activity. If a patient does not have a history of adrenal insufficiency and you would like the patient to get a ACTH stimulation test while admitted you can give 4mg of IV dexamethasone. Of note, dexamethasone only has glucocorticoid activity. 

In patients with known adrenal insufficiency, who are not in adrenal crisis, it is important to double the daily oral glucocorticoid dose in patients with acute illness.

Case 3 - Hypertensive Emergency

October 2017 ACC/AHA guidelines define SBP >120 and DBP >80 as abnormal and elevated. 

Hypertensive urgency is defined as a BP >180/120 AND otherwise stable without evidence of target end-organ damage. These patients should be managed with reinstitution or intensification of antihypertensive medications. Based on these new guidelines, there is no indication for referral to the ED or immediate reduction of BP while in the ED. These patients are not recommended to come to the ED. ACEP recommends no routine role of screening labs or EKG in asymptomatic patients who present to the ED with hypertension. However in patients with poor follow up you can consider checking a creatinine. Initiation of medications are not indicated however can be considered in patients with poor follow up. A large 2009 Brazilian meta-analysis recommends PO ACE-I or clonidine for PO medical management of hypertensive urgency. 

Hypertensive emergency is defined as BP >180/120 AND evidence of target end-organ damage. Target end-organ damage is defined as hypertensive encephalopathy, ICH or ischemic stroke, acute heart failure with acute pulmonary edema, aortic dissection, acute MI or unstable angina. Recommended BP reduction is no more than 25% in the first hour. After the first hour, reduce the BP to 160/100 over the next 2-6 hours. ICU level of care is recommended. First line medications are short acting, IV, titratable agents such as nicardipine (contraindication in critical aortic stenosis), esmolol/labetalol (use with caution in patients with COPD, asthma, or in patients with bradycardia), or nitroprusside. 

In the management of cocaine induced hypertensive emergency the AHA recommends the use of nitroglycerin or calcium channel blockers. 

Chronic hypertension changes the autoregulation of the brain. This is thought to be due to chemical and vascular changes in the brain that maintain cerebral perfusion however evidence supporting this is lacking. 

    Global Health Case series with Drs. Liebman, Banning, and Owens

    Shirati, Tanzania

    Case 1: Lymphatic Filariasis

    • Caused by the parasitic roundworm Wucheria bancrofti and spread via a mosquito vector. It often takes many mosquito bites, over many months before symptoms develop.

    • The adult roundworms mate in the lymphatic system causing the release millions of microfilariae. The parasitic roundworm damages the lymphatic system causing lymphedema. Over time, the skin becomes hardened and thickened, causing elephantiasis.
    • Males can also present with scrotal edema or a hydrocele.
    • Diagnosis is made with either a blood smear, best obtained at night when microfilariae are active, or with antifilarial IgG.
    • Diethylcarbamazine (DEC) is the treatment of choice but is contraindicated if onchoceriasis is present as this may lead to encephalopathy and death. 

    Case 2: Scabies

    Treatment is with either topical permethrin or oral Ivermectin. It is also important to treat all close contacts even if they are asymptomatic and to wash all bedding and clothing in hot water. However, in many parts of the world permethrin and oral Ivermectin are not available. Alternative treatment options are benzyl benzoate emulsion (BBE) and sulfur based soaps. 

    Chocola, Guatemala 

    Case 1: Leishmaniasis

    • Caused by the protozoan Leishmania parasite and is transmitted by the female sandfly.
    • There are three manifestations of leishmaniasis; cutaneous, mucocutaneous, and visceral also known as kala-azar. Cutaneous leishmaniasis is characterized by small painless papules that over time develop into painless ulcers, often called Chiclero’s ulcer. Diagnosis of cutaneous disease is made based on skin scrapings stained with a Giemsa stain. Mucocutaneous disease, most commonly seen in the nose, is thought to be due to spread of cutaneous leishmianasis.
    • Risk factors for leishmaniasis are poverty, urbanization, deforestation, crowding, and poor nutrition status.
    • There are 0.6-1 million new cases annually. Leishmaniasis is endemic to Guatemala. 
    • Treatment of cutaneous disease is most commonly with cryotherapy, heat, or Paromomycin cream. If there is concern for systemic disease the gold standard treatment is intramuscular Pentavalent which is an antimonial.

    R4 Soapbox: Firearm Violence with Dr. Grace Lagasse

    Firearm-injuries are defined as penetrating and non-penetrating injuries from a weapon that uses a powder charge to fire a projectile.  Firearms are the leading cause of violent death in the US and are responsible for over 30,000 deaths annually.

    Firearm violence represents a public health emergency. It is an extremely lethal heath event. Unlike most other causes of injury where death compromise only a fraction of the total burden of injury, firearm deaths make up a large proportion of the total burden of injury. Victims of firearm violence who present to the ED cost our health system billions of dollars a year and are often uninsured or on Medicaid. 

    ACEP supports a multifaceted public health approach to combating firearm violence. 

    A 1993 NEJM article reported a strong and independent associated between gun ownership and homicide with an adjusted OR of 2.7. In 1996 the Dickey Amendment was passed which limited the CDC's ability to fund and preform gun control research. In response to the Newton school shooting in 2012, President Obama signed an Executive Order to allow the CDC to research gun violence. However, this Executive Order did not include funding to support this research.

    Child Access Protection (CAP) laws impose criminal penalties for improper firearm storage and have been enacted in 14 states and the District of Columbia. These laws have reduced both firearm suicides and unintentional firearm deaths. Studies in Wisconsin and Alabama have also shown that increased background checks led to decreased firearm suicide and homicide rates.

    There is a historical precedent for ED based interventions. Why can't this also include firearm violence? Evidence has shown that 40% of violently injured youths return to the ED with future violence related injuries and of these patients that return to the ED, 20% are victims of homicide within 5 years. Baltimore, Chicago, Milwaukee, and Oakland have all enacted ED based interventions and have shown positive but not statistically significant results.

    Consultant of the Month: Dentistry with Drs. McMahon and Dagher

    Fractured teeth are defined by Ellis classifications.

    • Class I involves the enamel only.
    • Class II involves the enamel and dentin.
    • Class III involves the enamel, dentin, and pulp. 

    Management of fractured teeth can be done with Temp-Bond and is for symptomatic control. This usually occurs in patients with class III fractures and sometimes in patients with class II fracture. In patients with class III fractures they will ultimately require a root canal with dentistry but by covering the exposed tooth gives patients significant pain control. 

    Stabilizing teeth can be preformed with Coe-pak. Tips and tricks- need wet hands when manipulating the Coe-Pak and need to dry the teeth that you are applying the Coe-pak on to! Want to splint the affected tooth with two teeth on each side. This can be done for subluxed, luxated, and avulsed teeth. Patients may need anesthesia to tolerate this procedure. If an avulsed tooth is grossly dirty (has fallen on the ground) it is OK to gently irrigate with saline but do not scrap or wipe the tooth. Generally, these patients do not need antibiotic prophylaxis but if you are going to give antibiotics penicillin or amoxicillin is considered first line. For patients who are penicillin allergic clindamycin is considered first line.

    • Subluxed tooth is loose but not displaced
    • Luxated tooth is displaced. 
    • An avulsed tooth needs to be replaced a quickly as possible (within 1-2 hours) and need to have close follow up. 

    Dry socket occurs 3-5 days post op from tooth extraction. Patients often present with increased pain, bad odor, and bad taste in the mouth. It occurs due to a loss of the blood clot leading to exposed bone. The socket may have necrotic debris in it. Treatment options include irrigation with peridex, curette to induce bleeding and placement of a dressing such as a paste or eugenol.