Grand Rounds Recap 1/20

/

Quarterly Simulation and Oral Boards

How do you approach the undifferentiated patient in arrest?

  • Your demographics and any initial history can differentiate the hyperkalemic arrest from recent chemo from the rhabdo from prolonged down time from overdose, etc.

Running a code is an art and a science

  • Mental modeling is something that causes us angst but it works. Close your loop with your drugs and plan. Being loud with your summary reasserts your control of the situation and can quell the peanut gallery.
  • Assign your roles and know your nurses and medics, introducing yourself mid-compressions is poor form and can decrease code efficiency
  • We like to keep our fingers on the femoral pulse. It decreases pulse check time, let's you dictate timely next moves.

Tumor Lysis Syndrome

What is it?  - Rapid lysis of tumor cells leading to massive release of intracellular contents into the blood stream

  • Purine Nucleic acids -> Hypoxanthine -> xanthine -> Uric Acid (precipitates in distal renal tubules leading to renal failure)
  • Phosphorous (4x higher concentration in malignant cells as compared to normal cells) -> calcium-phosphate precipitation in renal tubules -> worsened renal failure -> worsened hyperphosphatemia
  • Potassium - hyperkalemia exacerbated by renal failure

Clinical manifestations - nausea, vomiting, diarrhea, anorexia, edema, fluid overload, hematuria, CHF, dysrhythmia, seizure, muscle cramps, tetany, syncope, sudden death

Who’s at risk? - NHL, Burkitt’s lymphoma, ALL, AML

  • High tumor cell proliferation rate, large tumor burden, tumor chemrsensitivity, increased LDH levels, pre-existing renal insufficiency

How prevalent? Varies based on underlying malignancy, linically-relevant TLS in 6% in NHL by 26% in B-ALL

How do you treat it?

  • Aggressive IV fluids
  • Alkalinization is no longer recommended.
  • Allopurinol (blocks xanthine and hypoxanthine metabolism to uric acid) - however can also lead to build up of uric acid precursors which can crystalize and cause renal failure and can reduce the clearance of the purine-based chemotherapeutic agents
  • Recombinant urate oxidase (Rasburicase) - urate oxidase is an enzyme present in most mammals but not humans (due to a non-sense mutation in the gene sequence).  Converts uric acid to allantoin which is 5-10x more soluble in urine

Oral boards Tips

  • Come up with a system - it is easy to get derailed and knowing what you are prone to forget 'repeat vitals' 'talk to family' 'treat pain' can be helpful reminders
  • E-oral boards (to be ~30% of total encounters) are coming and we tried them out this week - remember to keep you system and continually keep an eye on the monitor for updates and changes that may not be announced by the examiner
  • Hyperthyroidism case - when dealing with altered patient go broad and aggressive when in doubt, in real life you would second guess a head CT and LP, in oral boards just do it. Also remember traditional dogmas and respond appropriately. Cocaine use? No beta blockers..
  • Body packer case - don't do it, kids. Massive cocaine ingestion requires large benzodiazepine doses and these patients have a propensity for decompensation. In your stable patients you can consider . Symptomatic patients warrant engaging GI and surgery for EGD vs enterotomy for removal.
  • MI Case - 64 yo female with substernal chest pain who presents hypotensive and with inferior MI on EKG.
    • Consider dissection and obtain CXR
    • Give IV fluids and avoid nitro.
    • Cardiac catheterization lab unavailable so administer thrombolytics

INFLAMMATORY BOWEL DISEASE WITH DR. SABEDRA

Inflammatory bowel disease encompasses Crohn’s disease (CD) and ulcerative colitis (UC), which involve chronic GI tract inflammation.  While UC affects only the mucosa/submucosa of the rectum and colon, CD can affect any part of the GI tract and is transmural.  Our role is to recognize potential new cases, identify serious complications, and determine appropriate disposition.  It is important to ask about family history and risk factors for infection.  Patients often present with nonspecific symptoms including abdominal pain, diarrhea (+/- blood), and may also have fever, nocturnal diarrhea (which distinguishes from IBS), and weight loss or growth failure.  Perianal fistula, skin tags, or fissures may suggest an inflammatory process.   They may also have extraintestinal manifestations including oral ulcerations, rash, eye inflammation, liver abnormalities, or arthritis.  While there are many things on the differential for abdominal pain and diarrhea, many of these things can exist concurrently with IBD.  For example, an infection can precipitate a IBD flare, and many IBD patients frequently have IBS as well.

As IBD is an inflammatory process and workup should include ESR and CRP.  In addition, studies have shown the presence of fecal calprotectin is highly sensitive and specific for identifying adults with IBD.  There is also high sensitivity, but lower specificity in children.  If you suspect underlying infection additional stool studies including culture, O&P, and C. difficile toxin should be sent as well.  Finally, these patients should get a CBC as many develop anemia that can be severe and require transfusion.  Imaging studies are limited in the ED to identifying suspected complications.

Pain is the most common reason for presentation to the ED.  Patients are often on chronic opioids at baseline and can have high narcotic requirement.  However caution is advised in using these and antispasmodics as both can precipitate worsening dysmotility, and narcotics can also induce ileus, toxic megacolon, and narcotic bowel syndrome.

Disease severity and response to outpatient therapy can help guide disposition.  Disease activity is based on ability to maintain hydration, pain level, and signs of systemic toxicity.  Patients with mild to moderate activity can be managed outpatient with a steroid burst and taper.  If underlying infection is suspected they may also benefit from antibiotics.  In this case it is often prudent to refrain from steroids.  All discharged patients should have referral for GI follow-up.

Complications to be vigilant for include fistulae, abscesses, obstruction, and toxic megacolon.  Our main intervention for fistulae is antibiotics if secondary infection has developed.  Abscesses can be identified on CT and can be treated with IV antibiotics and/or percutaneous drainage.  Surgery is another option and is the most effective treatment for reducing risk of recurrent abscess.  Obstruction can occur for various reasons but usually can be managed the same as obstructions in non-IBD patients.  Toxic megacolon patients are very ill-appearing.  It can be precipitated by many of the medications used by IBD patients and is diagnosed on plain film.  Management consists of broad spectrum antibiotics, IV steroids (unless infectious etiology suspected), and surgical consultation.

TAMING THE SRU - Neurogenic shock WITH DR. AXELSON

Neurogenic shock is rare. In a hypotensive trauma patient, aggressively pursue sources of bleeding, and then pursue them again, before making an empiric diagnosis of neurogenic shock.

The classic presentation of neurogenic shock is hypotension, bradycardia, and warm extremities. Interestingly, bradycardia for the purposes of neurogenic shock (in the only two published definitions of neurogenic shock), is actually defined as HR < 80 (not 60 as typically is taught).

The number of spinal cord injury patients who actually present in neurogenic shock is small. One study in Resuscitation reported that 19% of trauma patients with isolated cervical spinal cord injury present with the classic definition of neurogenic shock, and only 14% of all comers with traumatic, isolated, spinal cord injury fit the definition of neurogenic shock.

Neurogenic shock is not the same as spinal shock. Spinal shock refers to flaccid areflexia below the level of a spinal cord lesion. It has no hemodynamic implications.

Despite what is classical taught, neurogenic shock can, in fact, present with tachycardia. If your spinal cord lesions is below the level of ~T5/T6, your sympathetic outflow to the heart is maintained. You lose sympathetic outflow below the level of the lesion, so in the case of a mid/high thoracic spinal injury, this results in pooling of blood in the abdomen, and resultant hypotension from absence of sympathetic tone to the splanchnic mesentary. But because you maintain sympathetic outflow to the heart, you can mount a tachycardia in response.

There is no consensus single pressor agent that is literature proven for treatment of neurogenic shock. Norepinephrine is probably your best choice because it is easily titratable, it gives alpha and beta squeeze, both of which you lose in neurogenic shock.

The consensus of both the American Association of Neurological Surgeons and the Congress of Neurological Surgeons is that you should target a MAP of 85-90mmHg in true, imaging confirmed neurogenic shock. This is based on class III evidence (retrospective, or flawed RCT data), that does suggest some improvement in neurologic outcomes at these higher MAPs for 7 days post injury. 

Case Follow up with Dr. Renne

Air emboli are a rare but likely underdiagnosed complication of central lines that can be catastrophic 

They are caused by an increase in the gradient between atmospheric pressure and the pressure in the central venous circulation, usually by a rapid decrease in the central venous pressure while the vasculature is exposed to air (i.e., deep inspiration during insertion or removal of a central line)

In one large study of 11,000 central venous catheter insertions, air emboli occurred on insertion in 15 patients with nearly an even split between IJ and SC lines; the prevalence may be even more common than realized because of the diverse presentations of air emboli

Symptoms of air emboli range from none to dyspnea/hypotension/hypoxia/dysrhythmia to cardiac arrest

In the ~1/4 of population with a PFO, air may migrate through a potential R-to-L shunt into the arterial circulation and cause debilitating strokes or MIs

Prevention of air emboli is key and involves the following:

  • Head down positioning (increases CV pressure when cannulating an IJ, minimizing air-to-vein pressure gradient)
  • Occluding open hub on insertion and using occlusive dressing over site after removal
  • Having patient hum/valsalva (if awake) or performing an inspiratory hold (if on ventilator); credit to Dr. Bonomo for the insp hold tip

Diagnosis of air emboli is best done with echocardiogram (bedside or formal) or CT; ETCO2 and SWAN are less specific modalities

Treatment of air emboli must be implemented swiftly and aggressively once identifying it; one can use the “4 Hs"

  • Head down and left side positioning (again, increases CV pressure to reduce amount of air entrained AND traps air in RA/RV to prevent migration into pulmonary vasculature AND theoretically protects coronary ostia from air)
  • High flow oxygen (facilitates emboli dissolution and mitigates hypoxia)
  • Hemodynamic support (fluids, pressors)
  • Hyperbarics (reports of positive neuro outcomes even when used 21 hours out from inciting event) and Heroics  (thoracotomy for direct air aspiration or aortic cross-clamping; alternatively extracorporeal support might be an option)

R4 Capstone - Global health with Dr. Selvam

One of the fundamental tenets of global health is the concept of the’ global commons’ or the idea that our health is inexorably linked to the health of other people around the world.

The United States has 293 physicians per 100,000 population; this accounts for 40% of the global health care workforce, though we have only 10% of the world’s disease burden

Meanwhile, Sub-Saharan Africa bears 25% of the world’s disease burden with only 3% of the global health care work force

Tanzania has only 8 physicians per 1 million population, one of the lowest ratios in the world

What is Global Health?

  • “Global health emphasizes transnational health issues, determinants, and solutions; involves many disciplines within and beyond the health sciences and promotes interdisciplinary collaboration; and is a synthesis of population based prevention and individual-level clinical care.” (Koplan et al)

Neglected Tropical Diseases (NTDs)

  •   Impact 2.7 billion people in 142 countries
  • Diseases include:  Hookworm, Ascariasis, Trichuriaisis, Lymphatic filariasis, Schistosomiasis, Trachoma, Leishmaniasis, Chagas disease, Trypanosomiasis, Onchocerciasis, Leprosy
  • When combined, the NTDs rank second to only HIV/AIDS (and ahead of malaria and TB) in terms of global burden/morbidity
  • DALYs = Daily adjusted life years lost
  • Kala Azar (aka Visceral Leishmaniasis) accounts for approximately 200,000 deaths and is the 2nd largest parasitic killer in the world
  • Onchocerciasis (aka River Blindness) leads to vision loss in almost 1 million people (1.99 million DALYs lost)

Global Pharma

  • Over the past 30 years, only 10 drugs developed for NTDs, 18 if you consider Malaria, and 21 if you count TB
  • This accounts for 1% of new chemical entities (NCEs) launched until 2007

Road Traffic Accidents (RTAs)

  • Account for 23% of all injury deaths worldwide (1.3 million deaths/yr)
  • 2.1% of all deaths globally
  • 20-50 million injured/disabled
  • RTAs rank 2nd (behind only HIV/AIDS) as a killer; RTAs tied with TB and ahead of malaria
  • Do local populations experience health inequities within countries just as is seen globally between countries?
    • In a recent report the US ranked 3rd in the world in total health care expenditures (as a percentage of GDP) but 32nd in life (HIA Report 2011)
    • ”…We have not sufficiently recognized and appropriately dealt with the inequities underlying average health statistics.  This has meant that even when overall progress has been made, large parts of populations, and even whole regions of the world, have been left behind” (WHO 2010)