End of Life Discussion

1. Introduce yourself and your role. I would like to discuss the next steps in taking care of X.
2. Setting up the scene. Determine what the pt / family already knows.* Determine pt’s functional status prior to illness.
3. Deliver bad news. I would like to provide you with an update on X’s medical condition
  • don’t focus on the medical, but rather on what is pt-centered: function, quality, and time of remaining life
  • summarize condition with a bottom-line: ‘getting worse,’ ‘not going to improve,’ ‘dying and time is likely very short.’
4. Listen. Whether or not you use the word dying, when you have presented bad news (such as information about disease progression), the next step is for you to allow silence, and let the family/patient respond.
5. Respond to the questions as well as the emotions. Name and validate.
If the emergency physician recognizes that the patient is likely to die during this hospitalization, regardless of critical interventions, it would be reasonable to express to the surrogate “worry” about how dire the situation appears. It is also reasonable in such a situation to ask the surrogate about whether the patient had expressed, or if the surrogate has an understanding of, the patient’s goals, values, and perspective on medical priorities near the end of life. Had the patient talked about whether “dying on machines” was acceptable or unacceptable? Does “being comfortable in a peaceful situation if I am dying” sound more consistent? – from ACEPnow
  • Determine the legal decision maker if available and review any completed advance directives.
  • Complete a rapid goals of care discussion (see Fast Facts #223-227).
  • Make recommendations. For example, ‘According to what you want for [the patient], I would/would not recommend….
If comfort is the priority, then hospice involvement or a palliative care consultation might be the most important intervention.
* if you do not know the patient or family well, take a moment to build relationship. Ask a non-medical question such as I am just getting to know you. I had a chance to look at your chart and learn about your medical condition but it does not say much about your life before you got sick. Can you tell us about the things you liked to do before you got sick? Similarly, if the patient is not able to participate in the meeting, ask family to describe the patient prior to his becoming ill: As we get started, can you describe what Mr. Jones was like before he became ill?
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-Could you please share with me what is important to you (to him/her) regarding what quality of life you would want for the rest of your life? I want to make sure I understand so I can what I can to help you get there.
-Thank you for sharing this. Knowing that [] would want X, …
-It’s really hard not knowing whether or not you’re going to survive.  Can I offer to contact a patient rep if you would like help contacting your loved ones during this difficult time?
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This “resuscitation menu,” or asking “should we do everything if your heart stops?” is an ineffective way to have goals of care conversations. From the patient perspective, our medical expertise and knowledge mean that when we offer a treatment or a menu of options, they are reasonable and realistic options – when in reality, they may not be appropriate or in keeping with the patient’s values around the quality of life. Studies show that patients often have a poor understanding of CPR, intubation, and unrealistically optimistic expectations.
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-for renal pts: hydromorphone (dilaudid) is the longer lasting choice compared to fentanyl

O2 Therapy in Severe Viral Pneumonias

A Protocol for O2 Escalation (goal sat low 90s, unless end stage lung disease):
1. up to 6L nc (40% FiO2). Treat pleuritic pain to prevent splinting.
2. 12-15L facemask (50-60% FiO2)
3. HFNC if available. Use ROX index to determine failure.

Who to definitely intubate? End organ injury/hypoperfusion (ex elevated lactate), AMS, hypotension, respiratory acidosis/hypercapnea (w/o hx of CHF or COPD)

CPAP failure: PEEP >8? and 100% FiO2, not cooperative

Use ROX Index to determine failure of HFNC:
ROX = (SpO2/FiO2) / RR
ROX < 4.88 – intubate
failure with trial of HFNC @2h: ROX < 2.85,     @6h: ROX < 3.47,      @12h: ROX < 3.85

Note that PF ratio is meant for intubated pts (FiO2 is most accurate on vented pt).


From literature:

Noninvasive ventilation:
-NIV may be useful in preventing ETI if concomitant COPD or CHF – NIV shown to work for hypercapnea

-the vast majority of pts with hypoxemic respiratory failure with previously normal lungs (ie PNA, ARDS) fail NIV and need mechanical ventilation. The risk of a trial of NIV is delaying needed intubation, worsening end-organ damage (mechanical ventilation reduces energy expenditure on respiration), and possibly worsening volume-induced lung trauma for ARDS pts.
-some studies suggest mortality benefit to NIV and reduced need for intubation for early hypoxemic respiratory failure as compared to Venturi or NRB mask in carefully selected pts: no shock or end-organ dysfunction (including arrhythmia), can clear secretions, and are cooperative.
–however, evidence from different RCTs on both mortality and need for intubation is conflicting!
–if pursue, use CPAP only as tachypneic pts can pull excessive tidal volumes on BIPAP and further damage ARDS lungs
–if no clinical improvement after 1 hour, consider it a failure of NIV
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In ARDS patients, it has been shown that the use of noninvasive inspiratory pressure support can decrease the inspiratory effort compared with no inspiratory assistance only if sufficient pressure support is added [69]. Of concern, the tidal volume can also be significantly higher during NIV, especially when substantial inspiratory pressure is delivered, and further exacerbated by the high inspiratory demand seen in patients with acute hypoxic respiratory failure [70]. Therefore, the total pressure dissipated to inflate the lungs can be excessive during NIV. Such large transpulmonary pressures and the resulting large tidal volumes may exacerbate lung injury if prolonged over time. It is possible, although not proven, that NIV is especially useful in patients who do not substantially increase their tidal volume, but further work is needed in this area
Invasive ventilation for hypoxaemic respiratory failure clearly reduces work of breathing and permits paralysis if total control of breathing is desired, effects that can redistribute blood flow from the respiratory muscles to other organs in patients with shock and hence help to treat shock itself [72]. The ability of NIV to achieve optimal pressures to reduce the work of breathing reliably in acute hypoxaemic respiratory failure is challenging because the high pressures often required increase air leaks, gastric insufflation and patient intolerance [69]. Thus, the ability to use lung protective ventilator strategies (such as maintaining a low tidal volume of 6 mL·kg−1 of predicted body weight) may be more difficult with NIV than with invasive ventilation [7374]. Some evidence even supports the idea that spontaneous ventilation can induce harm similar to ventilator-induced lung injury in situations of severe lung injury [7577], which raises a note of caution when using NIV that combines spontaneous effort with ventilator support.

NIV has also been studied as an alternative to intubation, with occasional reports showing benefit [84]. Positive studies on hypoxaemic, nonhypercapnic respiratory failure, mainly caused by community- or hospital-acquired pneumonia, have enrolled carefully selected patients who are cooperative with no associated major organ dysfunction, cardiac ischaemia or arrhythmias, and with no limitations in clearing secretions [29608587], which may explain the benefits seen.

Until recently, almost all studies on NIV for de novo ARF compared it with oxygen delivered with standard air entrainment (Venturi masks) or reservoir masks. Recently, high-flow nasal cannula therapy has been shown to offer several advantages compared with NIV, including better tolerance and dead space reduction [88]. One recent RCT reported a survival benefit of high-flow nasal cannula over standard oxygen therapy and bilevel NIV, although the primary end-point of intubation was not significantly different [67].

The main risk of NIV for the indication of de novo ARF is to delay a needed intubation [86]. Early predictors of NIV failure include higher severity score, older age, ARDS or pneumonia as the aetiology for respiratory failure, or a failure to improve after 1 h of treatment [89]. Although the reasons for a poorer outcome are not completely understood, patients with NIV failure have higher tidal volumes before intubation [71] and develop more complications after intubation [90]. Studies have shown that NIV failure is an independent risk factor for mortality specifically in this population, although careful patient selection seems to reduce this risk [9192].

References (reviews):

In summary: evidence of NIV on mortality and need for intubation is conflicting.
—Definite no’s: pts with shock, end-organ damage (including arrhythmias), poor cooperation, or poor secretion clearance
—Maybe: pts with concomitant hypercapneic failure from CHF or COPD, very early hypoxemic failure without other organ dysfunction, and pts not pulling large tidal volumes
Success rates in critically ill COVID-19-patients are limited, delayed intubation is associated with poor outcome and the treatment as well as a possibly necessary emergency intubation in cases of treatment failure increase the risk for transmission to staff []; however, in situations with an imbalanced resources-needs ratio, this approach could help bridge the time until decision-making and intubation, or it could also be a therapeutic option in cases of lacking ventilatory capacities.

Cognitive Forcing Strategies

Headache

  • Killers (11): SAH, ICH, meningitis, ENT/facial infection, CO poisoning, temporal arteritis, venous sinus thrombosis, cervical artery dissection, glaucoma, IIH, preeclampsia
  • Tx sequence: ivf, metoclopramide + benadryl, toradol, decadron. Sphenopalatine block.

Chest Pain

  • Killers (6): ACS, PE, ao dissection, tamponade, PTX, PNA
  • STEMI equivalents: aVR elevation, deep inverted/biphasic Ts (Wellens), ant precordial STD (posterior MI), hyperacute ST slope (deWinter), modified Sgarbossa in LBBB, *isolated TWI or STD in aVL*
  • Tx tips: ASA immed, NTG ointment, morphine worsens outcomes
  • Tips: pain above & below diaphragm = dissection w/u,

Syncope Plus

  • Structural/electrical heart disease or FH: arrhythmia
  • Exertion: HOCM
  • Young woman with abdominal pain: ectopic pregnancy
  • Older male with abdominal/flank pain: AAA
  • Sudden severe HA: SAH
  • Malignancy, SOB: PE

Dyspnea

Killers:

Agitated patient

  • Sequence: Must be undressed. Needs met? Verbal de-escalation, show of force, offer “something for the nerves” po, chemical + physical restraints (need to document & remove asap)
  • give home meds if possible, haldol 2-5mg IM +/- ativan 1-2mg IM, quetiapine/seroquel, olanzapine/zyprexa (safest for QTc)
  • Tips: avoid bzd in elderly and autistic, avoid antipsychotics if suspect tox, avoid benadryl in elderly

 

Procedural sedation
midazolam 0.05mg/kg IV, or haloperidol 5mg IV pretreatment to prevent recovery agitation after ketamine

Sick patient

  • eval: iv x 2 (io), O2, monitor, A-B-C-Dextrose
  • shock: empty tank (hypovolemia/hemorrhage), leaky tank (anaphylaxis, sepsis), pump failure (cardiogenic, dissection), obstructive (PE, tamponade)
  • Hs (5) & Ts (6): H’s, hypo/hyperK, hypoxia, hypovol, hypothermia; TPTX, tamponade, thrombosis ACS, thrombosis PE, tox, trauma
  • post ROSC (3): BP, EKG, gas, pressor
  • calling codes: unwitnessed arrest, nonshockable rhythm, no ROSC, age >60, pH<7, unknown downtime, pocus echo. K>12 futile.

 

Intubation

  • airway H&P (each with high LR+ for difficult airway): hx difficult tube, snoring, LEMON (Look externally [beard, retrognathia, obesity], Eval 3-3-2, Mallampati, Obstruction, Neck mobility), inability to exaggerate underbite (new!)
  • prep: SOAPME, position is ramped up, +/- push-dose pressor at hand (+bicarb if also severely acidotic), post-tube sedation +/- pressors hung, voice plan and backup to team

SCD patient

  • no O2 if not hypoxic!
  • no fluids if euvolemic (esp in AChS)! Only give D51/2NS, hypotonic fluids prevent further sickling. Bolus only for septic unstable patients.

Before discharge

  • have vitals normalized?
  • PO challenge? Road test?
  • review labs, imaging, & documentation – Does everything make sense? Any incidental findings?

 

Shoulder Reductions

elbow technique (new!)
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self-reduction
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scapular rotation: scapular tip pushed medially, acromion inferiorly (open-book)
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vertical pull (Spaso): lift arm vertically, fully externally rotate, and pull toward ceiling
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external rotation (Kocher): slowly rotate externally with humerus parallel to torso, then maintain externally rotate until cross midline
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lateral extension (Milch): while externally rotated and providing traction on the humerus, slowly extend laterally until above 90′
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traction-countertraction: tie sheets so that traction is pulled on humerus while body in place
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passive traction (Stimson): apply weight to extremity while pt prone (for young healthy pts only)
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oscillating method (Fares): while keeping traction, oscillate up and down while slowly extending laterally. Best if kept extremity in external rotation.
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up-close-and-personal (Cunningham): pt’s hand on your ipsil shoulder, put downward pressure on their elbow. With free hand, massage biceps and rotator cuff muscles.
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POSTERIOR dislocation traction-countertraction:
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INFERIOR dislocation traction-countertraction:
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Trauma

Burn transfer criteria:
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3 mL of lactated Ringer’s solution x weight in kilograms x % of body surface area burned (partial- and full-thickness burns)

Trauma in pregnant pts
–have a low threshold for giving Rhogam

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-types II & III may disrupt cribriform plate – look for CSF rhinorrhea

Traumatic iritis = inflam of ciliary body
-cycloplegic (homatropine. Relieve photophobia) +/- topical steroids (ONLY optho can Rx)

Globe rupture – elevate bed >30′ to reduce ocular pressure and prevent further extravasation (avoid sux if intubating – incr IOP)
-give abx prophyl

Infraorbital anesthesia is associated with this fracture due to injury to the infraorbital nerve. Other findings on physical exam include enophthalmos due to herniation of globe contents before the onset of edema. Diplopia on upward gaze occurs with entrapment of the inferior rectus muscle leading to binocular diplopia 

7 areas of ICH on CT Head: spinal cord, midbrain, 4th ventricle, lateral ventricles, gyri and sulci, gray-white matter differentiation

Spinal shock = cord concussion

3 types of pelvic fractures:
– lateral compression (T-bone MVC/pedestrian hit from side)
—look for vertical fracture of sacrum
—no benefit from pelvic binders
—mostly “elderly” (age >55) pts at risk of bleeding – calcified vessels break easily
—if suspect bleeding or binder already placed, benefits generally outweigh potential harm of overreduction so do not remove
– AP fracture (head on MVC)
– vertical shear (fall)

 

Hyponatremia & Hypernatremia

-Send serum osmolality!
-determine fluid status: hypo-, eu-, or hypervolemic
-Use formulas!

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Hyponatremia
-if asymptomatic, fluid restriction. Don’t give fluids!
-if altered/seizing,
-max rate of correction = 8 mEq/h
-Goal: <10-12 mEq total increase in 24h

Hypovolemic hyponatremia mechanism = decreased  arterial perfusion of kidneys -> ADH secretion -> reabsorption of free water
–fix the underlying problem: volume replete

Hypervolemic hyponatremia (CHF, cirrhosis) mechanism = depleted intravascular volume despite excess extravascular volume = decreased effective arterial perfusion of kidneys -> ADH secretion -> reabsorption of free water

Euvolemic hyponatremia
-SIADH – inappropriate excess ADH secretion
-psychogenic (excess free water intake), beer potomonia + “tea and toast syndrome” (inadequate solute intake)

Hypernatremia
-bolus NS if shock/hypoperfusion
-replace total body water (TBW) deficit

 

1. Treat Neurologic Emergencies Related to Hyponatremia

In the event of a seizurecoma or suspected cerebral herniation as a result of hyponatremia, IV 3% hypertonic saline should be administered as soon as possible according to the following guide:

  1. Administer 3% hypertonic saline 100-150cc IV over 5-10min
  2. If the patient does not improve clinically after the first bolus, repeat a second bolus of hypertonic saline.
  3. Stop all fluids after the second bolus of hypertonic saline to avoid raising the serum sodium any further

What if hypertonic saline is not readily available? –> Administer one ampule of Sodium Bicarbonate IV over 5min.

Ringer’s lactate has a sodium concentration of 128mmol/L which will be more isotonic to the hyponatremic patient. Although never shown in clinical studies, administering Ringer’s lactate will likely result is a slower rise in serum serum sodium than Normal Saline, and therefore have a lower risk of potentiating osmotic demyelination syndrome. Ringer’s lactate is therefore recommended by our experts as the fluid of choice for resuscitation of the hypovolemic/hyponatremic patient.

Practical Approach to the Differential Diagnosis of Hyponatremia

  1. Look at chief complaint: look for conditions which can increase output or decrease intake such as vomiting and diarrhea, pain or altered level of awareness
  2. Review Medication List: look for those that cause SIADH, especially thiazide diuretics and SSRIs; patients who have been on chronic steroids may have adrenal insufficiency
  3. Evaluate PMHx: Look for history of end organ failure (CHF, liver failure and renal failure) or cancers (a cause of SIADH)
  4. Lab work: glucose (hyperglycemia), potassium (hyperkalemia may suggest adrenal insufficiency), TSH (hypothyroidism)

Note: if by history the hyponatremia is acute, it is safe to correct it quickly. The patients who are at risk of central pontine demyelinolysis are those whose hyponatremia is chronic.

 

Other lytes concepts:
-replete low ionized Ca after PRBC transfusions (contains citrate)
-alkylosis (ex: primary hyperventilation) causes more Ca from its ionized state to be bound to albumin (may develop signs of hypoCa)
-severe hypocalcemia -> cardiovascular collapse (loss of contractility/inotropy)
-hypocalcemia -> QTc prolongation -> torsades
-CaCl2 = 3x more ions than Ca-gluconate

-beware of further increasing serum bicarb for a pt that is hypoventilating (ex CHF exacerbation) – will worsen compensatory respiratory acidosis (hypercarbia). This is why MICU gives acetazolamide to CHF pts on BIPAP
-Dialysis dysequilibrium syndrome (dizziness during dialysis) – due to the rather rapid removal of BUN, which has an osmotic effect
—–serum osmolality = 2x(Na) + glucose/18 + BUN/2.8

0.9% NS = 154 mEq Na
0.45% NS = 77 mEq
plasmalyte = 140 mEq
LR = 128 mEq
D5W = 0 mEq
3% hypertonic saline = 513 mEq (3 / 0.9 = 3.33 x 154mEq)

References:
https://emergencymedicinecases.com/episode-60-emergency-management-hyponatremia/
https://coreem.net/core/hypocalcemia/