2009

Question 1

Given patient in HFO ventilation and asked:

a. Of the three parameters (I:E ratio, Amplitude, and Frequency) which has the greatest effect on Tidal volume? Which has the least effect on tidal volume.
b. If the bias flow is decreased to 20L/min from 40L/min does this affect CO2 clearance? Explain your answer.

Answer 1

a)

greatest effect on tidal volume: amplitude

least effect on tidal volume: ? I:E ratio

b)

??? yes because bias flow washes out CO2 from the vent circuit and if it’s too low rebreathing will occur (reference)

Unlike mechanical ventilation at physiological breathing rates where changes in ventilator settings on contemporary ventilators inevitably affect both oxygenation and ventilation, traditional teaching of HFOV promoted changes in mean airway pressure as the means of influencing arterial oxygen tension and alterations to proximal pressure amplitude (ΔP) and frequency (f) of the oscillatory waveform as the determinants of arterial carbon dioxide tension (Pa,CO2).

from kemh website:

Clinically, when HFOV is used without volume guarantee, tidal volume is altered in response to blood gas/TcpCO2 trends by adjusting:

1. Amplitude or Delta-P (most important) Primary manipulations in PaCO2 are achieved by altering the oscillatory pressure amplitude (or power). Increasing the amplitude increases the displacement of the diaphragm/piston, increasing the VT delivered to the patient, lowering the PaCO2.
2. Frequency (Hz) Lowering the frequency in HFOV increases the tidal volume (when there is a fixed I:E ratio), thereby lowering the PaCO2. However, as frequency decreases, the percentage of the oscillatory amplitude transmitted to the proximal airways increases. The frequency, at which this amplitude increases significantly, is influenced by the mechanical properties of the lung. The appropriate frequency is dependent on the disease being treated. As a general rule for the SM3100A, higher frequencies (12-15 Hz) are used for low compliance (e.g. HMD), whilst lower frequencies (8-10 Hz) are used in the presence of high resistance (e.g. early phase meconium aspiration, CLD). Smaller babies with poorly compliant lungs require higher frequencies than more mature infants. Hybrid ventilators may have limited capacity to achieve required tidal volumes at high frequencies, in the absence of spontaneous breathing. It may be necessary to use lower frequencies in hybrid ventilators than previously selected when using the SM3100A. In general, the highest frequency achievable should be used, to reduce the risk of barotrauma when using HFOV mode in hybrid ventilators.
3. % I-Time I:E ratio is generally set at 1:2 for the Fabian and VN500, or 33 % (% inspiratory time) on the SM3100A. Increasing the I:E ratio to 1:1 (Fabian, VN500) or 50 % inspiratory time (SM3100A) may improve CO2 elimination at any given frequency. Increasing the absolute inspiratory time in this manner, permits more tidal volume to be delivered.

Question 2

Given pt with asthma attack on B-agonist therapy q1h for last 24 hours. Increased WOB for last 24 hours….Long stem to the question. End of the stem says patient develops lactate of 6. List 2 causes for lactic acidosis in this patient.

Answer 2

• medication-induced from B agonist
• direct effect of endogenous catocholamines
• hypoxia/hypoperfusion
• high demand of respiratory muscles

Question 3

Given patient admitted to ICU with severe pneumonia, ARDS, pneumothorax and chest tubes. Physiotherapist is concerned that there is ongoing leak in chest tubes. CT thorax is done and one slice is shown. List 3 abnormalities on the CT (there was s.c. emphysema, undrained pneumo, bilateral consolidation.

Answer 3

?anything to add?

Question 4

Given with COPD who has been tried on NIV for 12 hours and now failing. You proceed to intubate the patient. CO2 is detected when you connect up the detector. The patient is bagged at rate of 25b/m. Immediately after intubation BP is 65/30. List 4 possible causes for hypotension.

Answer 4

• dynamic hyperinflation
• pneumothorax/tension pneumothorax
• distributive shock component from induction meds
• pre-existing hypovolemia
• ?tube migration/incorrect placement (esophagela intubation?)

Question 5

Given COPD patient who is intubated. Question was: Aside from respiratory arrest and cardiac arrest, list 4 adverse effects of dynamic hyperinflation.

Answer 5

1. increases mean airway pressure increasing risk of barotrauma/pneumothorax
2. increases pt-ventilator dyssynchrony, in form of inadequate triggering since patient must achieve a higher negative presure or flow to reach atmospheric pressure then further negative pressure or flow to trigger breath
3. flattens diaphragm which puts it into a less ideal position for force generation
4. decreases cardiac output by decreasing venous return

Dynamic hyperinflation (DHI) is characterized by increased levels of intrinsic positive end-expiratory pressure (PEEPi or “auto-PEEP”). The hyperinflation is progressive (dynamic) because air accumulates in the lung with each breath as a result of a failure to achieve complete exhalation before the onset of the next breath. In patients with COPD who are intubated for respiratory failure, DHI can occur as a consequence of airflow obstruction due to bronchoconstriction, combined with a higher than normal minute ventilation (respiratory rate multiplied by tidal volume) delivered by the ventilator. DHI (spontaneous or ventilator-induced) creates elevated levels of auto-PEEP, which can lead to patient-ventilator dyssynchrony and increased work of breathing, barotrauma, cardiovascular collapse, and potentially even death.

Auto-PEEP is common in patients with COPD. In a prospective cohort study of 13 patients with COPD who were being mechanically ventilated, all of the patients had measurable auto-PEEP (mean 9.4 cm H2O), and seven had an auto-PEEP greater than 10 cm H2O. Auto-PEEP is responsible for up to one-third of the total work of breathing in patients mechanically ventilated with COPD [39].

Auto-PEEP can be detected in a number of ways. One practical and reliable method in patients with COPD is the demonstration on ventilator graphics of a progressive rise in peak airway pressures during mandatory tidal volume ventilation [40-43]. Alternatively, ventilator time-flow graphics may demonstrate the commencement of inspiratory flow before expiratory flow reaches zero (figure 7 and figure 4). These methods are not quantitative. While auto-PEEP can be quantitatively assessed by measuring airway opening pressure during an end-expiratory pause (Paw) (waveform 2) [44], this method is only accurate when the patient is paralyzed or exhibiting negligible abdominal and chest wall muscle engagement during exhalation, which is uncommon in COPD patients requiring mechanical ventilation.

Question 6

Given a pt with ventilatory parameters. Asked to give formula for static compliance, and dynamic compliance.

Answer 6

static lung compliance = tidal volume/(plateau pressure - total PEEP)

dynamic lung compliance = tidal volume/(peak inspiratory pressure - total PEEP)

total PEEP = intrinsic PEEP + ventilator PEEP

Question 7

Hypoxic patient on FiO2 1.0, PEEP 15. ph 7.24, PO2 48, PCO2 60. List four interventions that can assist with improving oxygenation of this patient.

Answer 7

1. prone positioning
2. NMB (now more controversial)
3. decrease oxygen consumption (treat fever, agitation etc)
4. ECMO?
5. conservative fluid strategy
6. inhaled pulmonary vasodilators
7. high PEEP strategy

Question 8

The use of etomidate has increased as a drug for intubation. List the one major
potential side effect of this drug.

Answer 8

Concerns with etomidate include adrenal suppression, myoclonus, and evidence of regional cerebral excitation (determined by electroencephalogram) after intubation [18,24,25]. Myoclonus has been misidentified as seizure activity, leading to incorrect recommendations that etomidate be avoided in patients with seizure disorders. Myoclonus during RSI is brief and minimal, because of the concomitant administration of a paralytic agent, and of no clinical significance. Etomidate decreases cerebral blood flow and cerebral metabolic oxygen demand, while preserving cerebral perfusion pressure [21]. Postintubation sedation with propofol or a benzodiazepine helps to prevent neuroexcitation.

Adrenocortical suppression — The major controversy surrounding etomidate stems from the reversible adrenocortical suppression associated with its use.

Although etomidate transiently inhibits cortisol biosynthesis, the preponderance of evidence suggests that this is not harmful in most clinical settings and does not preclude its use [46-50]. To avoid further suppression of cortisol, we do not administer multiple bolus doses or infusions of etomidate. In patients with suspected adrenal insufficiency, such as those on chronic glucocorticoid therapy, the clinician must weigh the risk of further cortisol suppression caused by etomidate against the risk of hemodynamic instability that may be caused by alternative induction agents.

Following a single induction dose of etomidate, reversible inhibition of 11-beta-hydroxylase (which converts 11-deoxycortisol to cortisol) causes adrenocortical suppression lasting <24 hours in both healthy and critically ill patients [46-55]. Although cortisol plasma concentrations may not appropriately rise in response to surgical stimulation after etomidate administration, concentrations do not necessarily fall below the normal range, and the clinical significance of this finding is uncertain.

In critically ill patients undergoing emergency tracheal intubation, a 2015 systematic review of eight randomized trials concluded that etomidate was not associated with increased mortality compared with any other induction agent (OR 1.17, 95% CI 0.86-1.60) [51]. Also, there is no definitive evidence that a single dose of etomidate increases mortality in critically ill patients diagnosed with sepsis [59]. However, use of etomidate in patients with frank septic shock may increase the likelihood of development of adrenal insufficiency [60]; thus, we usually select an alternative anesthetic induction agent in this circumstance.

Question 9

List 4 strategies to decrease incidence of VAP.

Answer 9

1. early mobilitiy
2. change vent circuit only if visibly solied or malfunctioning
3. elevate head of bed 30-45 degrees
4. chlorhexidine oral wash
5. minimize sedation
6. minimize invasive mechanical ventilation (use NIPPV when possible)
7. daily SBT and SAT
8. use ETT with supraglottic secretion clearance for pts intubated >48-72h
9. perform SBT with sedation turned off

Question 10

Given balloon pump wave form:

a. What is the timing on the balloon?
b. Please mark with an “I” where balloon inflation occurs.
c. Please mark with a “D” where balloon deflation occurs.
d. Describe how balloon deflation assists cardiac function.

Answer 10

a) and b) and c)

Caption for the image: The timing of balloon inflation and deflation is adjusted in the 1:2 mode. The inflation point is moved rightward (later) until it occurs in late diastole, and the dicrotic notch is uncovered. The inflation timing is moved progressively earlier in the cardiac cycle until the dicrotic notch on the central aortic tracing just disappears. Examples of early, late, and correct inflation are shown in the top two tracings. Similarly, the deflation knob is moved leftward (earlier) and then slowly advanced toward the right (later in the cardiac cycle) until the end-diastolic pressure dips 10 to 15 mmHg below the patient’s unassisted diastolic pressure. This will produce a maximal lowering of the patient’s unassisted systolic pressure. Examples of early, late, and correct deflation timing are shown in the bottom two traces.

d)

diastolic augmentation (increases DBP)

• increases coronary perfusion pressure
• increases coronary blood flow
• increases myocardial oxygen supply

systolic unloading (decreases SBP, decreases HR, decreases mean pulm wedge pressure, increases CO)

• decreases LV wall tension
• decreases LVEDP
• increases cardiac output
• decreases myocardial oxygen demand

Question 11

Given patient with long stem basically describing RV infarct.

a. List 4 principles in the management of this patient.

Answer 11

1. optimize RV preload
   
   • typically through volume loading, but consideration for gentle diuresis could also be made
2. decrease RV afterload
   
   • In patients with predominant RV dysfunction, RV afterload reducing therapy is not indicated and may worsen the hemodynamic profile. In patients with RVMI and significant left ventricular dysfunction, the use of an intraaortic balloon pump, and occasionally afterload reducing agents, may be effective in unloading the left ventricle and subsequently the right ventricle (I don’t get this…aside from the situation where pulmonary vasodilation increases LV preload and the LV can’t deal with it but why would this happen in isolated RV infarct???)
3. optimize heart rate and AV syncrhony
   
   • The ischemic right ventricle has a relatively fixed stroke volume and therefore right ventricular output is dependent upon heart rate and optimal transport of blood from the right atrium to the RV (referred to as atrioventricular [AV] transport).

As a result, bradyarrhythmias can significantly worsen the hemodynamic status. Atropine may be beneficial to increase heart rate, but right ventricular or atrioventricular sequential pacing (to provide an atrial contribution and AV synchrony) may be necessary

4. optimize inotropy and RV perfusion (MAP)
   
   • When fluid resuscitation is insufficient, hypotension should be rapidly corrected with an inotropic agent that also exerts vasoconstrictor effects. Uptodate says to use dopamine then maybe dobutamine, and if that fails consider mechanical support (IABP)…I’m not sure I agree and would suggest milrinone +/- vasopressin…
5. mechanical support
   
   • IABP (if also have cardiogenic shock from poor LV). Although there are little data on its benefits in shock due to RVMI, we have found it helpful in stabilizing aortic pressure and improving systemic perfusion in some patients and thus may be temporizing in refractory hypotension while performing emergency percutaneous revascularization and subsequently awaiting recovery of RV function
   • RVAD
6. anti-ischemic drug therapy
   
   • Beta blockers and calcium channel blockers, which might be considered as tools to improve ischemia (and in particular, angina), can reduce heart rate and contractility and slow AV conduction.

These drugs should be avoided in patients with RVMI, and in particular, those who are hemodynamically unstable. They can be tried with careful monitoring in those who are stable and have a clear indication.

Question 12

List 4 echocardiographic findings suggesting a patient has a Pulmonary embolus.

Answer 12

1. RV dilation
2. RV dysfunction with normal or slightly elevated RVSP (<60mm Hg, i.e. if it’s really high suggests chronicity)
3. short pulmonary artery acceleration time (<60ms)
4. dilated IVC
5. clot in transit (or in pulmonary arteries)
6. McConnell’s sign (RV free wall akinesia with apical sparing)
7. TR

Question 13

Post Heart Transplant patient with RV failure or something like that. iNO started and ordered at 20ppm. You find out that 30 mins later the iNO was accidentally set to 2000 ppm.
a. what is your next immediate step with the iNO.

b. The patients sats begin to fall to 85% and CO level 3%. What is the cause of this?
c. What is the treatment for this?

Answer 13

a) stop it or decrease to 20ppm and monitor for rebound pulmonary hypertension…not sure which I’d do though (stop vs decrease to typical dose)

b)

methemoglobinemia

Clinical clues to the diagnosis of acute toxic methemoglobinemia include the following:

• Sudden onset of cyanosis with symptoms of hypoxia and/or clinical symptoms of reduced oxygen availability after administration or ingestion of an agent with oxidative potential (table 1). (See ‘Signs and symptoms’ above.)
• Hypoxia that does not improve with an increased administration of oxygen.
• Abnormal coloration of the blood observed during phlebotomy. The blood in methemoglobinemia has been variously described as dark red, chocolate, or brownish to blue in color, and, unlike deoxyhemoglobin, the color does not change when the blood is exposed to oxygen
• Methemoglobinemia is strongly suggested when there is clinical cyanosis in the presence of a normal arterial pO2 (PaO2). Thus, arterial blood gas analysis may be deceptive because the PaO2 is generally normal in individuals with excessive levels of methemoglobin.

Routine pulse oximetry is generally inaccurate for monitoring oxygen saturation in the presence of methemoglobinemia and should not be used to make the diagnosis of this disorder. The reason is that methemoglobin absorbs light at the pulse oximeter’s two wavelengths, and this leads to error in estimating the percentages of reduced and oxyhemoglobins. A high concentration of methemoglobin causes the oxygen saturation to display as approximately 85 percent, regardless of the true hemoglobin oxygen saturation.

• Blood gas analysis measures arterial oxygen partial pressure and estimates oxygen saturation by comparison with a standard curve. Since arterial oxygen partial pressure is normal in patients with methemoglobinemia, blood gas analysis will give falsely high levels of oxygen saturation in the presence of methemoglobin.

As noted above, suspected methemoglobinemia should be confirmed by co-oximetry and, when available, re-confirmed via the Evelyn-Malloy method.

Pathogenesis:

Methemoglobin is an altered state of hemoglobin in which the ferrous (Fe++) irons of heme are oxidized to the ferric (Fe+++) state. The ferric hemes of methemoglobin are unable to reversibly bind oxygen. In addition, the oxygen affinity of any remaining globins’ ferrous hemes in the hemoglobin tetramer are increased. As a result, the oxygen dissociation curve is “left-shifted”.

The net effect is that patients with acutely increased concentrations of methemoglobin have a functional anemia (ie, the amount of functional hemoglobin is less than the measured level of total hemoglobin). The circulating methemoglobin-containing hemoglobin molecules are unable to deliver oxygen and the remaining oxyhemoglobin has increased oxygen affinity, resulting in impaired oxygen delivery to the tissues. Those with chronically increased methemoglobinemia and functional anemia may develop compensatory polycythemia/erythrocytosis.

c)

Treatment of methemoglobinemia:

1. stop offending medication/chemicals (see list below)
   
   • In lesser degrees of methemoglobinemia (ie, an asymptomatic patient with a methemoglobin level <20 percent), no therapy other than discontinuation of the offending agent(s) may be required
   • Patients with symptomatic and severe degrees of methemoglobinemia should be managed in the intensive care unit for stabilization of their airway, breathing, and circulation. This may require the use of oxygen supplementation, inotropic agents, and mechanical ventilation
   • Blood transfusion, especially in anemic subjects, or exchange transfusion may be helpful in patients who are in shock; hyperbaric oxygen has been used with anecdotal success in severe cases
2. methylene blue or vitamin C
   
   • While there have been no randomized trials comparing these two agents, the general experience has been that the action of a single dose of MB in this setting rapidly reduces toxic levels of methemoglobin to non-toxic levels (eg, <10 percent) within 10 to 60 minutes, whereas treatment with ascorbic acid requires multiple doses and may take 24 or more hours to reach similarly low levels and is therefore a poor alternative in emergency situations.
   • Accordingly, since high levels of methemoglobin constitute a medical emergency requiring urgent intervention, the more rapid and more dramatic action of MB in reducing methemoglobin levels has made MB the treatment of choice. When MB is not available or when its use is contraindicated (eg, as in glucose-6-phosphate dehydrogenase [G6PD] deficiency), ascorbic acid, and, in life-threatening situations, red cell blood exchange transfusions, are the only reasonable alternatives, although responses to these therapies are less marked and dramatic than they are to MB.
3. red blood cell transfusions

List of meds/chemicals that can cause methemoglobinemia

Medications

• Amino salicylic acid (also called p-aminosalicylic acid or 4-aminosalicylic acid)
• Clofazimine
• Chloroquine
• Dapsone
• Local anesthetics, topical sprays and creams including benzocaine (in teething rings and ointments), lidocaine, and prilocaine
• Menadione
• Metoclopramide
• Methylene blue*
• Nitroglycerin
• Phenacetin
• Phenazopyridine
• Primaquine
• Rasburicase
• Quinones
• Sulfonamides

Chemicals and environmental substances

• Acetanilide (used in varnishes, rubber, and dyes)
• Anilines and aniline dyes (eg, diaper and laundry marking inks, leather dyes, red wax crayons)
• Antifreeze
• Benzene derivatives (used as solvents)
• Chlorates and chromates (used in chemical and industrial synthesis)
• Hydrogen peroxide (used as a disinfectant and cleaner)
• Naphthalene (used in mothballs)
• Naphthoquinone (used in chemical synthesis)
• Nitrates and nitrites (eg, amyl nitrite, farryl nitrite, sodium nitrite, nitrate- and nitrite-containing foods, nitric oxide, well water)
• Nitrobenzene (used as a solvent)
• Paraquat (used in herbicides)
• Resorcinol (used in resin melting and wood extraction)
• Inherited disorders (extremely rare)
• Cytochrome b5-reductase deficiency
• Hemoglobin M disease

Question 14

Patient presents with Aortic dissection and BP of 180/100.

a. Over what time period would you proceed to lower his blood pressure?

b. Nitroprusside is one the drugs that can be used to lower BP in this
situation. What is a side effect of nitroprusside?

Answer 14

a) ?immediate

guidelines seem to differ whether to target SBP <140 or SBP <120 but I think most argue for a little more aggresive targets in the acute setting. Canadian guidelines seem to suggest target <140/90 in stable pts (but <130/80 in those with cardiovascular disease or major risk factors)

b)

cyanide toxicity (although I don’t think I’d call it a “side effect”)

Sodium nitroprusside, when administered by intravenous infusion, begins to act within one minute or less, and once discontinued, its effects disappear within 10 minutes or less. Frequent monitoring is required since this drug can produce a sudden and drastic drop in blood pressure.

Nitroprusside is metabolized to cyanide, possibly leading to the development of cyanide (or, rarely, thiocyanate) toxicity that may be fatal [10]. This problem, which can manifest in as little as four hours, presents with altered mental status and lactic acidosis. Risk factors for nitroprusside-induced cyanide poisoning include a prolonged treatment period (>24 to 48 hours), underlying renal impairment, and the use of doses that exceed the capacity of the body to detoxify cyanide (ie, more than 2 mcg/kg per minute).

Nitroprusside can result in dose-related declines in coronary, renal, and cerebral perfusion.

• Nitroprusside should not be given to pregnant women, patients with Leber optic atrophy, or patients with tobacco amblyopia. In addition, nitroprusside should be avoided, if possible, in patients with impaired renal function.

Nitroglycerin is also administered by intravenous infusion and is similar in action and pharmacokinetics to nitroprusside except that it produces relatively greater venodilation than arteriolar dilation. It has less antihypertensive efficacy compared with other drugs used to treat hypertensive emergencies, and its effects on blood pressure are variable from person to person and, potentially, from minute to minute. However, it may be useful in patients with symptomatic coronary disease and in those with hypertension following coronary bypass.

Question 15

List three hormonal therapies recommended for a donor with EF found to be <40%.

Answer 15

1. thyroid hormone replacement
2. methylprednisolone
3. vasopressin

I couldn’t find the effect of inotropes on this question (previously question said aside from inotropes but one heart donation criteria on uptodate said “inotropic support less than 10mcg/kg/min of dopamine or dobutamine”

In a retrospective analysis of data on 66,629 donors, thyroid hormone therapy was associated with increased procurement of hearts, lungs, kidneys, pancreases, and intestines, but not livers.

from 2006 Canadian guidelines: Weight of currently available evidence in a large retrospective cohort study by the United Network for Organ Sharing (UNOS)10 in the United States suggests a substantial benefit of triple hormone therapy with minimal risk. A multivariate logistic regression analysis of 18 726 brain-dead donors showed significant increases in kidney, liver and heart utilization from donors receiving 3 hormonal therapies. Significant improvements in 1-year kidney graft survival and heart transplant patient survival were also demonstrated. A prospective randomized trial has not been performed.

Question 16

Post op cardiac surgery patient with pacer wires. What is the rhythm? List 2 non-pharmacological therapies to address this rhythm.

Answer 16

• vagal maneuvers (on ventilator kind of like a recruitment maneuver, or carotid sinus massage)
• synchronized cardioversion
• overdrive pacing (aka pace termination)

Nonpharmacologic therapy to convert back to normal sinus rhythm including direct current cardioversion, pace termination, or catheter ablation are reasonable treatments if the patient is having adverse hemodynamic consequences from the arrhythmia, if pharmacologic therapies are unsuccessful or not tolerated, or if the patient has pre-excitation syndrome.

Question 17

List 2 tools used to assess patient for delirium.

Answer 17

Confusion Assessment Method ICU (CAM-ICU)

1. Acute onset and fluctuating course
   
   • Usually obtained from a family member or nurse and shown by positive responses to the following questions:
   • “Is there evidence of an acute change in mental status from the patient’s baseline?”;
   • “Did the abnormal behavior fluctuate during the day, that is, tend to come and go, or increase and decrease in severity?”
2. inattention
   
   • Shown by a positive response to the following:

“Did the patient have difficulty focusing attention, for example, being easily distractible or having difficulty keeping track of what was being said?”

3. disorganized thinking
   
   • Shown by a positive response to the following:

“Was the patient’s thinking disorganized or incoherent, such as rambling or irrelevant conversation, unclear or illogical flow of ideas, or unpredictable switching from subject to subject?”

4. altered level of consciousness
   
   • Shown by any answer other than “alert” to the following:

“Overall, how would you rate this patient’s level ofconsciousness?”

    * Normal = alert
    * Hyperalert = vigilant
    * Drowsy, easily aroused = lethargic
    * Difficult to arouse = stupor
    * Unarousable = coma

Intensive Care Delirium Screening Checklist (ICDSC)

see image

Question 18

List 4 adverse outcomes/complications that delirium can lead to in the ICU patient.

Answer 18

• cognitive impairment at 3 months
• cognitive impairment at 12 months
• longer hospital LoS
• mortality
• +/-costs although not really pt centered (uptodate)

Woah, interesting statement from the PADIS guidelines:

Questions: What are the short- and long-term outcomes of delirium in critically ill adults and are these causally related?

Ungraded Statements: Positive delirium screening in critically ill adults is strongly associated with cognitive impairment at 3 and 12 months after ICU discharge (316–319) and may be associated with a longer hospital stay (257, 279, 316, 320–327).

Delirium in critically ill adults has consistently been shown NOT to be associated with PTSD (328–333) or post-ICU distress (316, 333–336).

Delirium in critically ill adults has NOT been consistently shown to be associated with ICU LOS (257, 258, 272, 279, 318, 320–326, 334, 337–352), discharge disposition to a place other than home (257, 342, 344, 353, 354), depression (330, 356), functionality/dependence (330, 334, 350, 353, 354, 357–360), or mortality.

uptodate, not specifically on ICU pts, but pts with delirium in general:

Delirium has an enormous impact upon the health of older persons. Patients with delirium experience prolonged hospitalizations, functional and cognitive decline, higher mortality, and higher risk for institutionalization, even after adjusting for baseline differences in age, comorbid illness, or dementia.

Delirium can be disturbing for affected patients and relatives and is associated with worse outcome, and much higher ICU and hospital LOS and costs.

Question 19

Describe one difference that distinguishes a donor after neurological determination of death and donor after cardiac death.

Answer 19

not sure exactly what they are getting at here…

Donation after neurologic determination of death (DNDD) — Most (80 to 90 percent) organs from deceased donors are procured after declaration of death by neurologic criteria, also known as “brain death.” Brain death is the complete and irreversible cessation of cerebral and brainstem function; in most countries and situations, this is considered to be equivalent to cardiopulmonary death. Brain death is a relatively uncommon event, occurring in approximately 1 percent of all deaths [2]. The three most common causes of brain death are trauma, cerebrovascular accident, and anoxia, with the incidence of anoxic brain death increasing, in part due to nonmedical drug overdose.

Donation after circulatory determination of death (DCDD) — Because of the severe shortage of donated organs and the limited number of brain-dead donors, another option for organ donation is donation after circulatory determination of death.

If the patient expires in the allotted time, usually 60 minutes from withdrawal of ventilatory support, and is declared dead by cardiorespiratory criteria (permanent absence of respiration, circulation, and responsiveness) by the attending clinician, a mandatory waiting period of at least two minutes and not more than five minutes is observed for autoresuscitation.

Although kidneys are procured most frequently after DCDD, liver, pancreas, and lungs may also be procured. Cardiac transplantation after DCDD occurs in Australia and the United Kingdom and is being contemplated in the United States

Question 20

List 5 physical signs required for neurological determination of death.

Answer 20

do you agree all of the bolded ones would count as physical signs?

We recommend use of the following minimum clinical criteria
as a Canadian medical standard for NDD:

• Established etiology capable of causing neurological death in the absence of reversible conditions capable of mimicking neurological death
• Deep unresponsive coma with bilateral absence of motor responses, excluding spinal reflexes
• Absent brain stem reflexes as defined by:
  
  • absent gag
  • absent cough reflexes
  • bilateral absent corneal responses
  • bilateral absent pupillary responses to light, with pupils at mid-size or greater
  • bilateral absent vestibulo-ocular responses
• Absent respiratory effort based on the apnea test
• Absent confounding factors

Question 21

List 4 factors that would preclude you from performing neurological determination of death by physical exam only.

Answer 21

We recommend that, at the time of assessment for NDD, the
following confounding factors preclude the clinical diagnosis:

• Unresuscitated shock
• Hypothermia (core temperature < 34°C)
• Severe metabolic disorders capable of causing a potentially reversible coma
• Severe metabolic abnormalities, including glucose, electrolytes (including phosphate, calcium and magnesium), inborn errors of metabolism, and liver and renal dysfunction may play a role in clinical presentation. If the primary etiology does not fully explain the clinical picture, and if in the treating physician’s judgement the metabolic abnormality may play a role, it should be corrected.
• Peripheral nerve or muscle dysfunction or neuromuscular blockade potentially accounting for unresponsiveness
• Clinically significant drug intoxications (e.g., alcohol, barbiturates, sedatives, hypnotics); however, therapeutic levels or therapeutic dosing of anticonvulsants, sedatives and analgesics do not preclude the diagnosis.

Question 22

List one ancillary test to determine neurological determination of death.

Answer 22

The demonstration of the absence of intracerebral blood flow is considered the standard as an ancillary test for NDD. Currently validated imaging techniques are cerebral angiography and radionuclide angiography (aka …CT perfusion….Mo says is different from nuclear scan, or perfusion scintography).

CT angiography (according to Mo)

We recommend that an ancillary test be performed when it is impossible to complete the minimum clinical criteria as defined in Recommendation A.1. At a minimum, 2 particular clinical criteria must be met before ancillary tests are performed:

• An established etiology capable of causing neurological death in the absence of reversible conditions capable of mimicking neurological death
• Deep unresponsive coma

We recommend that demonstration of the global absence of intracerebral blood flow be considered as the standard for NDD by ancillary testing.

Question 23

Patient who had ventricular drain placed few weeks back for head trauma. He was discharged from ICU and now returns a week later with ↓ LOC and diagnosis of ventriculitis is made.

a) what are the diagnostic criteria for healthcare-associated ventriculitis or meningitis?
b) what is the treatment for it?

Answer 23

a)

The United States Centers for Disease Control and Prevention’s National Healthcare Safety Network has described healthcare-associated ventriculitis or meningitis as being present in patients who meet at least one of the following criteria:

• An organism cultured from the CSF
• At least two of the following signs or symptoms with no other recognized cause in patients aged >1 year of age: fever >38°C or headache, meningeal signs, or cranial nerve signs, or at least two of the following signs or symptoms with no other recognized cause in patients aged ≤1 year of age: fever >38°C or hypothermia <36°C, apnea, bradycardia, or irritability and at least one of the following:
  
  • Increased CSF white blood cell count, elevated CSF protein, and decreased CSF glucose
  • Organisms seen on a CSF Gram stain
  • Organisms cultured from the blood
  • Positive nonculture diagnostic test from the CSF, blood, or urine
  • Diagnostic single-antibody titer (immunoglobulin M) or fourfold increase in paired sera (immunoglobulin G) for organism

b) treatment

There are no randomized trials addressing optimal treatment of CSF shunt infections. Management of CSF shunt infection should include:

• removal of the device
• external drainage
• parenteral antibiotics
  
  • Parenteral antibiotic selection should be guided by the results of CSF Gram stain and culture. Pending these results, for adults, we recommend empiric therapy, taking into account local in vitro susceptibility results and bacteria previously isolated from the patient [4]. For most patients, we give vancomycin (15 to 20 mg/kg intravenously [IV] per dose every 8 to 12 hours, adjusted to a trough level of 15 to 20 mcg/mL; not to exceed 2 g per dose) and an agent to cover gram-negative bacilli, including P. aeruginosa. For adults, an agent to cover healthcare-associated gram-negative bacilli (ceftazidime [2 g IV every 8 hours], cefepime [2 g IV every 8 hours], or meropenem [2 g IV every 8 hours]) is appropriate. For adults with severe beta-lactam allergies (eg, anaphylaxis) and for whom meropenem is contraindicated, aztreonam (2 g IV every 6 to 8 hours) or ciprofloxacin (400 mg IV every 8 to 12 hours) should replace the cephalosporin or carbapenem.
• and shunt replacement once the CSF is sterile. If device removal is not feasible, intraventricular antibiotics may be useful.

Question 24

Patient with crush injury develops rhabdomyolysis with dark urine.

a. List two lab tests that you could perform to confirm diagnosis of rhabdomyolysis.
b. List 2 therapies to minimize the risk of renal injury.

Answer 24

a) these answers seem too easy…am I missing something?

• serum creatine kinase
• serum myoglobin
• urine myoglobin

urine findings and myoglobinuria - Myoglobin, a heme-containing respiratory protein, is released from damaged muscle in parallel with CK. Myoglobin is a monomer that is not significantly protein-bound and is therefore rapidly excreted in the urine, often resulting in the production of red to brown urine. Visible changes in the urine only occur once urine levels exceed from about 100 to 300 mg/dL, although it can be detected by the urine (orthotolidine) dipstick at concentrations of only 0.5 to 1 mg/dL. Myoglobin has a half-life of only two to three hours, much shorter than that of CK. Because of its rapid excretion and metabolism to bilirubin, serum levels may return to normal within six to eight hours.

Thus, it is not unusual for CK levels to remain elevated in the absence of myoglobinuria. In rhabdomyolysis, myoglobin appears in the plasma before CK elevation occurs and disappears while CK is still elevated or rising. Therefore, there is no CK threshold for when myoglobin appears. As above, rhabdomyolysis does not occur unless CK is elevated five times or more above the upper limit of normal.

b)

• volume administration
• bicarb administration

In addition to treating the underlying rhabdomyolysis or hemolysis, the general goals for prevention of AKI in all patients at risk for heme pigment-induced AKI are twofold:

●Correction of volume depletion if present

●Prevention of intratubular cast formation

The underlying conditions and factors that have led to rhabdomyolysis or hemolysis must also be addressed to avoid continued heme pigment release.

Volume administration — The prevention of AKI requires early and aggressive fluid resuscitation. The goals of volume repletion are to maintain or enhance renal perfusion, thereby minimizing ischemic injury, and to increase the urine flow rate, which will limit intratubular cast formation by diluting the concentration of heme pigment within the tubular fluid, wash out partially obstructing intratubular casts, and increase urinary potassium excretion.

Intravenous isotonic saline should be administered as soon as possible after the onset of injury (even while the patient is being rescued) or detection of hemolysis and continued until the muscle injury or hemolysis has resolved.

For patients who are at risk for heme-associated AKI due to rhabdomyolysis from any cause, we suggest initial fluid resuscitation with isotonic saline at a rate of 1 to 2 L/hour. The plasma creatine kinase (CK) concentration correlates with the severity of muscle injury, and concentrations >5000 unit/L identify patients who are at risk for the development of AKI. However, it may be difficult to identify patients who are at high risk for AKI based upon the initial plasma CK value since the CK level may still be rising from ongoing muscle injury. Thus, sequential CK measurements are critical in tailoring therapeutic interventions.

All patients should be initially treated with vigorous fluid repletion until it is clear from sequential laboratory values that the plasma CK level is stable and not increasing. Patients who have a stable plasma CK level <5000 unit/L do not require intravenous fluid, since studies have shown that the risk of AKI is low among such patients.

Bicarbonate — Patients with rhabdomyolysis who are appropriately monitored may benefit from bicarbonate therapy. We generally administer a bicarbonate infusion to patients who have severe rhabdomyolysis, such as those with a serum CK above 5000 unit/L or clinical evidence of severe muscle injury (eg, crush injury) and a rising serum CK, regardless of the initial value. In such patients, bicarbonate may be given, providing the following conditions are met:

• Hypocalcemia is not present
• Arterial pH is less than 7.5
• Serum bicarbonate is less 30 mEq/L

We generally do not administer bicarbonate to patients with hemolysis, unless another indication is present (such as concurrent rhabdomyolysis, which may occur in the settings of envenomation and poisonings).

Among patients with rhabdomyolysis, we infuse approximately 130 mEq/L of sodium bicarbonate (150 mL [3 amps] of 8.4 percent sodium bicarbonate mixed with 1 L of 5 percent dextrose or water) via an intravenous line separate from that used for the isotonic saline infusion. The initial rate of infusion is 200 mL/hour; the rate is adjusted to achieve a urine pH of >6.5.

If bicarbonate is given, the arterial pH and serum calcium should be monitored every two hours during the infusion. The bicarbonate infusion should be discontinued if the urine pH does not rise above 6.5 after three to four hours, if the patient develops symptomatic hypocalcemia, if the arterial pH exceeds 7.5, or if the serum bicarbonate exceeds 30 mEq/L. If the bicarbonate solution is discontinued, volume repletion should be continued with isotonic saline.

Question 25

List 4 ways to minimize the risk of contrast nephropathy.

Answer 25

1. avoid NSAIDs
2. IV fluid loading
3. minimize contrast load
4. avoid volume depletion
5. avoid back to back contrast studies (separate by >48-72hrs)

Identifying patients at risk — At-risk patients include the following:

• All patients with estimated glomerular filtration rate (eGFR) <60 mL/min/1.73 m2 who have significant proteinuria (defined as albuminuria >300 mg/day, which corresponds to proteinuria > 500 mg/day).
• All patients with eGFR <60 mL/min/1.73 m2 and comorbidities including diabetes, heart failure, liver failure, or multiple myeloma.
• All patients with eGFR <45 mL/min/1.73/m2 even in the absence of proteinuria or any other comorbidities.
• Patients who have eGFR <45 mL/min/1.73 m2 and have proteinuria and diabetes or other comorbidities and all patients with eGFR <30 mL/min/1.73m2 should be considered at highest risk.

Preventive measures

Avoid volume depletion and NSAIDs — Patients who are to receive intra-arterial contrast should avoid volume depletion and withhold nonsteroidal anti-inflammatory agents (NSAIDs) for 24 to 48 hours prior to the procedure. Both volume depletion and NSAIDs can increase renal vasoconstriction, which increases the risk of contrast nephropathy.

We do not withhold angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs). There are insufficient data to support a benefit of withholding ACE inhibitors and ARBs, and there are risks associated with resulting hypertension.

Dose and type of contrast agent — We use the lowest effective dose possible of contrast and avoid performing repeated studies that are closely spaced (within 48 to 72 hours).

Fluid administration — For all at-risk patients undergoing procedures involving intra-arterial contrast administration, if there are no contraindications to volume expansion, we administer intravenous isotonic saline prior to and continued for several hours after contrast administration.

Our preferred protocols are as follows:

• Outpatients ─ We give 3 mL/kg over one hour preprocedure and 1 to 1.5 mL/kg/hour during and for four to six hours postprocedure, with administration of at least 6 mL/kg postprocedure.
• Inpatients ─ We give 1 mL/kg/hour for 6 to 12 hours preprocedure, intraprocedure, and for 6 to 12 hours postprocedure.

Rationale — Intravenous volume administration prior to intravascular contrast administration for patients at risk for contrast-induced nephropathy is the standard of care despite an absence of adequately designed randomized trials demonstrating benefit [44]. Further studies that compare prophylactic fluid administration to no fluid administration are required to determine the role for prophylactic fluid administration, particularly in the highest-risk patients.

Acetylcysteine - We do not give acetylcysteine prior to angiography. Meta-analyses examining acetylcysteine have yielded conflicting results. In general, modest benefits were noted in meta-analyses that did not account for a large degree of heterogeneity between studies. However, the largest randomized trial, which was published after the meta-analyses, did not find improved outcomes with oral acetylcysteine in 4993 high-risk patients undergoing scheduled angiography

Question 26

There were three different diagrams of renal replacment circuits. You had to figure out what time (?type) of renal replacement each was based on the diagram. One diagram had pre and post filter fluid replacement, another had dialysate and fluid replacement and the last just had dialysate.

Answer 26

This is how I would reason this question:

• pre and post fluid replacement - CVVH
• dialysate and fluid replacement - CVVHD
• dialysate - CVVD
• no dialysate and no replacement - SCUF

overall review here

aims of RRT are achieved through diffusion or convection, which are respectively referred to as hemodialysis or hemofiltration. Middle molecules are preferentially cleared by convective methods, rather than smaller molecules that are more reliably cleared by diffusion.

• Diffusion = hemodialysis
• Convection = hemofiltration
• CVVH = continuous veno-venous hemofiltration
• CVVHD = continuous veno-venous hemodialysis
• CVVHDF = continuous veno-venous hemodiafiltration​
• majority of ICU RRT is CVVHF or CVVHDF

HEMOFILTRATION

Haemofiltration is a convective process whereby a hydrostatic pressure gradient is used to filter plasma, water, and solute across a membrane. This is analogous to the process within the renal corpuscle. The underlying mechanism is that of ‘solute drag’ where appropriately sized molecules are pulled along with the mass movement of solvent, traditionally termed ultrafiltration (UF). The convective transport is independent of solute concentration but determined by the direction and magnitude of the transmembrane pressure (TMP). Measures that result in a higher flow rate will increase UF production and in turn increase solute clearance. Equally, measures that increase the negative pressure across the membrane, including the pump on the effluent line, can have a marked effect. This fluid, known as effluent, is discarded. Owing to the high volumes produced, the circulating volume of the patient is replaced with a balanced crystalloid buffer solution.

HEMODIALYSIS

In haemodialysis, solute clearance is achieved by diffusion across the membrane. The space outside the blood-containing fibres within the ‘filter’ is filled with dialysate, which is pumped in a counter-current fashion to the flow of blood. Dialysate is reconstituted to include a buffer (which may be either acetic acid or bicarbonate) and essential electrolytes dissolved in ultrapure water rendered devoid of toxins and impurities. Diffusion occurs down concentration gradients allowing rapid equilibration of solutes across the membrane. The purpose of this counter-current flow system is to maintain a waste-solute concentration gradient (i.e. always lower on the dialysate side of the membrane, similar to solute movement within the Loop of Henle).

RRT Membrane

Two types of RRT membrane exist: cellulose based or synthetic. Exposure to an extracorporeal circuit and the interaction between blood and the membrane is known as biocompatibility. Less biocompatible membranes increase the likelihood of harmful side-effects associated with RRT.

Cellulose-based membranes trigger activation of inflammatory pathways, which may increase the longevity of AKI. Studies suggest that the use of more biocompatible membranes may lead to faster restoration of renal function and improved patient outcomes.3 In short, it can be assumed that the most biocompatible membrane available should be used for RRT.

Filter Fluid

During haemofiltration, bicarbonate ions are freely filtered and therefore need to be replaced. Previously, standard lactate-based fluids were used as buffers, with the lactate subsequently being metabolized in the liver. In the context of critical illness, impaired hepatic function can lead to lactic acid accumulation. To compensate for this, bicarbonate-based buffer solutions have become commercially available. These fluids may be added to the circuit before the haemofilter (pre-dilution) or mixed with the blood in the venous drip chamber (post-dilution). Pre-dilution replacement reduces the incidence of filter clotting but reduces the effective clearance of solutes. Post-dilution replacement is, therefore, the ideal, but a compromise is often made to maintain the integrity and lifespan of the filter. Although there is no mortality benefit associated with the use of bicarbonate-based fluids, there is evidence for improved control of acidosis and cardiovascular instability.

RRT Dosing

For continuous techniques, dose is the sum of all effluent fluids expressed as millilitres per kilogram body weight per hour. It is important to note that the addition of dialysate and the targeting of negative fluid balance both add to the summative dose. Dosing of intermittent techniques is difficult because of urea kinetics and fluid shifts in the critically ill: because of this, most studies assessing IHD measure dose in relationship to frequency and duration of sessions.

Question 27

Describe two factors that affect the clearance of drugs on dialysis.

Answer 27

Drug characteristics that affect clearance by all CRRT modalities include:

• degree of protein binding
• volume of distribution
• interactions of the drug with the dialyzer/hemofilter membrane
• potentially, molecular weight.

Details here:

Protein binding — The degree of protein binding is a major determinant of the extent to which the drug is removed by CRRT.

Only unbound drug can be removed by CRRT. The degree of protein binding is determined by pH, molar concentration of both the drug and protein, and the presence of displacing drugs as well as by circulating bilirubin, heparin, and free fatty acids.

Volume of distribution — The apparent volume of distribution is the theoretical volume of water the drug would occupy if the body were a single homogenous reservoir whose concentration is equal to the plasma concentration. Drugs that are lipid soluble or highly tissue bound have a large volume of distribution. Drugs with a large distribution volume are removed less efficiently by CRRT. Drugs that are limited to intravascular compartment have a small volume of distribution and are efficiently removed by CRRT.

Among critically ill patients, the volume of distribution is often increased because of severe volume overload. The volume of distribution may also be increased by other factors including mechanical ventilation, hypoalbuminemia, and extracorporeal circuit volumes.

Molecular weight — The efficiency with which solutes, including drugs, are removed by CRRT is affected by molecular weight, and, for higher molecular weight solutes, the CRRT modality.

Drugs ≤2000 Daltons readily cross the membrane and are small enough to be removed equally by all CRRT modalities.

For drugs between 2000 and 15,000 Daltons, the membrane’s pore size becomes a limiting factor in CRRT clearance, with increasing hindrance as molecular weight goes up.

Characteristics of membrane — Characteristics of the dialysis membrane/hemofilter that affect clearance include permeability (molecular weight cut-off) and factors such as charge that may influence binding to the drug.

Membrane permeability is an important determinant of drug removal. All membranes used for CRRT today are high flux. High-flux membranes have greater permeability for larger molecules compared with conventional membranes that may be used for intermittent hemodialysis.

Question 28

Adult patient who has PMH of streptococcal glomerulonephrits as a child. Patient now post op or something like that and they give you a bunch of physical findings (lowish BP, tachycardic, oliguric, urine Na 5mmol, Cr 500. There was more information.

a. Give formula for FeNa.
b. List lab values that would suggest patient is hypovolemic.

Answer 28

a) see images

FeNA = fractional excretion of sodium

The FENa can be measured in patients suspected of having AKI due to either prerenal disease or acute tubular necrosis (ATN). A variety of studies have confirmed that the FENa more clearly differentiates between these two conditions than other laboratory tests.

In general, a FENa below 1 percent suggests prerenal disease, where the reabsorption of almost all of the filtered sodium represents an appropriate response to decreased renal perfusion. In comparison, a value between 1 and 2 percent may be seen with either disorder, while a value above 2 percent usually indicates ATN. However, a FENa below 1 percent is not diagnostic of prerenal disease, since it can be seen in a variety of other causes of AKI.

The above cut-off values apply only in patients with advanced AKI. The FENa values that define prerenal disease are lower in patients with less severe disease since the filtered sodium load is much higher, being as low as 0.1 percent in patients with normal kidney function. Another potential problem is that the glomerular filtration rate (GFR) cannot be estimated from a single serum creatinine measurement, since the serum creatinine is not stable.

The relatively high FENa in ATN can be due to one or both of the following factors: inappropriate sodium wasting due to tubular damage and/or an appropriate response of the remaining, well-preserved nephrons to volume expansion.

Limitations of fractional excretion of sodium — There are at least four important limitations to the use of FENa in establishing the cause of AKI:

• The FENa criterion of less than 1 percent to diagnose prerenal disease applies only to patients with a marked reduction in GFR.
• Single measurements of serum creatinine may not provide an accurate estimate of the GFR.
• There are a number of causes of AKI other than prerenal disease in which the FENa can be less than 1 percent.
• The FENa may be above 1 percent when prerenal disease occurs in patients with chronic kidney disease or any cause of sodium wasting, such as diuretic therapy while the diuretic is still acting.

b)

• Urine sodium concentration — A low urine sodium concentration (or low urine chloride concentration in patients who have metabolic alkalosis) is strongly suggestive of reduced tissue perfusion, and it is usually present in hypovolemic patients unless there is a salt-wasting state (eg, diuretics, underlying renal disease), selective renal ischemia (eg, acute glomerulonephritis or bilateral renal artery stenosis), or a very low-sodium diet.

However, the presence of a low urine sodium does not necessarily mean that the patient has true volume depletion, since edematous patients with heart failure, cirrhosis with ascites, and the nephrotic syndrome also avidly conserve sodium. These disorders are characterized by reduced effective arterial blood volume due to a primary reduction in cardiac output (heart failure), to splanchnic vasodilatation and sequestration of fluid in the peritoneal cavity and arterial shunts (cirrhosis), and to a low plasma oncotic pressure (in some patients with severe or acute nephrotic syndrome).

The response of the kidney to true volume depletion and reduced effective arterial blood volume is to conserve sodium and water in an attempt to expand the extracellular volume. With the exception of those disorders in which sodium reabsorption is impaired, the urine sodium concentration in hypovolemic states should be less than 20 mEq/L and may be as low as 1 mEq/L. There are two additional exceptions in which the urine sodium concentration may be higher than 20 mEq/L despite the presence of hypovolemia:

• When there is also a high rate of water reabsorption; in this setting, the rate of sodium excretion and urine volume are low, but the urine sodium concentration is higher than expected due to concentration of the urine.
• When sodium is excreted with another anion [10]. This most often occurs in metabolic alkalosis due to vomiting or nasogastric suction. In such disorders, the metabolic alkalosis is associated with a high filtered bicarbonate load. The stimuli that increase renal sodium and bicarbonate reabsorption (volume depletion and hypokalemia) may sometimes be inadequate to remove all of the filtered sodium and bicarbonate from the urine. Under these conditions, urinary bicarbonate excretion occurs (with sodium as the accompanying cation). This occurs early in the disorder and also intermittently during established alkalosis, usually when transient further increases in serum bicarbonate occur (disequilibration phases of metabolic alkalosis). In such settings, the urine chloride concentration remains low (ie, below 20 mEq/L) and is a better index of extracellular fluid volume.
• elevated BUN
  
  • (However, an elevation in the BUN can also be produced by an increase in the rate of urea production or tubular reabsorption. As a result, the serum creatinine concentration is a more reliable estimate of the GFR since it is produced at a relatively constant rate by skeletal muscle and is not reabsorbed by the renal tubules)
• elevated Cr
• Hypernatremia and hyponatremia — A variety of factors can influence the serum sodium concentration in hypovolemic states, and it is the interplay between them that determines the level observed in a given patient. Primary water loss, as in insensible losses or diabetes insipidus, results in hypernatremia. On the other hand, salt and water loss may be associated with hyponatremia. Volume depletion stimulates the release of antidiuretic hormone (ADH), which will tend to cause retention of ingested water.
• Hypokalemia and hyperkalemia — Either hypokalemia or hyperkalemia can occur in hypovolemic patients. The former is much more common because of potassium loss from the gastrointestinal tract or in the urine. However, there may be an inability to excrete the dietary potassium load in the urine because of renal failure, hypoaldosteronism, or volume depletion itself since the delivery of sodium and water to the potassium secretory site in the cortical collecting tubule will be reduced.
• Metabolic alkalosis and acidosis — The effect of fluid loss on acid-base balance also is variable. Although many patients maintain a normal extracellular pH, either metabolic alkalosis or metabolic acidosis can occur. Patients with vomiting or nasogastric suction or those given diuretics tend to develop metabolic alkalosis because of hydrogen ion loss and volume contraction. On the other hand, bicarbonate loss (due to diarrhea or intestinal fistulas) can lead to metabolic acidosis. In addition, lactic acidosis can occur in shock and ketoacidosis in uncontrolled diabetes mellitus.
• Hematocrit and serum albumin concentration — Since red blood cells and albumin are essentially limited to the vascular space, a reduction in the plasma volume due to volume depletion tends to elevate both the hematocrit (ie, relative polycythemia) and serum albumin concentration. However, these changes are frequently absent because of underlying hypoalbuminemia and/or anemia, due, for example, to bleeding.

?Helpful

• Urine osmolality — In hypovolemic states, the urine is relatively concentrated with an osmolality often exceeding 450 mosmol/kg [11-13]. This response may not be seen, however, if concentrating ability is impaired by renal disease, an osmotic diuresis, the administration of diuretics, or central or nephrogenic diabetes insipidus. As an example, both severe volume depletion (which impairs urea accumulation in the renal medulla) [14] and hypokalemia (which induces antidiuretic hormone [ADH] resistance) can limit the increase in the urine osmolality in some patients. Thus, a high urine osmolality is consistent with hypovolemia, but a relatively isosmotic value does not exclude the disorder. Urinary concentration can also be assessed by measuring the specific gravity. The results are less reliable than the urine osmolality because specific gravity is determined by the mass rather than number of solute particles in the urine. A value above 1.015 is suggestive, but not diagnostic, of a concentrated urine, as is usually seen with hypovolemia. The urine specific gravity is misleadingly high with proteinuria or after administration of radiocontrast agents.

Not that helpful

• Urinalysis — Examination of the urine is an important diagnostic tool in patients with elevations in the BUN and plasma creatinine concentration. The urinalysis is generally normal in hypovolemic states since the kidney is not diseased. This is in contrast to most, but not all, of the other causes of renal insufficiency in which the urinalysis reveals protein, cells, and/orcasts.

Question 29

Patient with esophageal varices. List four non-pharmacological therapies to
manage esophageal varices.

Answer 29

• TIPS
• endoscopic variceal ligation (banding)
• endoscopic sclerotherapy
• Blakemore balloon tamponade
• esophageal stent placement
• porto-caval shunt surgery

Variceal bleeding

1. pharmacologic therapy (octreotide, pantoprazole)
   
   • if bleeding continues…
2. endoscopic therapies (endoscopic variceal ligation, or endoscopic sclerotherapy)
   
   • if initially successful but then rebleeds can consider repeat endoscopy
   • if initally unsuccessful then move to… (can temporize with esophageal stent or balloon tamponade
3. TIPS or surgical shunting

TIPS

Absolute contraindications to TIPS placement include:

• heart failure
• polycystic liver disease
• severe pulmonary hypertension
• uncontrolled systemic infection or sepsis
• severe tricuspid regurgitation.

Relative contraindications include:

• hepatocellular carcinoma (particularly if central)
• portal vein thrombosis
• severe coagulopathy or thrombocytopenia.

Complications of TIPS placement include:

• portosystemic encephalopathy
• technical complications (eg, cardiac arrhythmias, traversal of the liver capsule)
• TIPS stenosis

Balloon-occluded retrograde transvenous obliteration (BRTO) is a procedure that has been used for bleeding gastric varices as well as ectopic varices (eg, small bowel varices). BRTO is an interventional radiologic technique that involves occluding blood flow by inflation of a balloon catheter within a draining vessel, followed by instillation of a sclerosant proximal to the site of balloon occlusion. BRTO requires the presence of a spontaneous shunt into which a balloon catheter is retrogradely introduced. In the case of gastric varices, there frequently is a spontaneous gastrorenal shunt. Small bowel varices usually drain into dilated collateral vessels that connect to the portal vein through systemic shunts.

Question 30

List 2 other factors in FFP other than vitamin K dependent factors.

Answer 30

factor VIII

factor V

…factor XIII, factor XII, factor XI,

fibrinogen (would this count as a “factor”?…I think so cause it’s also called factor I)

FFP contains all coagulation factors except platelets.

Fresh Frozen Plasma (FFP) is prepared from single units of whole blood or from plasma collected by apheresis techniques. It is frozen at -18 to -30°C within eight hours of collection and, when appropriately stored, is usable for one year from the date of collection. Standard FFP units derived from a single unit of whole blood have a volume of approximately 200 to 250 mL. FFP contains all of the coagulation factors and other proteins present in the original unit of blood, slightly diluted by the citrate-containing anticoagulant solution used to collect the blood.

Vitamin K dependent factors (think 1972)

II

VII

IX

X

…and protein C and S which are Vitamin K dependent proteins that are ANTI COAGULANT

Question 31

Other than FFP list two methods of correcting coagulopathy in a bleeding patient on Coumadin.

Answer 31

vitamin K

prothrombin complex concentrate (aka octaplex in Canada) (the 4 factor PCC one contains: factors II, VII, IX, X, protein C, protein S…and apparently for the excipient: antithrombin III and human albumin)

As an aside:

Cryoprecipitate contains most of the fibrinogen (factor I), factor VIII, factor XIII, von Willebrand factor (VWF), and fibronectin derived from one unit of Fresh Frozen Plasma (FFP). Thus, one unit of Cryoprecipitate contains the following proteins in a volume of approximately 5 to 20 mL:

• Fibrinogen
• Factor VIII
• Factor XIII
• von Willebrand factor

Question 32

A girl suffers some abdominal trauma and is taken to OR and has multiple bowel
perforations and massive hemorrhage. The surgeons repair what they can and
then pack the abdomen witn sponges and leave it open & covered with plans to
have a second look the following day. What 3 things can you do to assist and
minimize bleeding in this patient over night.

Answer 32

• temperature control (prevent hypothermia)
• avoid hypocalcemia
• avoid acidosis
• treat resuscitation-associated coagulopathy (?use thromboelastography-guided management?)

Acute traumatic coagulopathy

Etiologies that upset this balance include classic elements of the “vicious triad”: acidosis related to tissue injury and shock, hypothermia from exposure and fluid administration, and hemodilution due to fluid or component blood product administration. Systemic consumption of clotting factors manifesting as disseminated intravascular coagulation (DIC) may occur early after injury due to inadequate clotting factor repletion in the face of ongoing consumption, or later in the hospital course triggered by secondary insults (eg, sepsis). Distinct from these, acute traumatic coagulopathy (ATC) is a biochemical response to injury and shock leading to hyperfibrinolysis and hypocoagulability that appears to be mediated by dysregulation of the protein C system.

Question 33

A trauma patient with closed head injury & coma:

a. Based on TBI guidelines list 2 indications for extraventricular drain in this patient.
b. Based on TBI guidelines what the recommended Cerebral perfusion pressure.

Answer 33

a) CSF Drainage from TBI guidelines 4th Ed.

Level I and II

• There was insufficient evidence to support a Level I or II recommendation for this topic.

Level III

• An EVD system zeroed at the midbrain with continuous drainage of CSF may be considered to lower ICP burden more effectively than intermittent use.
• Use of CSF drainage to lower ICP in patients with an initial Glasgow Coma Scale (GCS) <6 during the first 12 hours after injury may be considered.

b) CPP Thresholds

Level I and II A

• There was insufficient evidence to support a Level I or II A recommendation for this topic.

Level II B

• The recommended target cerebral perfusion pressure (CPP) value for survival and favorable outcomes is between 60 and 70 mm Hg. Whether 60 or 70 mm Hg is the minimum optimal CPP threshold is unclear and may depend upon the patient’s autoregulatory status.

Level III

• Avoiding aggressive attempts to maintain CPP above 70 mm Hg with fluids and pressors may be considered because of the risk of adult respiratory failure.

ICP Thresholds

Level I and II A

• There was insufficient evidence to support a Level I or II A recommendation for this topic.

Level II B

• Treating ICP above 22 mm Hg is recommended because values above this level are associated with increased mortality.

Level III

• A combination of ICP values and clinical and brain CT findings may be used to make management decisions. *The committee is aware that the results of the RESCUEicp trial may be released soon after the publication of these Guidelines.

ICP Monitoring

Level I and II A

• There was insufficient evidence to support a Level I or II A recommendation for this topic.

Level II B

• Management of severe TBI patients using information from ICP monitoring is recommended to reduce in-hospital and 2-week post-injury mortality.

Question 34

Pt with MI has LV free wall rupture is presented. List 2 risk factors for LV free wall rupture. At what time after MI does LV free wall rupture occur.

Answer 34

• No history of previous angina or MI (due to absence of collaterals)
• ST-segment elevation or Q wave development on the initial electrocardiogram (ECG)
• Peak MB-creatine kinase above 150 international units/L
• anterior location of infarct
• age >70yrs
• female sex

Although fibrinolytic therapy accelerates the occurrence of rupture, the TIMI 9 study of 3759 patients found no association between cardiac rupture and the use of adjunctive thrombin inhibitors, including heparin and hirudin, or the intensity of systemic anticoagulation. The incidence of cardiac rupture may be lower in patients treated with percutaneous coronary intervention compared to those receiving a fibrinolytic agent.

Late reperfusion — A separate issue from the overall efficacy of reperfusion to reduce the incidence of free wall rupture is the value of late therapy. Initial suggestions that late administration of fibrinolytic therapy might increase the risk of cardiac rupture [21,22] were disproved by the Late Assessment of Thrombolytic Efficacy (LATE) trial [23]. In this study, 5711 patients were randomly assigned to receive alteplase or placebo 6 to 24 hours after the onset of symptoms. Late fibrinolysis did not increase the risk of cardiac rupture; it did, however, appear to accelerate the time of onset of rupture events, typically to within 24 hours of treatment.

Protective factors for free wall rupture

• beta blockers
• PCI (over thrombolytics)

Timing:

3-5 days

Myocardial rupture after acute myocardial infarction (AMI) may occur from 1 day to 3 weeks after infarction. Most ruptures occur 3-5 days after infarction

Becker and colleagues identified 3 morphological types of FWR. Type 1 rupture is characterized as an abrupt, slit-like myocardial tear and corresponds to the acute phase of MI (<24 hours). In type 2 rupture, an area of myocardial erosion is evident, indicating a slowly progressive tear. Type 3 rupture has marked thinning of the myocardium and perforation in the central portion of aneurysm, which typically occurs during the late phase of MI (>7 days).

Question 35

List 4 anatomical areas that the FAST exam is performed in a Trauma.

List 2 areas that are not imaged well.

Answer 35

• hepato-renal recess (Morrison’s pouch)
• spleno-renal recess
• subxiphoid
• pelvic (around bladder)

retroperitoneum

bowels

diaphragm

?lung

Question 36

Patient who had major head trauma a few weeks ago is discharged, but returns to hospital feeling unwell. A bunch of lab work is given showing namely Na 108, elevated cortisol level.

a. List the major complication that can occur with treating the major abnormality.
b. What is the likely cause of these abnormaliies.
c. What test would you order to determine the cause of these abnormalities.

Answer 36

a) osmotic demyelination syndrome
b) chronic SiADH following TBI (or could it be cerebral salt wasting???)
c) ???

CSW versus SIADH — Some authorities suggest that the distinction between CSW and the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) is critically important, with possible adverse consequences if the incorrect therapeutic strategy is administered [5,36]. Others suggest that the distinction is less important since all hyponatremic patients (where due to CSW or SIADH) who have active intracranial pathology (eg, recent intracranial surgery or subarachnoid hemorrhage) should be treated with 3 percent (hypertonic) saline to ensure a prompt increase in the serum sodium concentration and to avoid a decrease in extracellular fluid volume [37].

In addition to hyponatremia, CSW and SIADH share the following features:

• The urine osmolality is inappropriately high in the presence of hyponatremia (which normally suppresses ADH release) due to increased release of ADH. This response is appropriate in CSW, due to the volume depletion, but inappropriate in SIADH.
• The urine sodium is usually >40 mEq/L due to volume expansion in SIADH and putative salt wasting in CSW.
• The serum uric acid concentration is typically reduced due to urinary losses, perhaps due to a putative hormone such as BNP in CSW and to volume expansion and a direct effect of ADH on the V1 receptor in SIADH.

It is only the presence of clear evidence of volume depletion (eg, hypotension, decreased skin turgor, elevated hematocrit, possibly increased BUN/serum creatinine ratio) despite a urine sodium concentration that is not low that suggests that CSW might be present rather than SIADH. By comparison, extracellular fluid volume is normal or slightly increased with SIADH.

Question 37

Patient had major abdominal trauma and is now hypotensive with Hgb 54g/L. A
CT scan was slice was supposed to be shown and they asked what the most
likely injury was and if the patient continued to bleed list 2 management options. Unfortunately there was no CT picture so we couldn’t do the question. But it was likely a splenic/liver laceration and they wanted you to suggest embolization or surgical resection.

Answer 37

For hemodynamically stable patients with liver injury with no other indication for abdominal exploration, we suggest nonoperative management over definitive surgical intervention, regardless of hepatic injury grade (Grade 2C). Observation involves monitored care, serial abdominal examination, and serial hemoglobin assessment and potentially hepatic embolization. Failure of nonoperative management (ongoing transfusion, hemodynamic instability) indicates the need for hepatic embolization or surgery.

For hemodynamically stable patients with liver injury who demonstrate pooling of intravenous contrast on initial or subsequent abdominal CT scan, we suggest hepatic embolization rather than nonoperative management without embolization (Grade 2C). Hepatic embolization requires specialized imaging facilities and an appropriately trained interventionalist experienced with celiac artery catheterization. Failure of hepatic embolization to control bleeding indicates the need for surgery.

Question 38

List two mechanism of action of Activated Protein C.

Answer 38

• promotes fibrinolysis
• inhibits thrombosis

It was hypothesized to benefit patients with sepsis because it modulates the procoagulant response that is believed to contribute to multisystem organ dysfunction.

Question 39

Given 85 y.o. female 48 hr post hip Sx and now oliguric, febrile, tachycardic, hypotensive (BP 90/50). It was clear that she was septic.
a. Give 2 clinical indicators that this pt is mounting SIRS response.

b. List 3 clinical goals in the management of this patient from the surviving sepsis guidelines (MVO2 >70, U/O >0.5ml/kg/hr, MAP>65, CVP>12)…this must be too old now…maybe change to list components of the 1 hour bundle?

Answer 39

a) SIRS criteria (must have >/=2)

HR >90bpm

temp >38, <36

RR >20 or PaCO2 <32

WBC >12 or <4 or >10% immature bands

b)

A. INITIAL RESUSCITATION

1. Sepsis and septic shock are medical emergencies, and we recommend that treatment and resuscitation begin immediately (BPS).
2. We recommend that, in the resuscitation from sepsis-induced hypoperfusion, at least 30 mL/kg of IV crystalloid fluid be given within the first 3 h (strong recommendation, low quality of evidence).
3. We recommend that, following initial fluid resuscitation, additional fluids be guided by frequent reassessment of hemodynamic status (BPS).

Remarks

Reassessment should include a thorough clinical examination and evaluation of available physiologic variables (heart rate, blood pressure, arterial oxygen saturation, respiratory rate, temperature, urine output, and others, as available) as well as other noninvasive or invasive monitoring, as available.

4. We recommend further hemodynamic assessment (such as assessing cardiac function) to determine the type of shock if the clinical examination does not lead to a clear diagnosis (BPS).
5. We suggest that dynamic over static variables be used to predict fluid responsiveness, where available (weak recommendation, low quality of evidence).
6. We recommend an initial target mean arterial pressure (MAP) of 65 mm Hg in patients with septic shock requiring vasopressors (strong recommendation, moderate quality of evidence).
7. We suggest guiding resuscitation to normalize lactate in patients with elevated lactate levels as a marker of tissue hypoperfusion (weak recommendation, low quality of evidence).

D. ANTIMICROBIAL THERAPY

1. We recommend that administration of IV antimicrobials be initiated as soon as possible after recognition and within 1 h for both sepsis and septic shock (strong recommendation, moderate quality of evidence; grade applies to both conditions).

1 hour bundle

• measure lactate level, remeasure if initial lactate is >2mmol/L
• obtain blood cultures prior to antibiotic administration
• administer broad-spectrum antibiotics
• begin rapid administration of 30mL/kg crystalloid for hypotension or lactate >/=4mmol/L
• apply vasopressors if patient is hypotensive during or after fluid resuscitation to maintain MAP >/= 65mm Hg

Question 40

List 2 pathophysiological abnormalities that occur at the microvascular level in sepsis.

Answer 40

• microthrombin formation
• increased microvascular permeability
• production of vasoactive products (bradykinin)
• decrease in number of functional capillaries, which causes an inability to extract oxygen maximally

Endotoxin reproduces many of the features of sepsis when it is infused into humans, including activation of the complement, coagulation, and fibrinolytic systems. These effects may lead to microvascular thrombosis and the production of vasoactive products, such as bradykinin.

Question 41

In an influenza pandemic list two ethical principles that you would use to triage patients in your ICU.

Answer 41

basic principles of medical ethics:

1. autonomy
2. justice
3. beneficence
4. non-maleficence

If these are what they are looking for I guess I would go with justice and beneficence…

Question 42

There was another question on influenza pandemic and the question listed some CMAJ 2006 article on influenza pandemic.

Answer 42

I suspect it was in reference to this article

Maybe something on triaging…?

Question 43

In examining the use of steroids in sepsis give 3 reasons why the CORTICUS trial showed such different results than other studies (Annane etc) that showed a difference with the use of steroids and fludrocortisone.

They might be more likely to ask about APROCCHS and ADRENAL…compare and contrast these.

Answer 43

Annane enrolled pts earlier (maybe benefit to early therapy as with IV fluids, Abx, etc in sepsis)

Annane had sicker pts overall (higher mortality rate overall) so these are maybe those most likely to benefit from steroids

CORTICUS was underpowered and only had 500 pts of the planned 800

good editorial comparison here

CORTICUS

• multicentre, randomized double blind, placebo controlled
• inclusion: septic shock within last 72H, hypoperfusion or organ dysfunction attributable to sepsis
• hydrocortisone 50mg IV q6H for 5d, then weaned for 6d
• Primary endpoint: no difference in 28d mortality in non-responders to corticotropin (no difference in those that responded to corticotropin either)
• reversal of shock faster if given steroids

ANNANE

• pts needed SBP <90 for >1H and enrolled by 8H after shock onset
• given hydrocortisone and fludrocortisone and abruptly stopped at 7d
• higher death rate than in CORTICUS (?sicker population)
• Primary outcome: 28d survival distriution from randomization in non-responders - significant improvement in steroid group, NNT 7
• median time to vasopressor withdrawal longer in placebo group (in non-responders)

APROCCHSS vs ADRENAL resident NEJM

other comparison paper on the two

Both trials included patients with clearly defined vasopressor-dependent shock and respiratory failure leading to the use of mechanical ventilation. Both trials also included details of antimicrobial therapy, assessment of 90-day all-cause mortality as the primary outcome, and robust secondary outcomes and adverse events. The combined sample size of more than 5000 patients (3658 and 1241, respectively) dwarfs those of previous studies.

APROCCHSS

• hydrocortisone 200/d + fludrocortisone 0.05/d vs placebo
• 1ary outcome favoured hydrocort + fludrocort

ADRENAL

• hydrocortisone 200/d vs placebo for 7d or discharge
• 1ary outcome not different between both groups

For secondary outcomes, both trials indicated that hydrocortisone was associated with an increase in the number of days free of shock or organ failure and more rapid cessation of mechanical ventilation. Rates of serious adverse events were low, with higher risk of hyperglycemia with bolus glucocorticoid doses. No differences were noted in rates of renal-replacement therapy or incidence of new-onset bacteremia or fungemia (ADRENAL trial).

Differences:

• ADRENAL had higher rate of surgical admissions
• ADRENAL had lower rates of RRT, blood infection, pulmonary infection and UTIs
• APROCCHSS had higher shock severity and mortality
• Second, the ADRENAL trial enrolled patients from 5 countries over 4 years, whereas the APROCCHSS trial was conducted over 7 years only in France. In total, 3,713 patients completed the evaluation in the ADRENAL trial, a number three times larger than the number of patients in the APROCCHSS trial. Third, the required vasopressor dosage and timing were lower and shorter, respectively, in the ADRENAL trial than in the APROCHSS trial. This might explain higher shock severity and mortality in the APROCCHSS.

Question 44

List 2 lab values to test for Cyanide toxicity (other than cyanide level).

Answer 44

• elevated lactate
• elevated venous PaO2

Of note, treatment with hydroxocobalamin affects a number of laboratory tests.

Anion gap acidosis — A severe metabolic acidosis with an increased anion gap is expected in cyanide poisoning. In addition to its inhibitory effects on cellular respiration, cyanide can induce cardiovascular collapse and seizures, which exacerbate anion gap metabolic acidosis.

Lactate — Cyanide-poisoned patients have an elevated blood lactate concentration. A retrospective study of 11 ICU patients with cyanide poisoning found that plasma lactate concentrations correlated closely with the severity of cyanide toxicity [32]. There were significant inverse correlations between lactate and systolic blood pressure, respiratory rate, and arterial pH. In fact, lactate concentrations of 10 mmol/ L or greater have been shown to be both sensitive and specific for cyanide poisoning in smoke inhalation victims [33]. Consequently, a normal serum lactate should lead the clinician to entertain other diagnoses, while serial lactate measurements can be used to monitor the progress of patients being treated for cyanide poisoning. Of note, a significant delay in laboratory processing of the patient’s blood sample may cause an artificial elevation in lactate concentration.

Venous PO2 — A narrowing of the venous-arterial PO2 gradient (ie, venous hyperoxia) may be seen in the cyanide-poisoned patient [34]. Cyanide inhibits cellular oxidative phosphorylation resulting in a marked decrease in peripheral tissue oxygen extraction from the blood. This results in elevated central venous oxygenation. On examination, the skin may appear flushed and the venules in the retina bright red. Laboratory evaluation may reveal a decreased arterial–venous oxygen gradient. Clinicians should keep in mind that a decreased oxygen gradient is nonspecific and can result from other inhibitors of oxidative phosphorylation, such as carbon monoxide, hydrogen sulfide, and azides.

Cyanide concentration (level) — Blood cyanide concentrations may be obtained for diagnostic confirmation but results are not available in time to be clinically useful. Even when available, the results of direct testing may be unreliable as both proper storage conditions and prompt blood draws are required. Furthermore, blood cyanide concentrations do not correlate directly with survival. Nonetheless, blood cyanide concentrations of 0.5 to 1 mg/L (12 to 23 μmol/L) generally correlate with tachycardia and flushing, 1 to 2.5 mg/L (23 to 58 μmol/L) with obtundation, 2.5 to 3 mg/L (58 to 69 μmol/L) with coma, and greater than 3 mg/L (>69 μmol/L) with death.

Hydroxocobalamin, a precursor of vitamin B12, contains a cobalt moiety that avidly binds to intracellular cyanide (with greater affinity than cytochrome oxidase) forming cyanocobalamin. This molecule is stable and readily excreted in the urine. Because hydroxocobalamin acts rapidly, does not adversely affect tissue oxygenation, and is relatively safe, many investigators recommend it be used as the first line agent in cyanide poisoning and we concur with this approach

Hydroxocobalamin, when given at the recommended dose, may cause a temporary reddish discoloration of the skin, plasma, urine, and mucous membranes [46,47]. These changes last for approximately two to three days, altering the laboratory values of tests performed using cooximetry or spectrophotometry. Blood tests that may be affected include creatinine, lactate, aspartate aminotransferase (AST) and alanine aminotransferase (ALT), bilirubin, and magnesium [18,48-50]. Common urinalysis tests may also be affected (eg, glucose, protein, ketones, and leukocyte and erythrocyte counts).

Question 45

List the drug or drug class, or receptors associated with the following presentations: There were 5 of them. I can remember 3.

a. bronchospasm, bradycardia, diarrhea etc.
b. metabolic acidosis, abdominal pain and hypocalcemia
c. muscle rigidity, diminished LOC…..can’t remember the rest.

Answer 45

a) cholinergic meds (?organophosphates)

• muscarinic signs:
  
  • SLUDGE/BBB – Salivation, Lacrimation, Urination, Defecation, Gastric Emesis, Bronchorrhea, Bronchospasm, Bradycardia
• It should be noted that these mnemonics do NOT take into account the critical CNS and nicotinic effects of these toxins. The nicotinic effects include fasciculations, muscle weakness, and paralysis via acetylcholine stimulation of receptors at the neuromuscular junction. This mechanism is analogous to the depolarizing effects of succinylcholine in producing neuromuscular blockade. Nicotinic and muscarinic receptors also have been identified in the brain, and may contribute to central respiratory depression, lethargy, seizures, and coma
• Medication Causes: Organophosphates have been used as insecticides worldwide for more than 50 years. The use of these agents has declined in the last 10 to 20 years, in part due to the development of carbamate insecticides, which are associated with similar toxicities [1]. Medical applications of organophosphates and carbamates include reversal of neuromuscular blockade (neostigmine, pyridostigmine, edrophonium) and treatment of glaucoma, myasthenia gravis, and Alzheimer disease (echothiophate, pyridostigmine, tacrine, and donepezil).

b) ?ethylene glycol or maybe propylene glycol toxicity (maybe from benzo preservative)

Propylene glycol is the diluent used in the parenteral formulations for these 2 benzodiazepines, and prolonged use can cause propylene glycol toxicity which includes skin and soft tissue necrosis, hemolysis, cardiac dysrhythmias, hypotension, significant lactic acidosis, seizure, and multisystem organ failure. While propylene glycol toxicity is rare, it must be considered when patients are receiving large or continuous infusions of parenteral benzodiazepines, for example when treating severe sedative or ethanol withdrawal syndromes such as delirium tremens. but I couldn’t find that it causes hypocalcemia or abdo pain

c) ?NMS

Question 46

Patient with Calcium channel blocker and Beta blocker overdose. Patient is now hypotensive and bradycardic. List 4 medications to manage this patient.

Answer 46

• IV fluids
• IV glucagon
• IV calcium
• vasopressors
• IV high dose insulin
• IV dextrose for insulin but pts can also have symptomatic hypoglycemia
• IV lipid emulsion
• IV atropine (give early and consider pretreating if intubating)

Looks like to me the mgmt is basically the same for CCB and BB but I vaguely remember hearing a difference when on tox (?more calcium for CCB overdoses?)

Question 47

Patient with terminal illness in ICU. You request palliative care to meet with the family. List 3 ways palliative care can assist.

Answer 47

1. eliciting pt values
2. communication with family
3. help with symptom management
4. second opinion to make the family more comfortable/confident in palliation

paper here

or here

Question 48

80 something old Female patient who had had massive intracranial bleed. No surgical intervention. Patient does not meet criteria for neurological death. Only family member is husband who wants to continue (“let God take her when she’s ready” or something like that he says). The neurosurgeon and neurologist are consulted and state there is no hope for a neurological recovery and the patient is in persistent vegetative state. List 3 things you can do to deal with this situation.

Answer 48

• explore if there are other factors of SDMs decision (fear of death, guilt, etc)
• offer spiritual care
• offer change of goals to palliative/comfort care
• offer second opinion (I mean fourth opinion, haha)
• explore pt’s previously expressed wishes (if known) or values and how they might help in this decision making