2016 Flashcards

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1
Q

Chest CT with pulmonary infiltrates / innumerable nodules, plus picture of lesions on hands, feet, and nose. What is characteristic finding on chest CT?
DDx? (list 4possibilities) Diagnostic Test? (skin Biopsy)

A

TB

sarcoid

vasculitis, i.e. GPA

other infections (nocardia, fungal, mycobacterial)

malignancy

syphillis (case reports)

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2
Q

Various Guyton Curves shown. Label each with clinical syndrome. There was one for CHF, hypovolemic, and hyperdynamic shock.

A

see image

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3
Q

ASD: list 5 complications in a patient with sepsis and known Atrial septal defect

A

***not sure how these are specific to sepsis***

atrial arrhythmias

intracardiac shunting -> RV volume overload (if L to R) eventually causing pulmonary vascular injury then pulm HTN then RV failure

shunting -> if R to L could cause hypoxia (typically via Eisenmenger’s syndrome)

systemic thromboembolism

?infective endocarditis

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4
Q

Patient with normal LVEF but low cardiac output and shock. List 5 possible etiologies or “cardiac findings” (meaning of latter was not clear. Physical findings? unclear question)

A
  1. mitral regurgitation
  2. aortic regurgitation
  3. hypovolemia (i.e. low LVEDV to begin with causing low SV)
  4. right heart failure (PE?) which can still have a “normal” LVEF but the LV would be small/underfilled
  5. cardiac tamponade, again a small/underfilled LV which is ejecting “normal” EF but small SVs
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5
Q

Match the following laws with their definitions: Laplace’s, Bernoulli, Poiseuille,
Henry’s, Boyle’s

A

Laplace - The larger the vessel radius, the larger the wall tension required to withstand a given internal fluid pressure

Bernoulli - an increase in the speed of a fluid occurs simultaneously with a decrease in pressure or a decrease in the fluid’s potential energy

Poiseuille - It states that the flow (Q) of fluid is related to a number of factors: the viscosity (n) of the fluid, the pressure gradient across the tubing (P), and the length (L) and diameter(r) of the tubing.

Henry - the amount of dissolved gas in a liquid is proportional to its partial pressure above the liquid. (relevant in nitrogen gas in diving I suppose)

Boyle - pressure of a given mass of an ideal gas is inversely proportional to its volume at a constant temperature.

Charles - volume of a gas proportional to temperature (i.e. when temperature of a gas increases so does volume)

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6
Q

ECMO - list benefits/drawbacks of VA vs VV ECMO

A

VA - provides cardiac and respiratory support

  • higher risks with vascular access (bleeding, limb ischemia)
  • always requires at least 2 catheters (VV can be one or two)
  • bypasses pulmonary circulation therefore can decrease pulmonary artery pressures
  • can be used in RV failure
  • overall VA ECMO has higher complications that VV ECMO (highest complication is bleeding and rates are higher in VA than with VV ECMO)

additional VA ECMO only complications from uptodate:

  • Pulmonary hemorrhage - Pulmonary edema and hemorrhage can occur in patients who have no left ventricular (LV) emptying during VA ECMO. Edema occurs when the left atrial (LA) pressure exceeds 25 mmHg. It is treated by venting the LA or LV
  • cardiac thrombus - There is retrograde blood flow in the ascending aorta whenever the femoral artery and vein are used for VA ECMO. Stasis of the blood can occur if left ventricular output is not maintained, which may result in thrombosis
  • Coronary or cerebral hypoxia – During VA ECMO, fully saturated blood infused into the femoral artery from the ECMO circuit will preferentially perfuse the lower extremities and the abdominal viscera. Blood ejected from the heart will selectively perfuse the heart, brain, and upper extremities. As a result, the oxyhemoglobin saturation of the blood perfusing the lower extremities and abdominal viscera may be substantially higher than that perfusing the heart, brain, and upper extremities. Cardiac and cerebral hypoxia could exist and be unrecognized if oxygenation is monitored using only blood from the lower extremity. To avoid this complication, arterial oxyhemoglobin saturation should be monitored in the right upper extremity. Poor arterial oxyhemoglobin saturation measured from the upper extremity is corrected by infusing some oxygenated blood into the right atrium (called VA-V access).
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7
Q

Malaria - Dx test and 7 complications

A

Dx test: thick and thin peripheral blood smear

  • Clinical tools for parasite-based diagnosis include microscopy (visualization of parasites in stained blood smears) and rapid diagnostic tests (RDTs; which detect antigen or antibody). Smear examination via light microscopy is the standard tool for diagnosis of malaria; RDTs should be used if microscopy is not readily available.
  • Two types of blood smears are used in malaria microscopy: thin and thick smears. Thin smear preparation maintains the integrity and morphology of erythrocytes so that parasites are visible within red blood cells. Thin smears allow identification of the infecting parasite species and can be used to measure parasite density. Thick smear preparation involves mechanical lysis of red blood cells so that malaria parasites can be visualized independent of cell structures. Thick smears allow the microscopist to review a relatively large quantity of blood and are typically used to screen for presence or absence of parasites and to estimate parasite density.

Following the bite of an infected female Anopheles mosquito, the inoculated sporozoites go to the liver within one to two hours. Individuals are generally asymptomatic for 12 to 35 days but can commence symptoms as early as 7 days (depending on parasite species), until the erythrocytic stage of the parasite life cycle (figure 1). Release of merozoites from infected red cells when they rupture causes fever and the other manifestations of malaria.

In most cases, the incubation period for P. falciparum infection is about 12 to 14 days (range 7 to 30 days); most infections due to P. falciparum become clinically apparent within one month after exposure.

Uncomplicated malaria — Malaria should be suspected in patients with any febrile illness if they have had exposure to a region where malaria is endemic [1,2,6]. The initial symptoms of malaria are nonspecific and may also include tachycardia, tachypnea, chills, malaise, fatigue, diaphoresis (sweating), headache, cough, anorexia, nausea, vomiting, abdominal pain, diarrhea, arthralgias, and myalgias [2,6]. Patients are considered to have uncomplicated malaria in the setting of symptoms of malaria and a positive parasitological test in the absence of signs of severe malaria [10].

Physical findings may include manifestations of anemia and a palpable spleen.

Laboratory evaluation may demonstrate parasitemia (usually <5000 parasites/microL of blood, <0.1 percent parasitized red blood cells [RBCs]), anemia, thrombocytopenia, elevated transaminases, mild coagulopathy, and elevated blood urea nitrogen (BUN) and creatinine.

Early in the course of malaria infection, febrile paroxysms occur at irregular intervals each day. The temperature of nonimmune individuals and children may rise above 40ºC and may occur in conjunction with tachycardia and/or delirium. Febrile convulsions may occur among children in the setting of malaria due to any species. However, generalized seizures are associated with falciparum and may herald the development of cerebral malaria.

Severe Malaria - Many of the clinical findings are the result of the parasitized (and nonparasitized) RBCs adhering to small blood vessels (“cytoadherence”) causing small infarcts, capillary leakage, and organ dysfunction; these include the following [6,14,15]:

  • Altered consciousness with or without seizures
  • Respiratory distress or acute respiratory distress syndrome (ARDS)
    • Noncardiogenic pulmonary edema (eg, adult respiratory distress syndrome) may be observed in adults with severe falciparum malaria [35]. The pathogenesis is uncertain but may be related to sequestration of parasitized red cells in the lungs and/or cytokine-induced leakage from the pulmonary vasculature.
  • Circulatory collapse
  • Metabolic acidosis
  • Renal failure, hemoglobinuria (“blackwater fever”)
  • Hepatic failure
  • Coagulopathy with or without disseminated intravascular coagulation
  • Severe anemia or massive intravascular hemolysis
  • Hypoglycemia (from: Diminished hepatic gluconeogenesis, Depletion of liver glycogen stores, Increase in the consumption of glucose by the host (and, to a much lesser extent, the parasite), Quinine-induced hyperinsulinemia)

Cerebral malaria is an encephalopathy that presents with impaired consciousness, delirium, and/or seizures; focal neurologic signs are unusual. The onset may be gradual or sudden following a convulsion. The severity depends on a combination of factors including parasite virulence, host immune response, and time between onset of symptoms and initiation of therapy.

Risk factors for cerebral malaria include age (children and older adults), pregnancy, poor nutritional status, HIV infection, host genetic susceptibility, and history of splenectomy.

Septicemia may complicate severe malaria, particularly in children [36]. In endemic areas, Salmonella bacteremia has been associated with P. falciparum infections [37]. Chest infections and catheter-induced urinary tract infections are common among patients who are unconscious for ≥3 days. Aspiration pneumonia may follow generalized seizures.

HIV infection — HIV and malaria often coexist. Both conditions induce cell-medicated immunodepression.

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8
Q

Family meeting with moribund patient. 4 strategies to approach family meeting. The meeting does not go well and the family is angry. What are 2 effects on the family?

A

SPIKES mnemonic

S - setting up the interview (privacy, involve significant others, sit down, connect w pt, manage time constraints/interruptions)

P - assessing the patient’s Perception, ask pt what they’ve been told or what they understand

I - obtain the pts Invitation

K - giving Knowledge and information

E - addressing the pt’s Emotion with Empathic responses

S - Strategy and Summary

Other: invite nurse, chaplain, social worker to family meeting

effects on the family

Psychological conditions are common among the family members of patients in the ICU. This was illustrated by a study of 920 family members, in which the prevalence of anxiety and depression was 69 percent and 35 percent, respectively [30]. In another report, approximately one-third of family members developed symptoms that suggested that they were at moderate to major risk of developing posttraumatic stress disorder (PTSD)

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9
Q

List 3 patient-centered reasons to withdrawing life sustaining therapy

A
  • discomfort/pain associated with intervention (non-maleficence)
  • limited chance for cure/positive outcome (beneficence)
  • autonomy over decisions and death process
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10
Q

List the qSOFA criteria for sepsis

A

Hypotension SBP <1/=00

Altered mental status (GCS<15)

Tachypnea (RR>/=22)

The score ranges from 0 to 3 points. The presence of 2 or more qSOFA points near the onset of infection was associated with a greater risk of death or prolonged intensive care unit stay. These are outcomes that are more common in infected patients who may be septic than those with uncomplicated infection. Based upon these findings, the Third International Consensus Definitions for Sepsis recommends qSOFA as a simple prompt to identify infected patients outside the ICU who are likely to be septic.

The diagnosis of infection was left to the clinician, while the TF recommended that an acute change of more than 2 sepsis-related organ dysfunction assessment (SOFA) points would identify sepsis.

But the SOFA score requires multiple laboratory tests and may not be available in a timely manner. To facilitate simple recognition in prehospital, ward, and the emergency department, the Task Force recommended a prompt called “qSOFA” for quick sepsis-related organ dysfunction assessment score.

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11
Q

Pulmonary hemorrhage secondary to U/S guided endobronchial Bx.
Management (4)

endobronchial management (3)

definitive management (2)

A
  • a) bleeding side down
  • inhaled TXA (has been tested in non-massive hemoptysis)
  • lung isolation via mainstem intubation
  • correct coagulopathy (plts if uremic or on antiplts, Vit K/octaplex, praxbind)
  • consider factor VII as rescue
    • b) lung isolation via bronchial blocker
  • ice cold saline via bronch
  • epinephrine via bronch
    • c) argon plasma coagulation
  • embolization
  • surgery
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12
Q

Post-CABG extubation questions - this was a repeat

A

???

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13
Q

Re-feeding syndrome - what are two most common labs are abnormal?

What are 4 labs that should be done to monitor?

What are 2 things to avoid when starting TPN?

A

a) hypophosphatemia, hypokalemia
b) PO4, K, Mg, and would probably choose Na over Ca
c) ?avoid starting feeds at full caloric needs (target 80% or 20kcal/kg/d)

?avoid feeds until given thiamine

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14
Q

Ebola - what are 3 components of extra PPE required not part of usual PPE?

A

Trained Observer - Because the sequence and actions involved in each donning and doffing step are critical to avoid exposure, a trained observer should read aloud to the healthcare worker each step in the procedure checklist and visually confirm and document that the step has been completed correctly. The trained observer has the sole responsibility of ensuring that donning and doffing processes are adhered to.

Impermeable garment:

  • Single-use (disposable) impermeable gown extending to at least mid-calf.

OR

  • Single-use (disposable) impermeable coverall.

Respiratory Protection: Either a PAPR (powered air purifying respirator) or disposable, NIOSH-certified N95 respirator should be worn in case a potentially aerosol-generating procedure needs to performed emergently. PAPRs with a full-face covering and head-shroud make accidental self-contamination during care more difficult (e.g., while adjusting eyeglasses); disposable N95 face piece respirators are less cumbersome and can be easier to doff safely.

Single-use (disposable) examination gloves with extended cuffs. Two pairs of gloves should be worn so that a heavily soiled outer glove can be safely removed and replaced during care. At a minimum, outer gloves should have extended cuffs.

Single-use (disposable) boot covers that extend to at least mid-calf.

Single-use (disposable) apron that covers the torso to the level of the mid-calf should be used over the gown or coveralls if patients with Ebola are vomiting or have diarrhea, and should be used routinely if the facility is using a coverall that has an exposed, unprotected zipper in the front.

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15
Q

SVT in asthmatic. What are two medications that can be used to Rx?

A

(Adenosine and Beta-blocker are CI)

non-dihydropyridine CCB (diltiazem, verapamil)

amiodarone

+/-procainamide

  • Procainamide, like quinidine and disopyramide, can significantly increase the ventricular rate in patients with uncontrolled atrial fibrillation or flutter. Two factors contribute to this response:
  • By slowing the atrial rate of atrial fibrillation or atrial flutter, procainamide increases the likelihood that a given impulse will pass through the AV node, thereby potentially increasing the ventricular rate.
  • Procainamide has a direct vagolytic action on the AV node, increasing conduction through the AV node.
  • Therefore, when administering procainamide for chemical cardioversion of atrial fibrillation, conduction through the AV node must be slowed and the ventricular response controlled (using ß-blockers, calcium channel blockers, or digitalis) before therapy with procainamide is initiated in these disorders
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16
Q

Drunk patient gets electrical shock from power lines. List 4 complications from electrical shock.

A

?rhabdomyolysis causing renal injury

cardiac arrhythmias (The overall estimate of arrhythmia following electrical injury is approximately 15 percent; most of these are benign and occur within the first few hours of hospital admission. However, acute electrical cardiac injury can result in sudden cardiac arrest due to asystole (usually with DC current or lightning) or ventricular fibrillation (AC current) prior to hospitalization. Ventricular fibrillation is the most common fatal arrhythmia.)

skin/surface burns: Superficial, partial-thickness, and full-thickness thermal burns can occur following electrical injury

weakness, decreased LOC, respiratory depression, autonomic dysfunction, memory disturbances. Damage to both the central and peripheral nervous systems can occur after electrical injury. Manifestations may include loss of consciousness, weakness or paralysis, respiratory depression, autonomic dysfunction, and memory disturbances. Sensory and motor findings due to peripheral nerve damage are common.

bone destruction: Because bone has the highest resistance of any body tissue, it generates the greatest amount of heat when exposed to an electrical current. Thus, the areas of greatest thermal injury are often the deep tissue surrounding long bones, potentially resulting in periosteal burns, destruction of bone matrix, and osteonecrosis.

compartment syndrome

electrical coagulation of small blood vessels

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17
Q

Pressure-time and flow-time curves shown for a patient on PCV. what is the
problem?

What are 4 mitigation strategies?

A

autopeep

  1. decrease tidal volume (i.e. Insp pressure in PCV)
  2. decrease I-time
  3. decrease RR
  4. ?technically you could decrease the inspiratory rise time to slightly decrease the tidal volume

treat possible bronchoconstriction?

Treatment of autoPEEP - Steps should be taken to correct auto-PEEP as soon as it is identified. Initial efforts should focus on determining and treating the underlying cause. When auto-PEEP persists despite management of its underlying cause, applied PEEP may be helpful if the patient has an expiratory flow limitation.

When a high minute ventilation is the presumed cause of auto-PEEP, the minute ventilation should be decreased by lowering the tidal volume or respiratory rate. This frequently requires a strategy of permissive hypercapnia. (See “Permissive hypercapnia during mechanical ventilation in adults”.)

When an expiratory flow limitation due to obstructive airways disease is the presumed cause of auto-PEEP, the duration of expiration should be prolonged. This can be accomplished by increasing the inspiratory flow, decreasing the tidal volume, or decreasing the respiratory rate.

Treatment with bronchodilators, steroids, and antibiotics may also be beneficial. In a study of 25 patients with COPD and acute respiratory failure, expiratory flow limitation was present in 96 percent of the patients at the initiation of mechanical ventilation [51]. The prevalence of expiratory flow limitation decreased to 47 percent at the time of extubation and 40 percent at the time of ICU discharge, indicating that expiratory flow limitation may respond to therapy.

When increased expiratory resistance is the presumed cause of auto-PEEP, the source of increased resistance should be identified and corrected. This may require sedation, pharmacologic paralysis, or replacement of the endotracheal tube or ventilator tubing.

Applied PEEP — Small amounts of applied PEEP can decrease auto-PEEP in patients who have an expiratory flow limitation [52-54]. This can be conceptualized as the applied PEEP holding open the narrowed airways during expiration, improving expiratory airflow, and allowing more complete expiration prior to the onset of the next breath. Additional benefits of using applied PEEP to offset auto-PEEP include decreased oxygen consumption and improved gas exchange. The latter is due to opening the small airways in the dependent lung zones and distributing inspired gas more homogeneously [55-57].

Applied PEEP should always be less than the measured auto-PEEP [58]. Otherwise, alveolar pressure may increase, placing the patient at increased risk for complications such as pulmonary barotrauma or hypotension (figure 5). One study even suggested that applied PEEP does not need to exceed the measured auto-PEEP for this to occur. Rather, it can occur if the applied PEEP is greater than 85 percent of the measured auto-PEEP [59]. Given the potential inaccuracy of auto-PEEP measurements, it is prudent to set applied PEEP to a level that is less than 50 percent of the measured auto-PEEP. Research has shown that mechanical ventilation with PEEP induces longitudinal atrophy by displacing the diaphragm in caudal direction and reducing the length of fibers. As a result, muscle fibers generate less force causing diaphragm weakness [60]. This may exacerbate diaphragm weakness in critically ill patients thus prolonging mechanical ventilation. This advocates for maintaining the lowest required PEEP setting.

Applied PEEP should not be used to counter auto-PEEP in patients who do not have an expiratory flow limitation. Applied PEEP may increase alveolar pressure and increase the risk of both barotrauma and hemodynamic compromise in this setting [61].

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18
Q

Hypoxemic respiratory failure with ARDS.

What are 2 ways to improve SpO2?

What are 3 strategies that have been proven to reduce mortality?

What are 2 strategies that can improve hypoxemia but do not improve mortality?

A

a) recruitment maneuvres, inhaled pulmonary vasodilators, high PEEP strategy
b) lung protective ventilation (low tidal volume), NMB, prone positioning
c) recruitment maneuvres, inhaled pulmonary vasodilators, HFO (by way of a higher mean airway pressure)

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19
Q

Echo image showing obviously dilated RV in patient with ARDS. What therapy can be used to mitigate this problem?

A
  • inhaled pulmonary vasodilators: inhaled nitric oxide, inhaled epoprostenol
  • prone positioning
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20
Q

4 hemodynamic profiles shown with CO, CI, SVR, PA pressures, wedge pressures, and CVP values given. Asked what can be added to help. There was one with LV failure, one RV failure, one with hypovolemic shock, and one with distributive shock / profound vasoplegia.

A

Normal values are:

cardiac output 4-8L/min

cardiac index 2.5-4L/min/m2

SVR 800-1200dynes/s/cm5

PA systolic 20-30mm Hg

PA diastolic 8-12mm Hg

PA mean 25mm Hg

wedge pressure 4-12mm Hg

CVP 2-6mm Hg

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21
Q

What is the oxygen delivery equation?
What is the transfusion threshold in sepsis?

A

a) see image

DO2=CO x [(1.34 x Hgb x SaO2) + (0.003 x PaO2)]

b) 70g/L

from guidelines: “1. We recommend that RBC transfusion occur only when hemoglobin concentration decreases to < 7.0 g/dL in adults in the absence of extenuating circumstances, such as myocardial ischemia, severe hypoxemia, or acute hemorrhage (strong recommendation, high quality of evidence).”

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22
Q
Toxidrome given (it was almost completely for sure anticholinergic) What are
3 things/syndromes that could match this?

What are 2 things that are characteristic of each of these possible syndromes (to differentiate them? unclear exactly what they wanted)

A

Anticholinergic toxidrome

  • “Red as a beet” – Cutaneous vasodilation occurs as a means to dissipate heat by shunting blood to the skin, in order to compensate for the loss of sweat production.
  • “Dry as a bone” (anhidrosis) – Sweat glands are innervated by muscarinic receptors, so anticholinergic medications produce dry skin.
  • “Hot as a hare” (anhydrotic hyperthermia) – Interference with normal heat dissipation mechanisms (ie, sweating) frequently leads to hyperthermia.
  • “Blind as a bat” (nonreactive mydriasis) – Muscarinic input contributes to both pupillary constriction and effective accommodation. Anticholinergic medications generally produce pupillary dilation and ineffective accommodation that frequently manifests as blurry vision.
  • “Mad as a hatter” (delirium; hallucinations) – Blockade of muscarinic receptors in the central nervous system (CNS) accounts for these findings. Manifestations may include: anxiety, agitation, dysarthria, confusion, disorientation, visual hallucinations, bizarre behavior, delirium, psychosis (usually paranoia), coma, and seizures. Hallucinations are often described as “Alice in Wonderland-like” or “Lilliputian type,” where people appear to become larger and smaller. Patients with altered mental status often present with agitation and may appear to grab invisible objects from the air [15]. Although central and peripheral anticholinergic effects are commonly seen together, in some cases, central effects may persist after resolution of peripheral symptoms.
  • “Full as a flask” – The detrusor muscle of the bladder and the urethral sphincter are both under muscarinic control; anticholinergic substances reduce detrusor contraction (thereby reducing or eliminating the desire to urinate) and prevent normal opening of the urethral sphincter (contributing to urinary retention).

Anticholinergic poisons

  • antihistamines
  • tricyclic antidepressants (amitriptyline)
  • sleep aids (doxylamine)
  • scopolamine
  • tainted illicit street drugs (heroin “cut” with scopolamine)
  • jimson weed
  • deadly nightshade (atropa belladonna)

While systemic effects generally improve spontaneously within several hours, treatment with physostigmine may be needed for severe toxicity

b) DDx:

?sympathomimetic

?serotonin

?salicylates

Any substance or condition that produces an alteration in mental status, tachycardia, urinary retention, or seizure should be included in the differential diagnosis. A wide range of medical conditions and drugs can cause agitated delirium.

Sympathomimetic overdose and serotonin toxicity may cause agitation, tachycardia, and hyperthermia, but can usually be differentiated from anticholinergic toxicity. Sympathomimetic overdose and serotonin toxicity generally cause diaphoresis, in contradistinction to anticholinergic overdose.

In agitated, hyperthermic patients with altered mental status, salicylate overdose should also be considered.

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23
Q

Ischemic colon - how to manage - 4 non-operative options

A
  • Nothing by mouth, nasogastric decompression.
  • Fluid therapy to maintain adequate intravascular volume and visceral perfusion and monitored as normal urine output.
  • Avoidance of vasopressors, which can exacerbate ischemia.
  • Antithrombotic therapy consists of anticoagulation (unfractionated heparin, weight-based protocol) to limit thrombus propagation and help alleviate associated arteriolar vasoconstriction with or without antiplatelet therapy [32].
  • Empiric broad-spectrum antibiotic therapy.
  • Proton pump inhibitors [33].
  • Supplemental oxygen [33].

Approach to treatment — Clinical evaluation and vascular imaging determine whether the patient is a candidate for vascular intervention and whether the occlusion is embolic or thrombotic, which has a bearing on the type of intervention offered. The goal of vascular intervention is to restore intestinal blood flow as rapidly as possible. The specific treatment chosen depends upon the clinical status of the patient and the etiology and location of the occlusion. Optimal treatment may include open, endovascular, or a combined approach. The ability to offer an endovascular approach depends upon local resources and the availability of vascular specialists. A hybrid interventional suite/operating room may be the ideal setting to manage acute mesenteric arterial occlusion, but these are generally available only at large vascular centers.

Some patients (eg, acute-on-chronic occlusion) who are hemodynamically stable and do not have clinical signs of advanced bowel ischemia can be observed while on heparin anticoagulation, if there is evidence of good collateral blood flow on vascular imaging studies. Antiplatelet therapy may be justified in this setting if the risk of progressive ischemia appears to be greater than the risk of bleeding [32,34]. The patient should have serial clinical assessment (laboratory, physical examination) with a low threshold to repeat abdominal imaging studies or, if abdominal symptoms progress, surgical or endovascular intervention.

A palliative approach may be the best option for poor-risk surgical candidates with extensive transmural infarction (eg, small bowel up to the midtransverse colon). Extensive bowel resection would be inappropriate for these patients and may also be inappropriate for a subset of patients who might otherwise be expected to tolerate the procedure but for whom lifelong parenteral nutrition would be unacceptable

Patients who are good-risk surgical candidates with indications for immediate laparotomy such as peritonitis or radiologic features of advanced bowel ischemia (free air, extensive pneumatosis) should be taken directly to the operating room for exploration. Resection of bowel should ideally be delayed until after mesenteric arterial revascularization can be performed to salvage as much bowel as possible; however, in practice, this sequence does not commonly occur. In situations where an individual with appropriate vascular expertise is not immediately available, resection of grossly necrotic or perforated bowel (leaving any questionable bowel) while awaiting intraoperative consultation is appropriate, or, alternatively, following resection, abdominal closure and transfer is also a reasonable option when required.

The traditional treatment for mesenteric embolism is open surgical embolectomy, which, in addition to expeditiously clearing the thrombus, allows direct assessment of bowel viability.

Open surgical treatment of mesenteric artery thrombosis is treated principally with mesenteric bypass. Thrombectomy alone is unlikely to offer a durable solution due to the presence of thrombogenic atherosclerotic plaques. Intraoperative retrograde superior mesenteric artery angioplasty and stenting is another option, particularly in the presence of gross contamination where bypass is more problematic.

Patients who are hemodynamically stable and who do NOT have clinical or radiologic signs of advanced intestinal ischemia may be candidates for a primary endovascular approach.

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24
Q

Aflutter post cardiac surgery. Adenosine is given and they show a strip. What
are pharmacological options to break it? If it persists, what must be done?

A

???

Rate control — Given the transient nature of the arrhythmia (see ‘Incidence and time course’ above), initial control of the ventricular response rate is an effective and relatively safe strategy in many patients who develop postoperative AF [44,128].

Rate control is most commonly achieved with beta blockers. The benefit is partly due to blockade of the augmented postoperative sympathetic state and to prevention of beta blocker withdrawal in patients on beta blockers preoperatively. Intravenous esmolol, a beta blocker with a short half-life, can be given for acute rate control if there is a concern for bradyarrhythmias, hypotension, or bronchospasm. Slowing of the ventricular rate in many AF patients receiving inotropic agents postoperatively can be achieved by lowering the dose or discontinuation of these agents.

Rhythm control — Restoration of sinus rhythm from well-tolerated postoperative AF is usually not necessary but occasionally can be beneficial. (See ‘Incidence and time course’ above.)

Restoration of sinus rhythm is indicated in symptomatic patients or in those when rate control is difficult to achieve. An attempt at the restoration of sinus rhythm can be beneficial in patients with a low ejection fraction. In addition, cardioversion in asymptomatic patients may be reasonable when well-tolerated AF occurs near the time of anticipated hospital discharge or when it does not spontaneously terminate within 24 hours, so that oral anticoagulation can be avoided; this is particularly true in patients at high risk of bleeding.

Our approach to postoperative anticoagulation — Among patients who develop AF following cardiac surgery, we suggest the following approach to anticoagulation:

  • For patients with multiple episodes of AF or one episode that lasts more than 24 to 48 hours, we recommend the initiation of oral anticoagulant therapy, but only if bleeding risks are considered acceptable. As the role of direct thrombin and factor Xa inhibitors has not been established for patients with postoperative AF, we suggest that warfarin be chosen for most patients (International normalized ratio 2.0-3.0).
  • We suggest continuation of anticoagulation for at least four weeks after return to sinus rhythm, particularly if the patient has risk factors for thromboembolism. Longer duration of anticoagulation is recommended by some of our experts in patients with high CHA2DS2-VASc scores (table 3), at low risk for bleeding based on the HAS-BLED score (table 4), or at high risk of AF recurrence.
  • Long-term anticoagulation should be considered for patients who remain in AF or who have paroxysmal AF at four weeks.
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25
Q

Apixiban and ICH, last dose 2h ago.

What 4 things can be done to reverse it?

What are major complications of Apixiban reversal?

A

a)

  • andexanet alpha
  • 4 factor unactivated PCC (i.e. Octaplex if andexanet alpha is not available)
  • antifibrinolytic agent (TXA)
  • oral activated charcoal (Intracranial hemorrhage associated with oral non-vitamin K antagonist anticoagulants (off-label use): Oral, enteral: 50 g within 2 hours of ingestion of an oral direct thrombin inhibitor (dabigatran) or an oral direct factor Xa inhibitor (eg, apixaban, edoxaban, or rivaroxaban).

Direct factor Xa inhibitors cannot be removed by hemodialysis.

b) adverse events: thromboses (arterial and venous) but a significant proportion occured >5d after getting andexanet alpha suggesting it may have been related to pts underlying thrombotic risk

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26
Q

Ruptured appendix in 40M. In ICU 5d, LFTs climbing. List 5 possible reasons.

A
  1. abscess (liver or peritoneal)
  2. drug related (acetaminophen, antibiotics = think amox-clav)
  3. pancreatitis?
  4. acalculous cholecystitis
  5. calculous cholecystitis
  6. hepatosplenic candidiasis
  7. right-sided pyelonephritis
27
Q

50F post-trach (decannulated) with new respiratory distress on floor. PFTs show image. What is Dx?

A

tracheal stenosis

from image:

A - normal

B - variable extrathoracic

C - variable intrathoracic

D - fixed upper airway obstruction (can be intra or extra-thoracic)

E - peripheral (i.e. lower airways) obstruction

28
Q

Post-ICH, has increased ICP episode and is given Mannitol. 2h later, urine
output is high. Na 151, Urine osmoles 358, serum Osmoles 318. What is Dx?

A

Mannitol diuresis

  • Mannitol is freely filtered by the glomerulus and does not undergo tubular reabsorption. Thus, it acts as an osmotic diuretic, increasing urinary losses of both sodium and electrolyte-free water. Lack of replacement of the fluid losses can lead to both volume depletion and hypernatremia that can be severe
  • Concerning findings associated with the use of mannitol include serum sodium >150 mEq, serum osmolality >320 mOsm, or evidence of evolving acute tubular necrosis (ATN). In addition, mannitol can lower systemic blood pressure (BP), necessitating careful use if associated with a fall in cerebral perfusion pressure (CPP). Patients with known renal disease may be poor candidates for osmotic diuresis.
29
Q

5 non-pharmacological things to Mx Variceal bleeding.

A
  • TIPS (or surgical shunting)
  • banding
  • sclerotherapy
  • balloon tamponade
  • esophageal stent
  • +/-BRTO (balloon retrograde total occlusion) for gastric or ectopic varices and also needs presence of a spontaneous shunt

Variceal bleeding

  • pharmacologic therapy (octreotide, pantoprazole)

if bleeding continues…

  • 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

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.

30
Q

Pancreatitis with necrotic capsule drained. 24h later develops frank bleeding
from drain and hypotension. 1 plan for Mx.

A

(IR for embolization)

Pseudoaneurysms are a rare but serious complication of acute pancreatitis that should be suspected when patients with acute pancreatitis have unexplained gastrointestinal bleeding, an unexplained drop in hematocrit, or sudden expansion of a pancreatic fluid collection.

Indications — The indications for embolization include the following [4,9,10]:

  • Massive upper or lower gastrointestinal (GI) bleeding (transfusion requirement of 4 units of blood or more in 24 hours)
  • Hemodynamic instability (hypotension with systolic blood pressure lower than 100 mmHg and heart rate of ≥100 beats per minute)
  • GI bleeding that fails to respond to conservative medical therapy or endoscopic control
  • Active GI bleeding demonstrated by nuclear scintigraphy or computed tomographic angiography examinations
  • Bleeding into pancreatic pseudocysts or from visceral artery aneurysms
  • Hemobilia
31
Q

Ludwig’s Angina: 2 organisms.

What 1 test do you want (it says to “be specific” - most thought CT head/neck/chest to assess for extent of infection into head and chest)

What 2 therapies are possible in addition to antibiotics?

A

Streptococcus anginosus

Peptostreptococcus species

Fusobacterium nucleatum

Actinomyces

Ludwig’s angina is typically a polymicrobial infection involving the flora of the oral cavity. The most common organisms isolated from deep neck space infections are viridans streptococci, reflecting their abundance in the mouth. Streptococcus anginosus (S. milleri) group of oral flora viridans streptococci are particularly virulent. Most abscesses originating from the teeth also harbor oral anaerobes, including Peptostreptococcus species, Fusobacterium nucleatum, pigmented Bacteroides, and Actinomyces spp.

In immunocompromised patients, Gram-negative aerobes may also be present. Furthermore, Staphylococcus aureus, including methicillin-resistant S. aureus, may contribute to deep neck space infections in immunocompromised patients, particularly in children and others with specific risk factors.

b)

Any signs or symptoms suggesting a deep neck space infection should prompt urgent investigation with imaging studies to diagnose a deep neck space infection, identify the precise site of infection, and evaluate for potential spread.

Computed tomography (CT) is generally the imaging modality of choice to diagnose and evaluate the site and extent of deep neck space infections [23]. CT allows the critical evaluation of soft tissues and especially bone from a single exposure (image 1). In addition, the axial imaging format of CT is particularly well suited to the head and neck. Because CT can localize a process and define its extent, particularly extension into the mediastinum or the cranial vault, it is also an invaluable tool for planning and guiding aspiration for culture or open drainage.

Additional imaging to evaluate the vasculature may be warranted in particular cases. As an example, CT angiography may be indicated if other imaging or clinical features suggest involvement of the neurovascular compartment within the carotid sheath.

c)

The treatment of Ludwig’s angina involves timely assessment and management of the airway, and empiric broad-spectrum antibiotics [7,11]. Surgery is not usually necessary since it is uncommon to have a drainable collection in the early stages of infection. Surgical drainage is important once abscesses are identified by CT or MRI.

Abx: immunocompetent pts:

  • ampicillin-sulbactam
  • ceftriaxone plus metronidazole
  • clindamycin plus levofloxacin
  • could use meropenem in penicillin allergic pts

c) after securing the airway

Early surgical decompression is unlikely to locate pus and, at best, may only moderately improve the airway. Abscesses develop relatively late (not usually in the first 24 to 36 hours) and are sometimes difficult to detect clinically.

If the patient is not responding adequately to antibiotics alone after this initial period, or if fluctuance is detectable or a collection is observed on imaging, needle aspiration or a more formal incision and drainage procedure under general anesthesia should be performed. This should be done with a cuffed tracheostomy in place. Additionally, when a tooth is implicated as the source of infection, it should be extracted.

When needle aspiration or incision and drainage is indicated, samples should be obtained for Gram stain and cultured for both aerobic and anaerobic microorganisms.

32
Q

SBT - 4 indications that the patient has passed

A

SBT passing criteria:

  • no change in mental status
  • no arrhythmias (HR<130-140)
  • no new hemodynamic deterioration
  • no worsened hypoxia
  • no respiratory acidosis (RR>8, RR<35)
  • no diaphoresis
  • no respiratory distress/use of accessory muscles/paradoxical breathing
33
Q

IO cannula - 2 absolute contraindications, 2 relative contraindications

A

a)

  • bone fracture
  • An extremity with vascular interruption, either from trauma or cutdown attempt, is not suitable for IO infusion because the fluid or drugs administered into the bone marrow will leak through the open blood vessel.

b)

  • overlying skin infection/burn
  • osteogenesis imperfecta
  • R to L cardiac shunt (eg, tetralogy of Fallot, pulmonary atresia), who may be at greater risk for cerebral fat or bone-marrow emboli
34
Q

List 5 reasons for an over-damped arterial line

A

Overdamping (This is defined when the oscillations following the downstroke are sluggish and can underestimate systolic pressure or overestimate diastolic pressure) Causes include:

  • Loose connections
  • Air bubbles
  • Kinks
  • Blood clots
  • Arterial spasm
  • Narrow tubing

Underdamping (This is defined when the oscillations are too pronounced and can lead to a false high systolic or a false low diastolic pressure):

  • Catheter whip or artefact
  • Stiff non-compliant tubing
  • Hypothermia
  • Tachycardia or dysrhythmia

Square Wave Test

When you squeeze the fast flush valve, you let the transducer taste some of the 300mmHg in the pressurized saline bag. This produces a waveform that rises sharply, plateaus, and drops off sharply when the flush valve is released again.

After the fast flush has ended, the transducer system returns to baseline. It does so as a harmonic oscillator, “bouncing” a couple of times before coming to rest. This “bounce” can be used to determine the resonance characteristics of the system. The accurate, responsive, adequately damped arterial line waveform will have the following features:

The time between oscillations will be short. This is the natural frequency of the system, and it should be less than 20-30 mmHg in order to resolve

There should be at least one “bounce” oscillation. If the system does not oscillate, there is too much damping.

There should be no more than two oscillations; a system which oscillates too much is underdamped.

There should be a distinct dicrotic notch. The dicrotic notch is resolved from high frequency waveforms, whcih are usually of low amplitude and therefore more susceptible to damping. If the arterial line is progressively becoming more and more damped, the dicrotic notch is the first feature to disppear.

The over-damped trace will lose its dicrotic notch, and there wont be more than one oscillation.
This happens when there is clot in the catheter tip, or an air bubble in the tubing. The higher frequency components of the complex wave which forms the pulse are damped to the point where they noi longer contribute to the shape of the pulse waveform.

The under-damped trace will overestimate the systolic, and there will be many post-flush oscillations.

The MAP remains the same in spite of damping.

http://ccn.aacnjournals.org/content/22/2/60.full

35
Q

What are 5 complications of IVIG?

A

aseptic meningitis

fever

Rate related reactions

  • Concurrent infections/phlogistic reactions — Phlogistic reactions are generalized inflammatory symptoms that may accompany the use of IVIG, especially in patients with an acute infection. This may be more likely in patients with an underlying immunodeficiency that puts them at risk of bacterial infections. Often, the reaction occurs in the setting of a chronic sinus or lung infection.
    • Symptoms may resemble those that accompany the onset of infection in individuals with intact immune function. Examples include chills (and even rigors), fever, flushing, flu-like myalgias, arthralgias, malaise, nausea, vomiting, and/or headache. Symptoms may be especially pronounced if the infection has not been treated with antibiotics and the patient is receiving IVIG for the first time.
  • Reactions resembling anaphylaxis — Reactions resembling anaphylaxis are usually rate-related and often occur midway through an IVIG infusion. Patients may develop urticaria, flushing; tachycardia; chest tightness, wheezing, or dyspnea; pain in the chest or lower back; nausea and/or vomiting; and/or a sense of impending doom or sudden anxiety.

Other transfusion reactions

  • TRALI
  • TACO

Anaphylaxis in IgA-deficient patients — Anaphylaxis during IVIG administration is extremely rare, but it may be life-threatening. Anaphylaxis with hypotension and/or respiratory compromise is a medical emergency and should be rapidly treated with epinephrine and other therapies. In the rare cases when anaphylaxis is seen, it generally occurs in patients with IgA deficiency, due to patient antibodies to IgA (ie, anti-IgA) that react with the IgA present in IVIG products

Delayed Reactions

  • Thromboembolic events
  • CNS effects - headache, aseptic meningitis
  • Renal complications - Boxed Warning about the risks of acute renal failure, osmotic nephrosis, and death from renal dysfunction. Additional complications such as hyponatremia can also occur.
  • Hematologic complications - hemolysis, neutropenia; usually transient

Late Reactions

  • dermatologic reactions - eczematous dermatitis
  • can impair response to live virus vaccines
  • theoretical risk of infections - ?prions, ?viruses
36
Q

Endocarditis. Given course of Vanco/Gent/(something else) then stepped down to Ceftriaxone when bug identified. New AKI without any casts seen on micro. What are 4 possible reasons for AKI?

A
  • endocarditis - Urinalysis may demonstrate microscopic hematuria, proteinuria, and/or pyuria. The presence of red blood cell casts on urinalysis is generally indicative of glomerulonephritis, which is a minor diagnostic criterion for IE.
  • Gentamycin
  • Vanco
  • septic emboli

ampicillin can cause acute interstitial nephritis (rarely)

37
Q

What is the formula for respiratory compliance?

How do you measure this on the ventilator (what manouver)?

List the causes (5?) of high plateau pressure.

A

a) compliance = tidal volume/ driving pressure = tidal volume / (plateau pressure - PEEP)
b) use end-inspiratory hold to determine plateau pressure

c)

  • pulmonary
    • low lung parenchymal compliance (ARDS, pulm edema, fibrosis)
    • overdistension (high tidal volume, autoPEEP)
  • extrapulmonary
    • chest - burn injury, chest wall deformity
    • pleural - pleural effusions
    • abdominal - abdo compartment syndrome/intra-abdominal hypertension
38
Q

CT head with acute stroke. What is shown on CT?

What 2 therapies are available?

What one test must you do before giving tPA?

A

tPA, endovascular clot retrieval

  • Mechanical thrombectomy is indicated for patients with acute ischemic stroke due to a large artery occlusion in the anterior circulation who can be treated within 24 hours of symptom onset or the time last known to be well at stroke centers with appropriate expertise, regardless of whether they receive intravenous alteplase for the same ischemic stroke event.

test glucose

  • The history, physical examination, serum glucose, oxygen saturation, and a noncontrast CT scan are sufficient in most cases to guide acute therapy (see ‘Immediate laboratory studies’ below). Other tests are considered based upon individual patient characteristics, but the absence or unavailability of any additional tests need not be a reason to delay therapy if otherwise indicated.
39
Q

COPD exacerbation with image showing of pseudocolitis and septic shock, also has renal failure. CT scan shows pancolitis. What 1 management option should you proceed with?

A

surgical consultation

Early surgical consultation is warranted for patients with CDI who meet one or more of the following clinical indicators that have been associated with poor prognosis (table 3) [98-102]:

  • Hypotension
  • Fever ≥38.5°C
  • Ileus or significant abdominal distention
  • Peritonitis or significant abdominal tenderness
  • Altered mental status
  • White blood cell count ≥20,000 cells/mL
  • Serum lactate levels >2.2 mmol/L
  • Admission to intensive care unit
  • End organ failure (eg, requiring mechanical ventilation, renal failure)
  • Failure to improve after three to five days of maximal medical therapy

Antibiotics for the treatment of severe CDI include oral vancomycin or oral fidaxomicin (see image).

Antibiotics for the treatment of fulminant CDI include the combination of enteral vancomycin plus parenteral metronidazole

40
Q

Inhalational injury in 20M, now has ST changes in lateral leads. What is most likely cause?

A

carbon monoxide poisoning - Acute myocardial injury is common among CO-poisoned patients and is associated with increased long-term mortality. A retrospective study of 230 patients with moderate or severe CO poisoning referred to a specialized center found evidence of myocardial ischemia (characteristic electrocardiographic changes or elevated serum cardiac biomarkers) in one-third of all cases.

I also looked up cyanide poisoning but couldn’t fit anything specific to ST changes, just listed bradycardia/arrhythmias.

41
Q

CT head with three arrows - name structures

A

internal capsule - The internal capsule is a white matter structure situated in the inferomedial part of each cerebral hemisphere of the brain. It carries information past the basal ganglia, separating the caudate nucleusand the thalamus from the putamen and the globus pallidus. The internal capsule contains both ascending and descending axons, going to and coming from the cerebral cortex. It also separates the caudate nucleus and the putamen in the dorsal striatum, a brain region involved in motor and reward pathways.

3rd ventricle

lateral ventricle

external capsule - The external capsule is a series of white matterfiber tracts in the brain. These fibers run between the most lateral (toward the side of the head) segment of the lentiform nucleus (more specifically the putamen) and the claustrum.

The white matter of the external capsule contains fibers known as corticocortical association fibers. These fibers are responsible for connecting the cerebral cortex to another cortical area.

42
Q

what are the 5 elements of choosing wisely in ICU?

A

dont start/continue life support unless in line w pt wishes

regular SAT

regular SBT

don’t daily CXR unless specific q

don’t routinely give blood for Hgb >70 (80 could be considerd for some)

  1. Don’t start or continue life supporting interventions unless they are consistent with the patient’s values and realistic goals of care.
  2. Don’t prolong mechanical ventilation by over-use of sedatives and bed rest.
  3. Don’t continue mechanical ventilation without a daily assessment for the patient’s ability to breathe spontaneously.
  4. Don’t order routine chest radiographs for critically ill patients, except to answer a specific clinical question.
  5. Don’t routinely transfuse red blood cells in hemodynamically stable ICU patients with a hemoglobin concentration greater than 70 g/l (a threshold of 80 g/L may be considered for patients undergoing cardiac or orthopedic surgery and those with active cardiovascular disease).
43
Q

List 5 scoring systems for severity of pancreatitis?

A
  1. Ranson’s criteria
  2. APACHE II score
  3. SIRS
  4. BISAP (bedside index of severity in acute pancreatitis)
  5. harmless acute pancreatitis score
  6. other organ failure-based scores (not specific to pancreatitis): SOFA, Marshall (or multiple) organ dysfunction score (MODS)
  7. CT severity index (aka Balthazar score) based on degree of necrosis, inflammation, and presence of fluid collections
44
Q

bronchoscopy images (3) - identify the location

A

test yourself

PIE website

ATS video

image in question is LUL (with lingular segments visible in middle)

image in answer is RUL bronchus

45
Q

Central line infection - what are 4 absolute indications for removal? what are appropriate antibiotics?

A
  • sepsis/hemodynamic instability
  • presence of endocarditis/evidence of metastatic infection
  • presence of suppurative thrombophlebitis
  • presence of bacteremia after 72hrs of appropriate antimicrobial therapy
  • subcutaneously tunnelled CVC tunnel tract infection or subcutaneous post resevoir infection\
  • candida
  • staph aureus

Catheter removal (in addition to administration of systemic antimicrobial therapy) is warranted in the following circumstances, given high likelihood of severe and/or progressive infection with antibiotic therapy alone:

  • Sepsis
  • Hemodynamic instability
  • Presence of concomitant endocarditis or evidence of metastatic infection
  • Presence of suppurative thrombophlebitis
  • Presence of a propagating clot
  • Persistent bacteremia after 72 hours of appropriate antimicrobial therapy
  • Subcutaneously tunneled central venous catheter tunnel tract infection or subcutaneous port reservoir infection

In addition, catheter removal is warranted in the setting of infection with the following pathogens, given relatively high virulence and relatively low likelihood of treatment response with antibiotic therapy alone:

  • S. aureus
  • P. aeruginosa
  • Drug-resistant gram-negative bacilli
  • Candida spp
46
Q

Venous Air embolism - 3 management strategies

A
  • trendelenburg positioning, left lateral
  • FiO2 1.0
  • aspirate through R IJ CVC
  • hyperbaric oxygen (if hemodynamic unstable and with evidence of cardiopulmonary compromise and/or end-organ damage due to air embolism)
  • life support care: mechanical ventilation, vasopressors etc
  • closed cardiac massage (i.e. compressions) can be a last resort therapy

positioning explanation:

A patient with venous air embolization should be immediately placed into the left lateral decubitus position (Durant’s maneuver), Trendelenburg position, or left lateral decubitus head down position [71]. These positions place the right ventricular outflow tract inferior to the right ventricular cavity, causing the air to migrate superiorly into a position within the right ventricle from which air is less likely to embolize [1,2,6,41]. The potential benefit of appropriate positioning was suggested by an animal experiment in which 40 percent of animals in the left lateral decubitus position survived the venous injection of a lethal amount of air (the experiment did not assess the left lateral decubitus head down or Trendelenburg position) [97].

In contrast, a patient with arterial air embolism should be placed in the supine position [71]. The reason that the optimal position differs for arterial and venous air embolism is that arterial blood flow is more forceful than venous blood flow and air bubbles are propelled forward by the arterial blood flow even if the patient is in a head down position. Since the head down positions have the potential to exacerbate the cerebral edema that is typically induced by cerebral air embolism, a flat supine position is also favored for this reason.

47
Q

Liver laceration with temporary closure of abdominal wall. What are 2 (maybe 4?) reasons to return to the OR immediately?

A

?evisceration

?massive bleeding from VAC

?enteric contents (feeds) coming out of VAC

abdominal compartment syndrome (I read up, and this can actually still happen)

48
Q

Define chronic critical illness. List 5 patient oriented strategies to manage chronic critical illness.

A

various definitions exist from LITFL:

  • a syndrome of ongoing “ventilator dependence, brain dysfunction, neuromuscular weakness, endocrinopathy, malnutrition, anasarca, skin breakdown and symptom distress” that occurs when patients with limited physiological reserve (due, often, to older age and chronic comorbidities)
  1. protocol implemented by RTs for ventilator weaning
  2. appropriate nutritional support to promote anabolism and avoid/minimize further losses in lean body mass, or adverse consequences of overfeeding
  3. integration of PT in a comprehensive rehabilitation model (optimize function and cognition)
  4. preventing complications: triple threat of infection, barrier breaches, and “immune exhaustion”
  5. integrate palliative care with restorative treatment
49
Q

Why is interprofesional care good? List 4 reasons.

A
  1. decreased LoS has been shown when a multidisciplinary approach is used for rounding
  2. Increased communication between providers and the inclusion of safety conversations in rounds leads to a reduction in adverse events and delays in initiation of appropriate therapy which translates into improved mortality rates
  3. Other markers for morbidity including weaning days, total days of mechanical ventilation, and prevention of complications such as stress ulcers, deep vein thrombosis, falls, skin breakdown, infection, and readmissions also show significant improvement with the multidisciplinary approach
  4. Staff satisfaction is also significantly improved with multidisciplinary rounds.

from https://www.ncbi.nlm.nih.gov/books/NBK507776/

50
Q

List 4 criteria for delirium

A

acute change or fluctuating course of mental status

AND

inattention (SAVEAHAART)

PLUS one of:

altered level of consciousness (RASS)

OR

disorganized thinking (stone float on water?)

51
Q

What is pulsus paradoxus?

what are 2 physiological reasons for it?

what are 3 causes besides tamponade?

what are three causes of tamponade that could cause pulsus? (might have asked for causes of tamponade that WOULDNT cause pulsus)

A

a) difference in systolic blood pressure >12mm Hg between inspiration and expiration

b)

  • change in intrathoracic pressure affects venous return to heart, less venous return means less cardiac output
  • increased pericardial pressure reduces RV compliance and thus with increased filling which happens during inspiration the RV pressure exceeds LV pressure causing bowing of the interventricular septum towards the LV and thus decreased LV filling and thus decreased LV stroke volume/cardiac output

c)

  • obstructive lung disease (COPD or asthma)
  • excessive respiratory efforts causing large changes in intra-thoracic pressure
  • constrictive pericarditis
  • RV infarct
  • restrictive cardiomyopathy
  • OSA
  • PE
  • tension pneumothorax
  • bilateral pleural effusions
  • marked obesity
  • hypovolemic shock
  • pectus excavatum

d) these answers are things that wouldn’t cause pulsus necessarily

  • positive pressure ventilation (although not listed on uptodate)
  • co-existing disease that elevates LV diastolic pressure (systemic HTN, AS) or RV diastolic pressure (pulm HTN with cor pulmonale)
  • intracardiac shunt with significant valvular regurgitation (AR)
  • ???aortic dissection with resulting periardial effusion and cardiac tamponade
  • ???”low pressure tamponade” as in the presence of dehydration and hypovolemia where a pericardial effusion would otherwise cause cardiac compression can affect cardiac function
52
Q

Heart Tx patient, 2h later in persistent shock. what 2 things must be
R/Oimmediately?

A

(tamponade, bleeding)

53
Q

Transplant medication question. How does Tac work?

What complications can be caused by calcineurin inhibitors?

A

a macrolide antibiotic that binds to FK binding proteins in the cytoplasms of most cells. The drug-receptor complex specifically and competitively binds to and inhibits calcineurin, a calcium- and calmodulin-dependent phosphatase [1-4]. This process inhibits the translocation of a family of transcription factors (NF-AT), leading to reduced transcriptional activation of cytokine genes for interleukin (IL)-2, tumor necrosis factor (TNF)-alpha, IL-3, IL-4, CD40L, granulocyte-macrophage colony-stimulating factor, and interferon-gamma.

similar side effects between cyclosporine and tacrolimus (both calcineurin inhibitors)

  • nephrotoxicity
  • HTN
  • neurotoxicity (tremor, headache, seizures, posterior leukoencephalopathy)
  • metabolic abnorm (glucose intolerance/diabetes, hyperlipidemia)
  • infections
  • malignancy (squamous cell and benign/malignant lymphoproliferative disorders)
  • GI (anorexia, n/v/d)
54
Q

Bad SAH - what 2 drugs can be used to prevent vasospasm?

what are 4 nonvasospasm complications of SAH?

A

nimodipine

statins

  1. rebleeding
  2. elevated ICP
  3. hydrocephalus
  4. hyponatremia
  5. seizures
  6. anemia
  7. pulmonary edema, cardiac arrhythmias
  8. decreased LV dysfunction, Takatsubo cardiomyopathy
  9. fever
  10. hypothalamic-pituitary dysfunction
55
Q

CCRT question - how does citrate work? how is citrate removed in dialysis?

what 2 tests do you need to monitor when using citrate?

What 2 other things would you do in a patient on CRRT with citrate if they arrest? (in addition to usual ACLS stuff)

A

The anticoagulant effect of sodium citrate relies on forming a complex with ionized calcium, thus removing an essential component of the coagulation cascade. Part of the citrate is removed in the extracorporeal circuit. Citrate reaching the systemic circulation is rapidly metabolized in the liver, muscle, and kidney, liberating the calcium and producing bicarbonate. The buffering effect of sodium citrate is proportional to the sodium ions it contains: a mole of trisodium citrate produces the same buffering effect as 3 moles of sodium bicarbonate; whereas preparations of citrate, including hydrogen citrate, have proportionally less buffering effect. Extracorporeal losses of calcium have to be compensated by an exogenous infusion.

During RCA, sodium citrate is infused into the inflow (“arterial”) limb of the extracorporeal circuit, chelating calcium and inhibiting clotting. The majority of the calcium citrate complex is removed across the hemofilter. Any calcium citrate complex that remains postfilter is returned to the patient and metabolized to bicarbonate by the liver, kidney, and skeletal muscle. Regional anticoagulation is reversed by dilution of citrate in the extracellular compartment and by its rapid metabolic clearance.

A systemic calcium infusion is required to replace the calcium that is lost in the effluent in order to maintain a normal ionized serum calcium concentration.

The use of RCA may require modification of the composition of dialysate or replacement fluid. The concentration of buffers (eg, bicarbonate, lactate) is usually reduced to prevent alkalosis since citrate provides alkali.

Ideally, the dialysate and replacement fluids should also be calcium free to prevent reversal of the citrate effect in the extracorporeal circuit, although this is not absolutely necessary. If calcium-containing replacement fluid is used, more citrate is required to chelate calcium in both the blood and replacement fluid. Calcium chloride or calcium gluconate is infused into the venous return line at an initial rate of 2 to 3 mmol/hour to replace calcium lost in the effluent when using calcium-free dialysate and replacement fluids. The rate is adjusted according to measurements of plasma calcium concentration to prevent hypocalcemia or hypercalcemia.

citrate accumulation is suggested by:

  • worsening metabolic acidosis with increasing anion gap
  • decreasing ionized calcium requiring escalating calcium infusion rates
  • increasing total calcium
  • ratio of total calcium to ionized calcium >2.5

b) two lab tests

  • total calcium
  • ionized calcium
  • (also could consider sodium to watch for hypernatremia and pH to watch for met acidosis)

c) cardiac arrest: idea from this article: https://academic.oup.com/ckj/article/2/6/439/346961

Calcium and Magnesium

Citrate anticoagulation is based on calcium chelation, and as calcium citrate is lost during passage through the dialyser/haemofilter, patients become hypocalcaemic. If this is not appropriately corrected, then arrhythmias and cardiac arrest may ensue [35]. Calcium is therefore infused either systemically or into the venous return of the extracorporeal circuit to maintain normal systemic ionized calcium of 0.95–1.2 mmol/l. Since many acutely ill patients are hypoalbuminaemic and acidotic, an infusion of acidic TCA increases the relative proportion of ionized-to-bound calcium and leads to increased dialysate/filtrate calcium–citrate losses [36]. Thus, many patients treated by CRRT using citrate-based anticoagulation develop a negative calcium balance, especially when compared to standard CRRT anticoagulated with heparin, as most commercially available dialysates/replacement solutions contain high concentrations of calcium [37].

Magnesium will be similarly lost due to binding to citrate and removal of the complex during passage through the dialyser/haemofilter, and also to the effect of predilution [24]. However, unlike calcium, magnesium is added to replacement solutions and dialysates. Depending upon the volumes exchanged, higher magnesium concentrations may be required to compensate for the losses.

56
Q

GSW in leg - what 5 things can be done while awaiting OR?

A
  1. local pressure
  2. tourniquet
  3. REBOA (resuscitative endovascular balloon occlusion of the aorta) (?no data according to EAST guidelines)
  4. traction on leg (?only if fractured?)
  5. blood transfusion
  6. TXA
  7. coagulopathy management (temperature, pH)
  8. factor VII (?rescue?)

EAST guidelines: https://www.east.org/education/practice-management-guidelines/penetrating-lower-extremity-arterial-trauma%2c-evaluation-and-management-of#h3

57
Q

RCT question - what test is appropriate with data given?

Why was trial negative?

Theoretical problems with meta analyses?

A

(t-test)

?

c)

  • identification and selection of studies (restricted to RCTs, or English language etc)
  • quality of included studies (affect internal and external validity)
  • publication bias (increases Type I error - false positive)
  • degree of heterogeneity
58
Q

What scoring systems can be used for nursing workload?

What populations are not included in APACHE score? SOFA score? MODS score?

A

Nursing Activities Score (NAS)

Therapeutic Intervention Scoring System (TISS-28)

Exclusions

APACHE II - peds, CABG, pt transferred from another hospital

SOFA - peds (<13yrs), pt admitted <48h after uncomplicated surgery, pt transferred from other units

MODS - pt admitted <24h, non-surgical pts

SAPS II - peds, CABG, burn

MODS

We studied a group of patients admitted for more than 24 hrs to the surgical ICU of a tertiary-level teaching hospital, the Victoria General Hospital, Halifax, NS, Canada, from May 1988 through February 1990. Clinical, laboratory, and radiographic data were collected daily throughout the entire ICU stay. Both ICU and hospital survival rates were documented. Glasgow Coma Scores were determined by the research nurse. To obviate the confounding effects of sedation or anesthesia, we recorded the best estimate of the Glasgow Coma Score in the absence of sedation. Thus, unless there were compelling reasons to assume a neurologic deficit, sedated patients were assigned a Glasgow Coma Score of 15. Acute Physiology and Chronic Health Evaluation II (APACHE II) scores were calculated over the first 24 hrs for all patients [23]. The recorded data were representive of the previous 24 hrs, and usually consisted of values obtained at the time of morning blood work. All recorded data were obtained during active ICU therapy; agonal values or those values reflecting further deterioration after a decision to discontinue active care were excluded. Obvious laboratory errors, or spuriously abnormal results associated with clinical interventions such as tracheal suctioning or sedation were omitted. Missing data were imputed as normal.

59
Q

5 vascular changes in sepsis (repeat)

A
  • microthrombin formation
  • increased microvascular permeability
  • production of vasoactive products (bradykinin)
  • decrease in number of functional capillaries, which causes an inability to extract oxygen maximally (Compared to normal controls or critically ill patients without sepsis, patients with severe sepsis have decreased capillary density [64]. This may be due to extrinsic compression of the capillaries by tissue edema, endothelial swelling, and/or plugging of the capillary lumen by leukocytes or red blood cells (which lose their normal deformability properties in sepsis).)
  • vascular hyporesponsiveness leads to an inability to appropriately distribute systemic blood flow among organ systems (therefore can’t redistribute blood from splanchnic circulation to heart/brain)
  • At the level of the endothelium, sepsis induces phenotypic changes to endothelial cells. This occurs through direct and indirect interactions between the endothelial cells and components of the bacterial wall. These phenotypic changes may cause endothelial dysfunction, which is associated with coagulation abnormalities, reduced leukocytes, decreased red blood cell deformability, upregulation of adhesion molecules, adherence of platelets and leukocytes, and degradation of the glycocalyx structure [65]. Diffuse endothelial activation leads to widespread tissue edema, which is rich in protein.

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.

60
Q

Dapsone - what is possible complication?

List 2 treatment options

A

a) methemoglobinemia
b) discontinue dapsone

methylene blue (or ascorbic acid if methylyne blue not available)

blood transfusion

supportive care (mechanical ventilation, vasopressors, etc)

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 [1]. As a result, the oxygen dissociation curve is “left-shifted”. See image.

General considerations — Offending agents in acquired methemoglobinemia should be discontinued (table 1).

  • 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 [66,67].
  • 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

Treatment

If the patient is symptomatic or if the methemoglobin level is >20 percent, which is often the case in deliberate or accidental overdoses or toxin ingestion, specific therapy is urgently indicated. The two treatments most often employed are methylene blue (MB) and ascorbic acid (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.

  • * While methylene blue is a recognized treatment for methemoglobinemia, it also has oxidant potential and may worsen the clinical status of individuals with G6PD deficiency because it induces acute hemolysis that can further decrease oxygen delivery to the tissues. In high doses, methylene blue can paradoxically increase methemoglobinemia.

Cimetidine, used as a selective inhibitor of N-hydroxylation, may be effective in increasing patient tolerance to dapsone, chronically lowering the methemoglobin level by more than 25 percent [82,83]. Since it works slowly, cimetidine is not helpful for the management of acute symptomatic methemoglobinemia arising from the use of dapsone.

61
Q

Pregnant with increased LFTs and anemia.

a) List 3 DDx.
b) List 2 important tests (lab, imaging) to do in this patient.

A

(liver U/S, Fetal assessment)

a)

  • thrombotic thrombocypenic purpura (TTP)
  • severe pre-eclampsia
  • pregnancy related hemolytic uremic syndrome
  • HELLP (hemolysis, elevated liver enzymes, low platelets)
  • acute fatty liver of pregnancy (although doens’t seem to cause anemia)

b)

blood smear

?liver ultrasound???

fetal assessment???

All women with acute fatty liver of pregnancy (AFLP) have elevations in aminotransferases (aspartate aminotransferase or alanine aminotransferase), usually ranging from 5 to 10 times the upper limit of normal, but not exceeding 500 int. unit/L (table 1) [22]. Other laboratory findings that may be present include:

  • Elevated serum bilirubin levels
  • Low serum glucose
  • Elevated serum creatinine
  • Elevated white blood cell count
  • Elevated ammonia level
  • Elevated uric acid level
  • Prolonged prothrombin time, international normalized ratio, activated partial thromboplastin time
  • Increased thrombin time
  • Reduced levels of coagulation inhibitors (eg, antithrombin)
  • Low platelet count
  • Low fibrinogen
  • Fragmented red blood cells and burr cells
  • Proteinuria
62
Q

Donor management

a) what are indications for hormone replacement (list 2 indications)?
b) 3 things that can/should be given.

A

a)

  • EF =40%
  • any hemodynamic instability
  • consideration for hormonal management should be done for all NDD patients

uptodate: There is a lack of consensus about when hormonal therapies should be initiated. Some experts recommend using them only in hemodynamically compromised donors, while others recommend broad use in most donors [20]. If hormonal therapy has been started by an organ procurement organization (OPO) in the intensive care unit (ICU), it should be continued through the procurement.

CMAJ article 2006:

Recommendation 5.1: Thyroid hormone, vasopressin and methylprednisolone

Combined hormonal therapy is defined as administration of

  • Thyroid hormone (tetraiodothyronine or T4), 20 μg IV bolus followed by 10 μg/h IV infusion
  • Vasopressin, 1 U IV bolus followed by 2.4 U/h IV infusion
  • Methylprednisolone, 15 mg/kg IV every 24 h.

We recommend that combined hormonal therapy be used in donors with an ejection fraction = 40%, based on 2-dimensional echocardiographic assessment, or hemodynamic instability. Consideration should be given to its use in all donors.

b) methylprednisolone

vasopressin

thyroxine

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.

63
Q

C-spine injury - 3 reasons to suspect vertebral injury or dissection of vertebral artery.

1 best investigation.

A

a)

any pt with neurologic abnormality that is unexplained by diagnosed injury

blunt injury pts with epistaxis thought to be from arterial source

consider screening in pts with risk factors:

GCS = 8

petrous bone #

DAI

cervical # esp C1-C3

cervical spine # esp with subluxation or rotational component

Lefort II or III #s

b)

diagnostic four vessel cerebral angiography is GOLD standard (CTA neither sensitive nor specific enough but for Level III evidence historical studies suggest it has similar diagnostic rate compared to four vessel cerebral angiography)

https://www.east.org/education/practice-management-guidelines/blunt-cerebrovascular-injury#h3

EAST guidelines for blunt cerebrovascular injury:

What patients are of high enough risk, so that diagnostic evaluation should be pursued for the screening and diagnosis of BCVI?

Level I: No level I recommendations can be made.

Level II:

  1. Patients presenting with any neurologic abnormality that is unexplained by a diagnosed injury should be evaluated for BCVI.
  2. Blunt trauma patients presenting with epistaxis from a suspected arterial source after trauma should be evaluated for BCVI.

Level III:

  1. Asymptomatic patients with significant blunt head trauma as defined below are at significantly increased risk for BCVI and screening should be considered. Risk factors are as follows:

* Glasgow Coma Scale score ≤8;

* Petrous bone fracture;

* Diffuse axonal injury;

* Cervical spine fracture particularly those with (i) fracture of C1 to C3 and (ii) fracture through the foramen transversarium;

* Cervical spine fracture with subluxation or rotational component; and

* Lefort II or III facial fractures

  1. Pediatric trauma patients should be evaluated using the same criteria as the adult population.

What is the appropriate modality for the screening and diagnosis of BCVI?

Level I: No level I recommendations can be made.

Level II:

  1. Diagnostic four-vessel cerebral angiography (FVCA) remains the gold standard for the diagnosis of BCVI.
  2. Duplex ultrasound is not adequate for screening for BCVI.
  3. Computed tomographic angiography (CTA) with a four (or less)-slice multidetector array is neither sensitive nor specific enough for screening for BCVI.

Level III:

  1. Multislice (eight or greater) multidetector CTA has a similar rate of detection for BCVI when compared with historic control rates of diagnosis with FVCA and may be considered as a screening modality in place of FVCA. Conflicting studies have been published however (see the Scientific Rationale section).

How should BCVI be treated? This refers a grading scheme proposed by Biffl et al.[6] Grading scale:

* Grade I—intimal irregularity with <25% narrowing;

* Grade II—dissection or intramural hematoma with >25% narrowing;

* Grade III—pseudoaneurysm;

* Grade IV—occlusion; and

* Grade V—transection with extravasation.

Level I: No level I recommendations can be made.

Level II:

  1. Barring contraindications, grades I and II injuries should be treated with antithrombotic agents such as aspirin or heparin.

Level III:

  1. Either heparin or antiplatelet therapy can be used with seemingly equivalent results.
  2. If heparin is selected for treatment, the infusion should be started without a bolus, a guideline for activated partial thromboplastin time goal cannot be determined.
  3. In patients in whom anticoagulant therapy is chosen conversion to warfarin titrated to a prothrombin time-international normalized ratio of 2 to 3 for 3 months to 6 months is recommended.
  4. Grade III injuries (pseudoaneurysm) rarely resolve with observation or heparinization, and invasive therapy (surgery or angiointerventional) should be considered. N.B. carotid stents placed without subsequent antiplatelet therapy have been noted to have a high rate of thrombosis in this population.[7]
  5. In patients with an early neurologic deficit and an accessible carotid lesion operative or interventional repair should be considered to restore flow.
  6. In children who have suffered an ischemic neurologic event (INE), aggressive management of resulting intracranial hypertension up to and including resection of ischemic brain tissue has improved outcome as compared with adults and should be considered for supportive management.

For how long should antithrombotic therapy be administered?

No recommendations can be made.

How should one monitor the response to therapy?

Level I: No level I recommendation can be made.

Level II:

  1. Follow-up angiography is recommended in grades I to III injuries. To reduce the incidence of angiography-related complications, this should be performed 7 days postinjury.

Level III: There are no level III guidelines for this question.

64
Q
A