2017 Flashcards
According to Sepsis 3:
a. How do they define organ dysfunction (1)
b. What is needed to define septic shock (2)
c. What are the qSOFA criteria (3)
a) life-threatening organ dysfunction caused by a dysregulated host response to infection
* organ dysfunction defined as increase in SOFA score of 2 or more points. Importantly, the SOFA score is an organ dysfunction score. It is not diagnostic of sepsis nor does it identify those whose organ dysfunction is truly due to infection but rather helps identify patients who potentially have a high risk of dying from infection.
b) patients who fulfill the criteria for sepsis (see above) who, despite adequate fluid resuscitation, require vasopressors to maintain a mean arterial pressure (MAP) ≥65 mmHg AND have a lactate >2 mmol/L
c)
- hypotension (SBP
- altered mental status (GCS <15)
- tachypnea (RR>/= 22)
On balance, qSOFA may not be as robust as originally thought and clinicians need to keep in mind that it was originally designed not as a diagnostic tool but rather as a predictive tool that calculates the risk of death from sepsis.
Patient with severe aortic stenosis goes to operating room for AVR. Has her valve done and post-pump TEE shows normal LV function with some LV hypertrophy. Valve gradients are normal and the valve is functioning well. She is bradycardic and requires pacing. In the ICU she becomes hypotensive and after 1L fluid has not recovered. You suspect she has dynamic LVOT obstruction. They give you a table of values that basically show her HR was paced at 90, and is still paced at 90. Cardiac index went from 3 ~1.6. PAWP went from 10-15, and BP was 120/80 now it is 80/60. They then ask:
a. What are 4 physiologic reasons why her LVOT obstruction is getting worse
b. What are 4 interventions you can perform to improve her hemodynamics
a)
- hypovolemia decreasing preload and therefore LVESV
- maybe decreased LVESV from arrhythmia, ie. that it’s paced and therefore doesn’t have atrial kick*** Mo agreed and said things that specific to operation
- low SVR from pump
- narrow LVOT diameter from hypertrophic LV septum
- abnormal length or position of mitral valve anterior leaflet
- hyperdynamic state which increases flow through LVOT thereby worsening Bernoulli effect on septum and mitral valve anterior leaflet
- post-bypass pump vasoplegia
- relative tachycardia shortening diastolic filling time
- ?mismatch between valve
b)
- decrease HR of pacemaker (this is a guess: try A-V synchronized pacing??? would need to program to VAO)
- increase preload with fluid bolus
- increase afterload without inotropy (i.e. phenylephrine or vasopressin)
- ???early beta blockers
Patient with diarrhea sees her GP and is found to have thrombocytopenia. He diagnoses ITP. She then gets worse and goes to the ED where they diagnose DIC. She seizes in the ED, CT head is normal. She is hemodynamically stable.
a. List 4 ways to differentiate DIC from ITP
b. What other diagnosis needs to be ruled out in this case?
a)
DIC
- INR prolonged
- PTT prolonged
- pt typically looks sick and there should be a precipitant (infection, cancer, trauma, obstetrical issue, etc)
- fibrinogen is low
- D-dimer is high
- blood smear may show schistocytes but this should prompt further investigation for TTP
ITP
- INR and PTT normal
- fibrinogen is normal
- D-dimer is normal
- red cells look normal on smear
b) TTP
- pts look sick
- schistocytes on smear
- normal INR and PTT (or slight increase)
- normal fibrinogen
- normal D-dimer (or slight increase)
What are the four criteria for major burns?
not sure which list they are asking for…
from uptodate a severe burn is one that is:
- complicated by major trauma
- inhalational injury
- chemical burn
- high voltage electrical burn
- any burn encompassing >20% of TBSA excluding superficial burns
Burn center referral criteria
- Partial-thickness burns greater than 10% of TBSA
- Burns that involve the face, hands, feet, genitalia, perineum, or major joints
- Third-degree burns in any age group
- Electrical burns, including lightning injury
- Chemical burns
- Inhalation injury
- Burn injury in patients with preexisting medical disorders that could complicate management, prolong recovery, or affect mortality
- Any patient with burns and concomitant trauma (such as fractures) in which the burn injury poses the greatest risk for morbidity or mortality. In such cases, if the trauma poses the greater immediate risk, the patient may be stabilized initially in a trauma center before being transferred to a burn unit. Physician judgment will be necessary in such situations and should be in concert with the regional medical control plan and triage protocols.
- Burned children in hospitals without qualified personnel or equipment for the care of children
- Burn injury in patients who will require special social, emotional, or rehabilitative intervention
Obese man with BMI >45, has known ACA aneurysm that is due to be coiled soon (but hasn’t been done yet), has limited mouth opening. What three factors will affect your airway management plan (worded slightly differently).
difficulty with BVM
- obese
difficulty with laryngoscopy
- limited mouth opening
hemodynamic control
- avoid excessive hypertension/cough due to unprotected aneurysm
List the formulas for the following:
a. O2 delivery equation
b. Oxygen extraction ratio
c. Shunt
d. Oxygenation index
a) oxygen delivery equation
DO2 = cardiac output X arterial O2 content
= HR X SV X [(1.34 X Hgb concentration X SaO2) + (0.0031 X PaO2)]
b) oxygen extraction ratio
O2 extraction ratio =
(arterial O2 content - venous O2 content) / arterial O2 content
* use arterial O2 content from above but use the following for venous O2 content
venous O2 content = (1.34 X Hgb concentration X SvO2) + (0.0031 X PvO2)
c) shunt
Q shunt / Q total cardiac output
= (pulmonary end-capillary O2 content - arterial O2 content) /
(pulmorary end-capillary O2 content - venous O2 content)
- pulmorary end-capillary O2 content is estimated from the PAO2
- arterial O2 content and venous O2 content are calculated from the arterial and mixed venous gas measurements
d) oxygenation index
OI = [mean airway pressure X FiO2 / PaO2] X 100
- a high OI (eg, ≥25) indicates severe hypoxemic respiratory failure
- OI is most commonly used in neonates with persistent pulmonary hypertension of the newborn to determine the severity of hypoxemia and to guide the timing of interventions
Liver transplant patient post-op day 1. Hemodynamically stable but INR and AST/ALT are increasing:
a. What are 4 reasons why the LFT’s are increasing?
b. What one test will you order?
a)
- hepatic artery thrombosis
- primary graft nonfunction—preservation injury
- biliary complication
- sepsis/septicemia
- too early for cyclosporine (or other drug) toxicity
b) liver ultrasound with doppler do this first…. (vs ?liver biopsy)
The differential diagnosis of liver transplantation dysfunction depends in part upon the time at which it occurs. Within the first few days after transplantation, abnormal liver tests may reflect technical or functional problems, such as hepatic artery thrombosis, preservation injury, biliary anastomosis leakage or stenosis, primary graft nonfunction, or even consequences of shock and septicemia. Although many of these problems may be evident clinically or on imaging such as Doppler ultrasonography, the biopsy findings may sometimes be the first sign of a problem.
We routinely obtain both a Doppler ultrasound and a liver biopsy on the same day when a transplantation recipient presents with hepatic dysfunction.
Acute cellular rejection is generally suspected based upon the development of hepatic biochemical test abnormalities, which may include elevations of some or all of the following: serum aminotransferases, alkaline phosphatase, gamma-glutamyl transpeptidase (GGT), and bilirubin levels. However, these abnormalities are neither sensitive nor specific for distinguishing acute cellular rejection from other causes of hepatic allograft dysfunction and do not correlate with the severity of the rejection episode.
Abnormalities in the hepatic biochemical tests in the short-term post-transplantation period are frequently a manifestation of preservation injury or acute cellular rejection. Preservation injury usually manifests with elevation of the alkaline phosphatase and GGT, without a significant increase in total bilirubin. By contrast, elevation of transaminases (alanine aminotransferase [ALT] and aspartate aminotransferase [AST]) together with rising bilirubin level and/or GGT should raise concern for acute cellular rejection.
Liver histology remains the gold standard for the diagnosis of acute cellular rejection.
a. What are 3 risk factors for MDR VAP?
b. What are 6 prevention strategies (previous years they have only asked for 4,
they wanted us to list 6 here)?
a)
Risk Factors for MDR VAP
- prior IV Abx use within 90d*
- septic shock at time of VAP
- ARDS preceding VAP
- >/= 5d of hospitalization prior to occurence of VAP
- acute RRT prior to VAP onset
*(also a risk factor for MDR HAP, MRSA HAP/VAP, and MDR Pseudomonas VAP/HAP)
b)
VAP prevention (specific guideline, see table 2 pg 920):
- use NIPPV (minimize invasive MV)
- manage pts without sedation whenever possible
- interrupt sedation daily
- assess readiness to extubate daily
- perform SBTs with sedatives turned off
- facilitate early mobility
- utilize ETT with supraglottic suction for pts expected to require >48-72hrs of MV
- change vent circuit ONLY if visibly soiled or malfunctioning
- elevate head of bed 30-45degrees
evidence that intervention improves outcomes but insufficient data on possible risks:
- selective oral/digestive decontamination
- ???regular oral care with chlorhexidine
no impact on VAP rates/average duration of MV/LoS/mortality:
- stress ulcer prophylaxis
- early tracheostomy
- monitoring gastric residuals
- early parenteral nutrition
List two benefits of small bowel over gastric feeding tubes.
may reduce the risk of gastroesophageal reflux and pneumonia.
increaes feedomg tolerance
Canadian guideline recommendation
2015 Recommendation:
Based on 16 level 2 studies, small bowel feeding compared to gastric feeding may be associated with a reduction in pneumonia in critically ill patients. In units where small bowel access is feasible, we recommend the routine use of small bowel feedings. In units where obtaining access involves more logistical difficulties, small bowel feedings should be considered for patients at high risk for intolerance to EN (on inotropes, continuous infusion of sedatives, or paralytic agents, or patients with high nasogastric drainage) or at high risk for regurgitation and aspiration (nursed in supine position). Finally, where obtaining small bowel access is not feasible (no access to fluoroscopy or endoscopy and blind techniques not reliable), small bowel feedings should be considered
for those
select patients that repeatedly demonstrate high gastric residuals and are not tolerating adequate amounts of EN intragastrically.
uptodate:
Post-pyloric feeding has theoretical advantages in critically ill patients. Impaired gastric emptying is relatively common and thus feeding beyond the pylorus has the potential to deliver adequate nutrition without the need for parenteral nutrition. In addition, compared to gastric feeding, it may reduce the risks associated with high gastric residuals such as aspiration pneumonia. The delivery of a continuous feed to the jejunum also prevents gastric distension, thus potentially allowing for better respiratory function [30]. The main disadvantages are the inconvenience, risks, and costs associated with placement of the tube beyond the pylorus.
A 2015 meta-analysis included 14 randomized controlled studies that compared gastric versus post-pyloric feeding in 1109 critically ill patients. There were no significant differences in duration of mechanical ventilation or mortality but post-pyloric feeding was associated with a reduction in pneumonia as compared with gastric feeding.
Canadian clinical practice guidelines also noted that small bowel feedings were associated with a lower incidence of pneumonia in critically ill adults (RR 0.77, 95% CI 0.60-1.0), and therefore recommend routine use of small bowel feedings in centers where this is feasible [34]. Canadian ICUs using these guidelines reported higher rates of adequacy of enteral nutrition (percentage of prescribed energy needs actually received) compared with sites less compliant with these guidelines
Crohns patient requiring TPN
a. What are two ways you can calculate his energy expenditure?
b. How many calories will you give from carbohydrates?
c. How much protein will you give?
a)
- Indirect Calorimetry
- Predictive Equations
- Simplistic weight-based equations
Differing opinions in the ASPEN vs Canadian Clinical Practice Nutrition Guidelines…
Canadian Clinical Practice Guidelines (2015, this statement not changed from 2013)
2013 Recommendation:
There are insufficient data to make a recommendation on the use of indirect calorimetry vs. predictive equations for determining energy needs for nutrition or to guide when nutrition is to be supplemented in critically ill patients.
2013 Discussion:
It was noted that both the included studies examined the role of Indirect
Calorimetry (IC) vs. Equations in unselected, heterogeneous patients. There are no randomized controlled trials of the use of IC in select patients (prolonged stay, obesity, for example). Given the differences in the methodological design of the 2 studies i.e. Singer (2011) used indirect calorimetry to guide supplementation of enteral nutrition with parenteral nutrition whereas Saffle (1990) compared the effectiveness of indirect calorimetry guided enteral nutrition to enteral nutrition guided by Curreri formula, the committee agreed not to combine the two studies in a meta-analysis. Similarly the assignment of values was also not thought to be meaningful because of the heterogeneous nature of the studies. There was no signal of benefit in clinical outcomes in either study and the committee noted the signal for harm associated with the use of indirect calorimetry in the Singer study (increase in length of stay, pneumonia and overall infections). The committee decided that there was insufficient evidence to put forward a recommendation.
ASPEN
- *A3a.** We suggest that indirect calorimetry (IC) be used to determine energy requirements, when available and in the absence of variables that affect the accuracy of measurement. [Quality of Evidence: Very Low]
- *A3b.** Based on expert consensus, in the absence of IC, we suggest that a published predictive equation or a simplistic weight-based equation (25–30 kcal/kg/d) be used to determine energy requirements. (See section Q for obesity recommendations.)
Clinicians should determine energy requirements to establish the goals of nutrition therapy. Energy requirements may be calculated through simplistic formulas (25–30 kcal/kg/d), published predictive equations, or IC. The applicability of IC may be limited at most institutions by availability and cost. Variables in the ICU that affect the timing and accuracy of IC measurements include the presence of air leaks or chest tubes, supplemental oxygen (eg, nasal cannula, bilevel positive airway pressure), ventilator settings (fractional inspiratory oxygen and positive end-expiratory pressure), continuous renal replacement therapy (CRRT), anesthesia, physical therapy, and excessive movement.26 More than 200 predictive equations have been published in the literature, with accuracy rates ranging from 40%–75% when compared with IC, and no single equation emerges as being more accurate in an ICU.27–32 Predictive equations are less accurate in obese and underweight patients. Equations derived from testing hospital patients (Penn State, Ireton-Jones, Swinamer) are no more accurate than equations derived from testing normal volunteers (Harris-Benedict, Mifflin St Jeor). The poor accuracy of predictive equations is related to many nonstatic variables affecting energy expenditure in the critically ill patient, such as weight, medications, treatments, and body temperature. The only advantage of using weight-based equations over other predictive equations is simplicity. However, in critically ill patients following aggressive volume resuscitation or in the presence of edema or anasarca, clinicians should use dry or usual body weight in these equations.
Table 2. Bundle Statements.
- Assess patients on admission to the intensive care unit (ICU) for nutrition risk, and calculate both energy and protein requirements
- to determine goals of nutrition therapy.
- Initiate enteral nutrition (EN) within 24−48 hours following the onset of critical illness and admission to the ICU, and increase to
- goals over the first week of ICU stay.
- Take steps as needed to reduce risk of aspiration or improve tolerance to gastric feeding (use prokinetic agent, continuous infusion,
- chlorhexidine mouthwash, elevate the head of bed, and divert level of feeding in the gastrointestinal tract).
- Implement enteral feeding protocols with institution-specific strategies to promote delivery of EN.
- Do not use gastric residual volumes as part of routine care to monitor ICU patients receiving EN.
- Start parenteral nutrition early when EN is not feasible or sufficient in high-risk or poorly nourished patients.
b)
Protein (MOST IMPORTANT macronutrient) 1.5g/kg/d, ~20-25% total calories
Carbs/Glucose 3g/kg/d, ~50-60% of total calories
Lipids 0.8g/kg/d, ~25-35% of total calories
Bottom Line: you want 1.5g/kg of protein
for every 1g protein you want 0.5g lipid
for every 1g protein you want 2g carbs
*note this is referring to grams not calories
** if concerned about refeeding give 20kcal/kg/d (down from the typical 25), consider 30 if pt hypermetabolic, head injury or in recovery phase. For obese pts with BMI>30, give 22-25kcal/kg/d and use weight as if their BMI was 25
c)
1.5g/kg of protein
short word on intentional underfeeding: hypocaloric enteral nutrition
2015 Recommendation:
Based on 4 level 2 studies, intentional underfeeding of calories (not protein) should be considered in patients at low nutrition-risk. However, this recommendation does not apply to patients at high nutrition risk.
2015 Discussion:
The committee noted that with the inclusion of 3 new trials (Charles 2014, Petros 2014 and Arabi in press) the effect of hypocaloric enteral nutrition on mortality was associated with a trend towards a reduction in ICU and hospital mortality and a reduction in mechanical ventilation. There was no effect on length of stay outcomes. The differences in calories received were 42-50% in the hypocaloric group vs. 72-75% energy needs in the comparison group yet protein delivery was not different. The committee struggled with the signal of benefit with restricting calories in a heterogeneous ICU patient population and a signal of benefit from optimizing caloric delivery in nutritionally high-risk patients. Given this, it was agreed that a weak recommendation be made for the use of hypocaloric nutrition without underfeeding of protein in nutritionally low-risk patients. It was agreed that the need for maintaining protein intake as demonstrated by recent evidence ought to be emphasized.
But you might intentionally underfeed obese and ARDS pts although most ICU pts are “high nutritional risk”. In those intentionally underfed consider using 5–75% of ideal daily intake (20kcal/kg/d is probably adequate)..however in these ptsa keep protein as is!!!
Young guy ~23M post ARDS extubated after 3 days with muscle cramping. You suspect he may have PRIS:
a. List 4 risk factors for PRIS
b. What 3 laboratory tests will be abnormal (EXCEPT CK)
a)
- high dose (>4mg/kg/hr)
- prolonged infusion (>48h)
- young age
- critical illness
- high fat and carbohydrate intake
- inborn errors of mitochondiral fatty acid oxidation
- concominant catecholamine infusion
- concominant steroid therapy
- traumatic brain injury
b)
- metabolic acidosis (combination of lactate and renal failure)
- rhabdomyolosis (increased CK and myoglobin) from direct muscle necrosis of both skeletal and cardiac muscle
- renal failure
- hypertriglyceridemia
- hyperkalemia
- lipemia
Trauma patient in periphery with head injury, hemo-pneumothorax, splenic laceration, pelvic fracture, has subclavian line in place, intubated. You are going to be transporting this patient to the trauma center (they don’t say by ground or air). List 6 emergencies you need to be prepared for.
- hemorrhagic shock from intra-abdominal or pelvic bleeding
- obstructive shock from worsening hemo-pneumothorax
- development of worsened head injury, increased ICP
- airway issue (are they intubated?)
- ?spinal shock from ?SCI
- ?injury from CVC insertion (bleeding or new pneumothorax)
77F with ischemic bowel who requires laparotomy. She has known CHF with EF 20%, COPD with FEV1 30% predicted, she is on CRRT, and has been trached with prolonged ventilation following her necrotizing pancreatitis. She is not doing well. You have a family meeting and the family thinks that she would want to pursue all active treatment including surgery. List two ethical principles that might suggest this is a bad idea, explain your reasoning.
non-maleficence
beneficence (should have net benefit for the pt)
Autonomy (was this discussed with the pt)
- Requires that the patient have autonomy of thought, intention, and action when making decisions regarding health care procedures. Therefore, the decision-making process must be free of coercion or coaxing. In order for a patient to make a fully informed decision, she/he must understand all risks and benefits of the procedure and the likelihood of success. Because ARTs are highly technical and may involve high emotions, it is difficult to expect patients to be operating under fully-informed consent.
Justice
- The idea that the burdens and benefits of new or experimental treatments must be distributed equally among all groups in society. Requires that procedures uphold the spirit of existing laws and are fair to all players involved. The health care provider must consider four main areas when evaluating justice: fair distribution of scarce resources, competing needs, rights and obligations, and potential conflicts with established legislation. Reproductive technologies create ethical dilemmas because treatment is not equally available to all people.
Beneficence
- Requires that the procedure be provided with the intent of doing good for the patient involved. Demands that health care providers develop and maintain skills and knowledge, continually update training, consider individual circumstances of all patients, and strive for net benefit.
Non-maleficence
- Requires that a procedure does not harm the patient involved or others in society. Infertility specialists operate under the assumption that they are doing no harm or at least minimizing harm by pursuing the greater good. However, because assistive reproductive technologies have limited success rates uncertain overall outcomes, the emotional state of the patient may be impacted negatively. In some cases, it is difficult for doctors to successfully apply the do no harm principle.
What are two hemodynamic profiles that you might encounter in a patient post cardiac arrest with post cardiac arrest syndrome (or something, I had no idea what they were looking for here).
- anoxic brain injury
- arrest-related myocardial dysfunction
- systemic ischemic-reperfusion response
- persistent precipitating pathology (ACS, chronic ischemic scar, PR, cardiomyopathies)
so for the hemodynamic profiles, I guess I would say hypotension from distributive shock, or cardiogenic shock due to stunning or primary cardiac problem (CM, PE, ACS)
Picture of purpuric rash on legs – with stem that reads: 19F university students presents with fever, myalgias, neck stiffness and this rash.
a. What is the causative organism
b. What type of precautions are required
a) Neisseria meningitidis
b) droplet and contact until 24hrs after initiation of appropriate antibiotic therapy
Manifestations of Meningococcal infection
Acute systemic meningococcal disease is most frequently manifest by three syndromes:
- Meningitis
- Meningitis with accompanying meningococcemia
- Meningococcemia without clinical evidence of meningitis
The typical initial presentation of meningitis due to N. meningitidis consists of the sudden onset of fever, nausea, vomiting, headache, decreased ability to concentrate, and myalgias in an otherwise healthy patient. The first classic symptom of meningococcal disease was rash, which sometimes evolved from nonspecific to petechial to hemorrhagic over several hours.
The petechial rash appears as discrete lesions 1 to 2 mm in diameter, most frequently on the trunk and lower portions of the body. The mucous membranes of the soft palate, ocular, and palpebral conjunctiva must be carefully examined for signs of hemorrhage. Over 50 percent of patients will have petechiae upon presentation [2,7]. Petechiae can coalesce into larger purpuric and ecchymotic lesions (picture 1). The petechiae correlate with the degree of thrombocytopenia and clinically are important as an indicator of the potential for bleeding complications secondary to disseminated intravascular coagulopathy (DIC).
A maculopapular eruption resembling a wide variety of viral exanthems, particularly rubella, can be an early finding in meningococcemia. This transient rash generally does not persist for more than two days and has frequently disappeared hours after its first observation; it is neither purpuric nor pruritic.
Purpura fulminans is a severe complication of meningococcal disease [16], occurring in approximately 15 to 25 percent of those with meningococcemia [17,18]. It is characterized by the acute onset of cutaneous hemorrhage and necrosis due to vascular thrombosis and disseminated intravascular coagulopathy. Initially, there is cutaneous pain followed by erythema and petechiae. Ecchymoses develop and these lesions, if the course is not altered with therapy, evolve into painful indurated, well-demarcated purple papules with erythematous borders. These areas progress to necrosis with formation of bullae and vesicles. Gangrenous necrosis can follow with extension into the subcutaneous tissue and occasionally involves muscle and bone.
b) Droplet precautions should be continued until 24 hours after institution of effective antibiotics in patients with suspected or confirmed N. meningitidis infection.
Chemoprophylaxis is indicated in close contacts of patients with meningococcal infection and should be given as early as possible following the exposure. Although “close contact” has not been clearly defined, it generally refers to individuals who have had prolonged (>8 hours) contact while in close proximity (<3 feet) to the patient or who have been directly exposed to the patient’s oral secretions during the seven days before the onset of the patient’s symptoms and until 24 hours after initiation of appropriate antibiotic therapy
Patient with difficult percutaneous tracheostomy. She develops subcutaneous emphysema and CXR shows a small right sided pneumothorax. They give you a Bronchoscopy picture which is blurry and unclear but shows a hole just above the carina.
a. What is the most important next management step?
b. What is shown in the picture?
c. Her volumes begin to drop and subcutaneous emphysema gets worse, what are the next two things you will do?
d. What are 2 absolute and 2 relative contraindications to percutaneous tracheostomy?
a)
?confirm appropriate placement of tracheostomy tube by bronch +/- end-tidal CO2
b)
?tracheal injury
c)
?insert right chest tube
?reduce airway pressures
?deepen ETT to try and bypass tracheal injury (bronch-guided)
call thoracic surgery
d)
From uptodate
absolute contraindications (they didn’t list any absolute contraindications)
relative contraindications
- age <15
- uncorrectable bleeding diathesis
- gross distortion of the neck from hematoma, tumour, thyromegaly, scarring
- tracheomalacia
- evidence of soft tissue infection of the neck
- obese/short necks which obscure landmarks
- inability to extend neck due to cervical fusion, RA, etc.
A study that evaluated the rates of bleeding complications during percutaneous tracheostomy showed that bleeding complications could be predicted by a platelet count less than 50,000, an activated partial thromboplastin time longer than 50 seconds, or the presence of two or more coagulation disorders [79]. Administration of prophylactic subcutaneous heparin did not increase the risk of bleeding.
absolute:
- infants
- infection at insertion site
- operator inexperience
- unstable cervical injuries
- uncontrollable coagulopathy
relative:
- enlarged thyroid glands
- presence of pulsatile vessel at insertion site
- difficult anatomy
- coagulopathy
- close proximity to burns/surgical wounds
- high PEEP/FiO2 requirements
- history of cervical injury or tracheostomy
- high riding inominate artery
- radiotherapy to cervical region in last 4wks
- controlled local infection
Percutaneous tracheostomy should NOT be performed if EMERGENCY
pt refusal
They give you a diagram of a transducer levelled to 10cm below a column of water.
a. The transducer is inserted to 10cm below the water column (right where the level is) what will the transducer read?
b. The transducer tip is then inserted to 40cm below the water column. What will the transducer read?
a) 0cm H2O
b) +30cm H2O
or +10 H2O and +40 H2O but if it’s levelled at 10 then I suspect this means it’s calibrated to zero at that level
levelling is not necessarily the same as zeroing
Patient with GBS:
a. List 2 evidence based treatments that will improve clinical course.
b. What respiratory parameters will you look for to suggest they may need to be intubated?
c) another test asked to list 2 physical exam features that may predict respiratory failure/needing intubation.
a)
Plasma exchange
IVIG
The main modalities of therapy for Guillain-Barré syndrome (GBS) are plasma exchange (also called plasmapheresis) and administration of intravenous immune globulin (IVIG). These treatments hasten recovery from GBS, as shown in randomized controlled trials. Patients recover sooner when treated early. The beneficial effects of plasma exchange and IVIG are believed to be equivalent, while combining the two treatments is not beneficial.
The choice between plasma exchange and IVIG is dependent on local availability and on patient preference, risk factors, and contraindications. Patients who are mildly affected and already recovering do not require disease-modifying therapy. When both therapies are equally available and there are no contraindications for either, we suggest treatment with IVIG. Intravenous immune globulin is given for five days at 0.4 gram/kg per day. Side effects include aseptic meningitis, rash, acute renal failure (mostly related to sucrose containing products), and (rarely) hyperviscosity leading to stroke. IgA deficiency can lead to anaphylaxis.
Aside from plasma exchange and IVIG, no other pharmacologic agents have been found to be effective for GBS. In particular, glucocorticoids are not beneficial. In a systematic review and meta-analysis of six trials with 587 participants, glucocorticoid-treated patients with GBS showed no significant difference in disability grade compared with patients who were not treated with glucocorticoids.
b)
The respiratory status of patients with Guillain-Barré syndrome (GBS) can deteriorate quickly and unpredictably. Many patients require mechanical ventilation. Respiratory features associated with progression to respiratory failure in patients with severe GBS include:
- Vital capacity less than 20 mL/kg
- MIP less than 30 cmH2O
- MEP less than 40 cmH2O, or a reduction of more than 30 percent in vital capacity
Clinical features associated with respiratory failure include:
- Time of onset to admission less than seven days
- Inability to cough
- Inability to stand
- Inability to lift the elbows
- Inability to lift the head
Bulbar dysfunction, autonomic dysfunction, and bilateral facial palsy are also associated with the need for mechanical ventilation.
Patient with recent infection, ascending paralysis and you suspect GBS:
a. What is the most common infectious cause for this syndrome
b. What are two other infections that cause this system (?syndrome)
a)
Campylobacter jejuni infection is the most commonly identified precipitant of GBS. Furthermore, campylobacter-associated GBS appears to have a worse prognosis, manifested by slower recovery and greater residual neurologic disability, than other forms of the disease.
b)
GBS also occurs in association with human immunodeficiency virus (HIV) infection, predominantly in those who are not profoundly immunocompromised.
Multiple reports have found an increased risk of GBS following influenza-like illnesses.
Less commonly, GBS has been reported following infection with varicella-zoster virus, herpes simplex virus, hepatitis A, B, C, and E viruses, and the bacteria Haemophilus influenzae, Escherichia coli, and Mycoplasma pneumoniae. The importance of these infectious agents as triggers of GBS is uncertain.
Trauma patient with traumatic injuries post-OR for damage control laparotomy, femur fractures bilaterally not fixed, abdomen packed:
a. 180/100, HR 130, Pulsus 20 what ONE management step will you take?
b. BP 120/60 HR 130 pulsus 20 on norepi 0.3mcg/kg/min what management step will you take?
c. BP 120/60 HR 130, pulsus 20, on NE 0.3mcg/kg/min patient has had 5L crystalloid 6U packed red cells and has ongoing transfusion requirements – what ONE management step will you take next?
d. BP 120/60 HR 130 Pulsus 20 on NE 0.3mcg/kg/min has sats of 90% and ECHO shows RV strain. What do you think the diagnosis is.
a) pain control
b) fluid/blood resuscitation
c) apply splint and traction to both legs…Mo said pericardial tamponade
d) fat embolism
Fat embolism syndrome (FES) typically manifests 24 to 72 hours after the initial insult, but may rarely occur as early as 12 hours or as late as two weeks after the inciting event [37]. Affected patients develop a classic triad: hypoxemia, neurologic abnormalities, and a petechial rash. None of these features are specific for FES.
Pulmonary manifestations are the most common presenting features of FES. Hypoxemia, dyspnea, and tachypnea are the most frequent early findings. In one series, hypoxemia was present in 96 percent of cases [38]. A syndrome indistinguishable from acute respiratory distress syndrome (ARDS) may develop. Approximately one-half of patients with FES caused by long bone fractures develop severe hypoxemia and require mechanical ventilation.
Neurologic abnormalities are also common and typically manifest after respiratory abnormalities, although rare case reports suggest neurological symptoms can occur in isolation [40]. Neurologic manifestations range from the development of an acute confusional state and altered level of consciousness to seizures and focal deficits.
The characteristic red-brown petechial rash may be the last component of the triad to develop and occurs in only 20 to 50 percent (on average one third) of cases (picture 1) [38,39,42]. It is found most often on the nondependent regions of the body including the head, neck, anterior thorax, axillae, and sub-conjunctiva.
The only therapy for fat embolism syndrome is supportive care.
Patient with burns to 65% BSA, mostly chest abdomen and extremities. He is admitted and you start resuscitation as per parkland formula. 5 hours later his peak pressures are reading 50cm H20 and plateau are 40cmH20. CXR is normal. CVP is 30. What are two causes for this and what is one thing you will do about each?
- abdominal compartment syndrome -> decompression with laparotomy
- chest wall rigidity/low compliance from circumferential burn -> chest escharotomy
- …less likely I guess might be pulmonary edema/ARDS for which you might reduce resuscitation and consider RRT/diuresis
Asthmatic girl intubated and put on RR 32, VC 600mL, PEEP 8, on FiO2 70%, you get called 15min later when BP is 70/30 what is the next step in management?
lacks enough detail to clearly answer but her RR and Vt are probably too high leading to dynamic hyperinflation. rule out pneumothorax
Immedicately I would disconnect pt from ventilator and push on chest/abdo then give IVF, reduce RR and Vt.
Patient with ARDS, intubated and on low tidal volume ventilation of 6mL/kg, PEEP 5, Volumes 360mL, Inspiratory trigger -0.5cmH2O. develops a bronchopleural fistula and has CT inserted to -20cmH2O. He is paralyzed with TOF 0 and no activity. RR set to 15 but persistently has RR 35 with alkalotic ABG and decreased CO2.
a. What is one ventilator change you can make to improve the blood gas?
b. What is one non-ventilator change you can make to improve the blood gas?
c. How is the best way to measure the air leak?
d. What are four ventilator strategies you can use to treat a bronchopleural fistula?
a) change to fully controlled mode of ventilation (or increase inspiratory trigger)
b) decrease chest tube suction pressure (i.e. less negative)
c)
A BPF can be quantified from ventilator graphics as volume that is “lost” – that is, the difference between the inspiratory and expiratory tidal volumes (see images)
d)
decrease mean airway pressure, decrease tidal volume more specific
decrease intrinsic PEEP
maximize negative pressure or spontaneous ventilation
extubate as early as possible
When any type of pulmonary barotrauma is detected, immediate attempts should be made at the bedside to lower the plateau airway pressure.
- minimize tidal volume and PEEP
- minimize chest tube suction
- use negative pressure (i.e. spontaneous breathing) rather than positive pressure ventilation (or minimize positive pressure ventilated breaths)
Guidelines for ventilator management in the patient with airleak from barotrauma and alveolopleural fistula
- Reduce both mean airway pressure and the number of positive-pressure breaths, using the lowest number of mechanical breaths that permits acceptable alveolar ventilation
- Wean patient completely if possible
- Partial ventilatory support (eg, low-rate SIMV or pressure support) is preferable to total ventilatory support (eg, assist/control, high-rate SIMV, or pressure control ventilation)
- Avoid or correct respiratory alkalosis (to minimize minute ventilation)
- Consider use of permissive hypercapnia (reducing minute ventilation and allowing arterial PCO2 to rise)
- Limit effective (returned) tidal volume to 5 to 8 mL/kg
- Minimize inspiratory time, and hence mean airway pressure:
- Keep inspiration-to-expiration ratio low (eg, 0.33)
- Use high inspiratory flow rate (eg, 70 to 100 L/min)
- Avoid inflation hold (end-inspiratory pause) and inverse-ratio ventilation
- Use low-compressible-volume (non-disposable) ventilator circuit
- Minimize PEEP (both dialed-in and auto-PEEP)
- Use least amount of chest tube suction that maintains lung inflation
- If spontaneous movement exacerbates leak, keep patient heavily sedated (in unusual circumstances neuromuscular blockade may also be necessary)
- Explore position differences, and avoid patient positions that increase the leak
- Treat bronchospasm and other causes of expiratory airflow obstruction
- Consider specific or unconventional measures (eg, independent lung ventilation, high-frequency jet ventilation, PEEP to chest tubes, etc) only if the air leak per se is clinically felt to be worsening the patient’s condition (eg, intractable hypotension or arrhythmias in association with respiratory acidosis)
- Treat underlying cause of respiratory failure, maintaining nutritional and other support, with goal of discontinuing mechanical ventilation as soon as possible
Patient post mitral valve and aortic valve replacement with cardiogenic shock post bypass on high doses of milrinone, epi, norepi. Has IABP inserted. You see blood in the gas line:
a. What is the problem?
b. What is your next step in management?
a) possible rupture of IABP balloon
b) ?early removal of IABP (before it thromboses) or call CV surgery and have them assess it (may need to be removed in OR)
Blood in the inflation catheter could imply rupture of the balloon. It needs to be notified immediately to the cardiothoracic surgical team. If the situation is not promptly attended to and clots form in the balloon it will not be able to be removed without causing femoral artery injury. The blood rapidly reacts with the helium causing a hard clot formation, which together with the tortuous atherosclerotic aortic environment results in entrapment of a semi-deflated balloon.
Balloon rupture and entrapment is a rare complication in patients treated with an IABP, and it is often difficult to detect. Management should be aimed at early rupture detection with a low threshold to remove the IABP before entrapment can occur. In case of IABP entrapment, either percutaneous removal in conjunction with local or systemic thrombolysis or surgical extraction should be performed, followed by repair of the damaged iliofemoral arteries.
a) What four electrolyte abnormalities do you see in tumor lysis syndrome?
b) What two drugs do you give to prevent/treat tumor lysis?
a)
hyperkalemia
hyperuricemia (from catabolism of nucleic acids)
hyperphosphatemia (and secondary hypocalcemia)
b) would these count as two drugs???
- rasburicase or allopurinol
- IV fluids
The main prophylactic strategies are intravenous (IV) hydration and the use of hypouricemic agents, such as allopurinol and rasburicase.
IV hydration — Aggressive IV hydration is the cornerstone of preventing TLS and is recommended prior to therapy in all patients at intermediate or high risk for TLS (table 3) [2]. The goal of IV hydration is to improve renal perfusion and glomerular filtration, and induce a high urine output to minimize the likelihood of uric acid or calcium phosphate precipitation in the tubules. A 2008 International Expert Panel on TLS recommended that both children and adults at risk for TLS initially receive 2 to 3 L/m2 per day of IV fluid.
Urinary alkalinization — The role of urinary alkalinization with either acetazolamide and/or sodium bicarbonate is unclear and controversial. In the past, alkalinization to a urine pH of 6.5 to 7 or even higher was recommended to increase uric acid solubility, thereby diminishing the likelihood of uric acid precipitation in the tubules. However, this approach has fallen out of favor.
Allopurinol can be used in intermediate risk pts, and rasburicase in high risk pts as a preventive treatment of TLS.
Treatment of established TLS
Patients who present with or develop TLS during therapy should receive intensive supportive care with continuous cardiac monitoring and measurement of electrolytes, creatinine, and uric acid every four to six hours [50]. Effective management of these cases involves the combination of treating specific electrolyte abnormalities, the use of rasburicase at 0.2 mg/kg (if it was not given initially) with repeated doses as necessary, attempting to wash out the obstructing uric acid crystals with fluids with or without a loop diuretic, and the appropriate use of renal replacement therapy.
Symptomatic hypocalcemia should be treated with calcium at the lowest doses required to relieve symptoms. In most situations, clinicians should use other oral phosphate binders, even though there are no good studies demonstrating efficacy.
You are a hospital administrator and you want to access a database containing illness severity data.
a. What are three things you can do with that information?
b. What is one measurement tool to assess staff workload on your unit (i.e. nursing workload)?
c. APACHE and SOFA are two scoring systems used to assess illness severity. What patient population is NOT included in the development of these scoring systems?
a)
predict hospital mortality
predict ICU length of stay
???resource allocation
therapeutic intervention scoring system-28 (TISS-28)
c) ???…ahh couldn’t find this after looking for sooo long but I might guess burn pts
“In addition, in most of the scores, specific populations were excluded from the original databases (for example, patients with burns, patients aged less than 16 or 18 years, patients with a very short length of ICU stay, and so on).”
Acute Physiologic and Chronic Health Evaluation (APACHE) — The APACHE scoring system is widely used in the United States, of which there are four versions (APACHE I through IV) [4-11]. APACHE instruments require the input of a large number of clinical variables, from which a severity score is derived. The resulting severity score is entered into a computer-generated logistical regression equation, which predicts hospital mortality and in some cases length of stay. The required variables differ among the versions but generally include factors such as age, diagnosis, prior treatment location, and numerous acute physiologic and chronic health variables.
Sequential (sepsis-related) Organ Failure Assessment (SOFA) — The SOFA score was initially designed to sequentially assess the severity of organ dysfunction in patients who were critically ill from sepsis. The original SOFA instrument was derived from a cohort of 1449 patients admitted to 40 ICUs in 16 countries [28]. Since multiple organ dysfunction is common in critically ill patients, it has since been used to predict mortality in those with organ failure from other causes including those with acute liver failure from acetaminophen overdose, chronic liver failure (CLIF-SOFA), and cancer, as well as in patients who have undergone cardiac surgery or hematopoietic stem cell transplant [29-34].
SOFA uses simple measurements of major organ function to calculate a severity score (calculator 3). The scores are calculated 24 hours after admission to the ICU and every 48 hours thereafter (thus, the term “Sequential” Organ Failure Assessment). The mean and the highest scores are most predictive of mortality. In addition, scores that increase by about 30 percent are associated with a mortality of at least 50 percent
a) What are the four criteria to be an organ donor after cardiac death (DCD)?
b) What are two recommendations for declaration of death in DCD?
Had trouble with both of these questions…???
a)
Before considering donation, the patient should be judged to have:
- A non-recoverable injury or illness
- Dependence on life-sustaining therapy
- Intention to withdraw life-sustaining therapy, and
- Anticipation of imminent death after withdrawal of life-sustaining therapy.
As a general rule, eligibility criteria are similar to those for organ donation after NDD and should be based on demographic, age and organ-function criteria detailed in the previous CCDT forum. Patients with a history of intravenous drug abuse, sepsis or serious systemic infection, or active malignancies and high-grade brain tumours are excluded. Bacteremic patients are not necessarily excluded. Patients with non-melanoma skin malignancies and some primary non-metastatic brain tumours may be eligible. Organs contaminated with hepatitis B, C or HIV may be transplanted into recipients already infected with these same viruses. Infections with human T-cell leukemia-lymphoma virus, systemic viral infection (e.g., measles, rabies, adenovirus), prion-related disease and herpetic meningoencephalitis are contraindications for organ donation.
b)
determination of fact of death - must be determined by 2 physicians in accordance with “accepted medical practice”
conflict of interest - no physician who has had any association with a proposed transplant recipient that might influence their judgement shall take any part in the determinatio nof death of the donor
prohibition on participation in transplant - no physician who took any part in the determination of the fact of death of the donor shall participate in any way in transplant procedures
determination of cardiocirculatory death -
- Beginning with the onset of circulatory arrest, there must be a 5-minute period during which the absence of palpable pulses, blood pressure and respiration are continuously observed by at least 1 physician and
- Death is determined by 2 physicians by documenting the absence of palpable pulses, blood pressure and respiration on completion of this 5-minute period.
The physician present during the 5-minute period of continuous observation and who makes 1 of the determinations of death must be a staff physician with the requisite skill and training.
COPD patient passess SBT.
a) What Is one evidence based way to prevent reintubation?
b) What are four risk factors for reintubation in someone who has passed an SBT?
a) extubation to NIPPV
b)
- reduced cough peak expiratory flow (PEF <60L/min) or unable to moisten index card held in front of ETT
- increased sputum volume (>2.5mL/hr)
- ???impaired neurologic function (inability to follow commands) ***but controversial and not always shown
results of one study also add:
- higher illness severity at admission
- higher amount of secretions
- higher minute ventilation
- higher number of failed SBTs
- lower oxygenation
advanced age
cardiac disease
hypercapneic resp failure
a) List 4 medications besides benzos to treat status epilepticus.
b) What are two ion channels and list what the drugs do (i.e. open, close, block)?Do not list the name of the drug.
c) What does the GABA agonist do to the action potential of the cell?
a) phenytoin: Stabilizes neuronal membranes and decreases seizure activity by increasing efflux or decreasing influx of sodium ions across cell membranes in the motor cortex during generation of nerve impulses.
valproic acid: Intravenous valproic acid is increasingly used in the treatment of status epilepticus. It is preferred over phenytoin in patients with primary generalized epilepsies, although these patients represent a relatively small proportion of those with GCSE. Causes increased availability of gamma-aminobutyric acid (GABA), an inhibitory neurotransmitter, to brain neurons or may enhance the action of GABA or mimic its action at postsynaptic receptor sites. Also blocks voltage-dependent sodium channels, which results in suppression of high-frequency repetitive neuronal firing.
levetiracetam: The precise mechanism by which levetiracetam exerts its antiepileptic effect is unknown. However, several studies have suggested the mechanism may involve one or more of the following central pharmacologic effects: inhibition of voltage-dependent N-type calcium channels; facilitation of GABA-ergic inhibitory transmission through displacement of negative modulators; reduction of delayed rectifier potassium current; and/or binding to synaptic proteins which modulate neurotransmitter release.
phenobarbital: Phenobarbital is a very effective anticonvulsant, especially in the acute management of seizures, but it was not the best initial treatment in the VA comparative trial [3]. Various studies have shown a rate of seizure control of approximately 60 percent when phenobarbital is used alone, similar to that with lorazepam alone or the combination of phenytoin and diazepam [3,60]. High doses of phenobarbital will control almost any seizure [61], but at the cost of substantial sedation and potential reduction of blood pressure and respiration. Despite its efficacy, phenobarbital is generally not used as a first-line treatment in adults because administration is slow, it causes prolonged sedation, and it may involve a higher risk of hypoventilation and hypotension than either benzodiazepines, phenytoin, valproate, or levetiracetam. Long-acting barbiturate with sedative, hypnotic, and anticonvulsant properties (?receptor?).
propofol: Propofol is a short-acting, lipophilic intravenous general anesthetic. The drug is unrelated to any of the currently used barbiturate, opioid, benzodiazepine, arylcyclohexylamine, or imidazole intravenous anesthetic agents. Propofol causes global CNS depression, presumably through agonism of GABAA receptors and perhaps reduced glutamatergic activity through NMDA receptor blockade.
b)????
c)
GABA agonists or positive allosteric modulators increase frequency of Cl channel opening, therefore higher concentration of Cl inside cell, therefore higher action potential, therefore lower chance of firing.
wikipedia: There are three receptors of the gamma-aminobutyric acid. The two receptors GABA-α and GABA-ρ are ion channels that are permeable to chloride ions which reduces neuronal excitability. The GABA-β receptor belongs to the class of G-Protein coupled receptors that inhibit adenylyl cyclase, therefore leading to decreased cyclic adenosine monophosphate (cAMP). GABA-α and GABA-ρ receptors produce sedative and hypnotic effects and have anti-convulsion properties. GABA-β receptors also produce sedative effects. Furthermore, they lead to changes in gene transcription.
Many commonly used sedative and anxiolytic drugs that affect the GABA receptor complex aren’t agonists. These drugs are known as positive allosteric modulators (PAMs) and while they do bind to the GABA receptors, they cannot induce a response from the neuron without an actual agonist being present. Drugs that fall into this class exert their pharmacodynamic action by increasing the effects that an agonist has when potentiation is achieved.
Most general anaesthetics are PAMs of GABA-A receptor. Positive allosteric modulators work by increasing the frequency with which the chloride channel opens when an agonist binds to its own site on the GABA receptor. The resulting increase in the concentration of Cl− ions in the postsynaptic neuron immediately hyperpolarizes this neuron, making it less excitable and thus inhibiting the possibility of an action potential. However, some general anesthetics like propofol and high doses of barbiturates may not only be positive allosteric modulators of GABA-A receptors but also direct agonists of these receptors.
Na channel - phenytoin, valproic, lacosamide
GABA - propofol, phenobarbit
Ca channel - phenobarb
A 70M with COPD was admitted to hospital 1 month ago presents with diarrhea and septic shock. He has renal failure. CT abdomen shows pseudomembranes. They show you an endoscopy picture. What is the MOST important next step?
call surgery
pseudomembranous colitis is caused by C difficile
- Vanco 500mg PO QID +/- Vanco retention enema if ileus present
- Metronidazole 500mg IV Q8H
- low threshold to consider colectomy
- ???which of these is the MOST important step???
Patients with severe or fulminant colitis should receive antibiotic therapy, supportive care, and close monitoring. Surgery should be considered if the patient’s clinical status fails to improve within the first few days of therapy and/or the serum lactate is ≥2.2 mmol/L [72]. Toxic megacolon should be suspected if the patient develops abdominal distention with diminution of diarrhea; this may reflect paralytic ileus resulting from loss of colonic muscular tone.
Antibiotic therapy — Antibiotics for the treatment of severe CDI include oral vancomycin or oral fidaxomicin (table 2).
Antibiotics for the treatment of fulminant CDI include the combination of enteral vancomycin plus parenteral metronidazole (table 2) [1,8,12,76]. For patients with concomitant ileus (and/or another condition preventing oral vancomycin from reaching the colon), rectal vancomycin may be administered as a retention enema, either in addition to oral vancomycin (if the ileus is partial) or in place of oral vancomycin (if the ileus is complete) (table 2) [8,77-79]. However, administration of rectal vancomycin is associated with risk of colonic perforation; therefore, use of intracolonic vancomycin should be restricted to patients who are unresponsive to standard therapies, and the procedure should be performed by personnel with expertise in administering enemas [8,77-79].
The standard duration of antibiotic therapy for C. difficile diarrhea is 10 days; the antibiotic course should be tailored to clinical circumstances for patients with severe disease. Those with an underlying predisposing infection requiring prolonged duration of concomitant antibiotic administration should continue CDI treatment throughout the antibiotic course plus one additional week after its completion.
Surgery — 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:
- 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
IDSA guidelines on CDiff
XXVIII. What are important ancillary treatment strategies for CDI?
Discontinue therapy with the inciting antibiotic agent(s) as soon as possible, as this may influence the risk of CDI recurrence (strong recommendation, moderate quality of evidence).
Antibiotic therapy for CDI should be started empirically for situations where a substantial delay in laboratory confirmation is expected, or for fulminant CDI (described in section XXX) (weak recommendation, low quality of evidence).
XXIX. What are the best treatments of an initial CDI episode to ensure resolution of symptoms and sustained resolution 1 month after treatment?
Either vancomycin or fidaxomicin is recommended over metronidazole for an initial episode of CDI. The dosage is vancomycin 125 mg orally 4 times per day or fidaxomicin 200 mg twice daily for 10 days (strong recommendation, high quality of evidence) (Table 1).
In settings where access to vancomycin or fidaxomicin is limited, we suggest using metronidazole for an initial episode of nonsevere CDI only (weak recommendation, high quality of evidence). The suggested dosage is metronidazole 500 mg orally 3 times per day for 10 days. Avoid repeated or prolonged courses due to risk of cumulative and potentially irreversible neurotoxicity (strong recommendation, moderate quality of evidence). (See Treatment section for definition of CDI severity.)
XXX. What are the best treatments of fulminant CDI?
For fulminant CDI*, vancomycin administered orally is the regimen of choice (strong recommendation, moderate quality of evidence). If ileus is present, vancomycin can also be administered per rectum (weak recommendation, low quality of evidence). The vancomycin dosage is 500 mg orally 4 times per day and 500 mg in approximately 100 mL normal saline per rectum every 6 hours as a retention enema. Intravenously administered metronidazole should be administered together with oral or rectal vancomycin, particularly if ileus is present (strong recommendation, moderate quality of evidence). The metronidazole dosage is 500 mg intravenously every 8 hours.*
*Fulminant CDI, previously referred to as severe, complicated CDI, may be characterized by hypotension or shock, ileus, or megacolon.
If surgical management is necessary for severely ill patients, perform subtotal colectomy with preservation of the rectum (strong recommendation, moderate quality of evidence). Diverting loop ileostomy with colonic lavage followed by antegrade vancomycin flushes is an alternative approach that may lead to improved outcomes (weak recommendation, low quality of evidence).
Bronchoscopy pictures – identify the bronchus (three images)
good place to test yourself here
Trachea
- right mainstem bronchus
- upper lobe bronchus
- apical segmental bronchus
- posterior segmental bronchus
- anterior segmental bronchus
- bronchus intermedius
- right middle lobe bronchus (really an extension of the bronchus intermedius)
- lateral segmental bronchus
- medial segmental bronchus
- right lower lobe bronchus
- superior
- medial
- anterior
- posterior
- lateral
- right middle lobe bronchus (really an extension of the bronchus intermedius)
- upper lobe bronchus
- left mainstem bronchus
- upper lobe bronchus
- apical
- posterior
- anterior
- …
- superior lingular
- inferior lingular
- lower lobe bronchus
- lateral
- posterior
- anterior
- medial
- superior
- upper lobe bronchus
70M undergoes aortic valve replacement. His TEE postoperatively showed normal LV function. He requires pacing, but when paced his cardiac output drops by 20%. A Rhythm strip is given that shows some spikes without capture, and some spikes right after a QRS. What three changes can you make to the pacemaker to improve cardiac output?
- increase pacing amperage (so it will capture mechanical beats)
- decrease the sensitivity threshold (so it can sense intrinsically paced beats)
- increase pacing rate (higher HR = higher CO, most of the time)
Vasculopath lady with a history of intestinal angina postprandial pain and nausea and HTN etc. Presents with worsening abdominal pain:
a. What are the three vessels that supply the bowel and which parts do they supply
b. You already know she has symptoms of ischemia from occlusion of which vessel?
c. What is wrong with these CT and angiogram images?
d. What is the next most important step?
from another version:
Old lady with abdominal angina, hx AobiFem bx 7 years ago. Imaging of coronal CT through aorta.
a. What 3 vessels perfuse the gut and describe the distribution
b. Based on her PMHx, what’s vessel is already compromised
c. Stem – 2 days later, inc abdo pain, lactate elevated, hypotension, angiogram done.
i. What is most important finding – SMA thrombus?
ii. What immediate treatment
a) celiac trunk -> stomach, spleen, liver, GB, abdominal esophagus, pancreas, duodenum
superior mesenteric artery -> duodenum to proximal 2/3rds of the transverse colon
inferior mesenteric artery -> distal 1/3rd of the transverse colon, splenic flexure, descending colon, sigmoid colon, rectum
b) ?which vessel is already compromised? I guess Aorta and/or iliac/femoral arteries
c)
d) treatment of SMA thrombus
Initial medical management for all patients with acute mesenteric ischemia includes the following, which are discussed in detail separately:
- 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 (algorithm 2 and algorithm 3), 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. (See ‘Surgical versus endovascular intervention’ below.)
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.
You are given a left ventricular diastolic pressure volume graph with pressure on the y axis and volume on the x axis. They have drawn the normal pressure volume trace. They then ask you to draw a trace for:
a. Dilated cardiomyopathy
b. Tamponade
DCM
DCM increases end-diastolic volume (EDV) and end-systolic volume (ESV). However, the weakening of the heart causes a decrease in end-systolic pressure (ESP). Thus, the slope of the end-systolic pressure volume relationship (ESPVR) decreases. The slope of the end-diastolic pressure volume relationship (EDPVR) decreases which signifies an increase in compliance (decrease in vascular stiffness). Stroke work and cardiac output are also depressed.
TamponadeDenault article
Mechanism of pericardial tamponade. a The normal venous return (VR) curve and cardiac output (CO) using the Starling relationship. Both VR and CO are equal at a specific right atrial pressure (Pra). The venous return is equal to the difference between the mean systemic pressure (Pms) and the Pra divided by the resistance to VR. The resistance to VR is a function of the slope of the VR. At a certain point on this curve, VR cannot increase because Pra becomes sub-atmospheric. This leads to collapse of the great vessels entering the intra-thoracic cavity. The corresponding normal pressure–volume relationship of the right and left ventricles are shown below. b Top In tamponade, VR and CO are reduced and Pra is increased. This is secondary to the rise in pericardial pressure. In addition, VR will now be limited by the pericardial pressure, not by the sub-atmospheric pressure. Therefore, VR is now equal to the difference between Pms and pericardial pressure divided by the resistance to VR. The VR slope is reduced by an increase in the resistance to VR. A normal compensatory increase in mean systemic pressure (Pms) will also be observed secondary to the activation of the autonomic nervous system. Bottom Bi-ventricular pressure–volume relationships in pericardial tamponade. The increase in pericardial pressure will be transmitted to both ventricles. Therefore, an upward shift of the horizontal part of the pressure–volume relationship will be observed. This is typically associated with equalization of end-diastolic pressures. As pericardial pressure increases and tamponade develops, bi-ventricular volumes will be further reduced. Consequently, left ventricular pressure and systemic pressure will be reduced. (see image in question)
Man with depression since his wife died four months ago. He is found unresponsive at home with bottles of verapamil, hydrochlorothiazide, and atorvastatin. His HR is 40, BP 80/40. The emergency physicians have tried volume resuscitation and atropine, and he is being transcutaneously paced without capture or improvement in BP, list four more treatment options you could try.
- IC calcium
- glucagon
- high dose insulin
- lipid emulsion
- ECMO
- norepinephrine
uptodate:
for severely symptomatic patients:
- Stabilization of the airway as necessary (avoid induction agents that exacerbate hypotension)
- Additional IV boluses of isotonic crystalloid
- IV calcium salts
- IV glucagon
- IV high-dose insulin and glucose
- IV vasopressor (eg, norepinephrine)
- IV lipid emulsion therapy
Atropine should be administered to any patient with symptomatic bradycardia; however, it is often ineffective after significant CCB exposure [15]. Atropine is administered in a dose of 0.5 to 1.0 mg IV every two to three minutes to a maximum of 3 mg.
Calcium salts are often used to overcome the cardiovascular effects of CCBs. However, treatment with calcium salts is often ineffective. This is because CCB poisoning interferes with both the serum concentration and the intracellular handling of calcium.
Glucagon increases intracellular levels of cyclic adenosine monophosphate (AMP) and, in animal models, has been shown to increase heart rate in CCB toxicity [21]. However, it has minimal effects on the mean arterial pressure. Glucagon has been effective in treating human cases of CCB toxicity [22-24]. The dosing regimen for glucagon in the treatment of CCB poisoning has not been established in human clinical trials. For the adult patient, an initial 5 mg IV bolus is a reasonable start and may be repeated twice at 10-minute intervals. A glucagon infusion can be started at the total dose at which a response is noted. Nausea and vomiting are common side effects of glucagon administration.
Vasopressors: uptodate recommends norepinephrine. Patients with profound CCB toxicity may require higher doses of vasopressors than those typically used in the treatment of severe sepsis or other causes of shock. In one series, patients with severe diltiazem or verapamil toxicity received vasopressor doses as high as 100 mcg per minute of norepinephrine, 150 mcg per minute of epinephrine, and 100 mcg/kg per minute for dopamine [25]. However, the arrhythmogenic effects of these drugs become more prominent at higher doses; thus, the risk of such high doses, particularly with multiple agents, may outweigh the benefits.
High-dose insulin therapy has positive inotropic effects in patients with CCB toxicity. Its effectiveness and safety have been noted in animal models and case reports [26-29]. Relative hypoglycemia and hypokalemia must be corrected prior to initiating high-dose insulin therapy. For patients with a serum glucose concentration below 8.25 mmol/L, we administer 50 mL of 50 percent dextrose (D50W) IV. For patients with a serum potassium concentration below 3 mmol/L, we administer 20 mEq of potassium IV. We initiate high-dose insulin therapy with a bolus of 1 unit/kg of regular, short-acting insulin given IV. Following this bolus, we begin a continuous infusion at 0.5 units/kg per hour IV and titrate upwards until hypotension is corrected or a maximum dose of 10 units/kg per hour is reached. CCB overdose often causes hyperglycemia that is refractory to high-dose insulin. Therefore, not all patients require supplemental dextrose. If necessary, euglycemia can be maintained by means of a continuous IV infusion of 5 to 10 percent dextrose. A reasonable initial rate for such an infusion is 0.5 to 1 g of dextrose/kg per hour. Titration of the dextrose infusion and additional boluses of 50 percent dextrose are provided based upon serum glucose measurements (finger stick glucose), which are obtained every 15 to 30 minutes until the concentration is stable and every hour thereafter until several hours after therapy is complete.
Lipid emulsions are the fats used in total parenteral nutrition (TPN). Initially used to treat overdoses of local anesthetics such as bupivacaine, IV lipid emulsion (ILE) is being studied as a therapy for poisonings involving a number of lipophilic medications. Studies of ILE therapy are preliminary. Systematic reviews of lipid emulsion therapy for acute poisoning have found the overall quality of studies supporting this treatment to be low or very low, but included human case reports provide some evidence of benefit in patients with toxicity from verapamil, beta blockers, some tricyclic antidepressants, bupivacaine, chlorpromazine, and some antidysrhythmics (eg, flecainide) [33-35]. We suggest consultation with a medical toxicologist or poison control center to determine whether ILE therapy is appropriate.
A transvenous pacemaker can be inserted to assist with electrical conduction. However, pacing does not counteract the negative inotropic effects of these drugs, and successful capture may not correct the patient’s hypotension [49]. If there are no contraindications, an intraaortic balloon pump may help correct intractable hypotension.
Extracorporeal membrane oxygenation — There are several case reports of patients with severe CCB poisoning who survived following treatment with extracorporeal membrane oxygenation (ECMO) [51-53]. We believe that ECMO should be considered a last resort and on a case-by-case basis in conjunction with guidance from a poison control center or medical toxicologist.
Extracorporeal removal — CCBs are highly protein bound; therefore, extracorporeal removal by hemodialysis is not effective.
Patient with COPD in the ICU for months, tracheostomy in place, is competent to make his own decisions and wants to keep going. We know that ventilator weaning depends on the balance of three factors:
a. What are the three factors of ventilator weaning
b. What two things must be present for you to decide that ventilator weaning is
futile.
a) what is this question asking exactly??? only three???
- systemic disease factors
- respiratory system mechanical factors (load/capacity balance)
- iatrogenic factors (inappropriate vent support, upper airway abnormalities, tracheostomies affecting swallowing and aspiration)
b)
- treatable conditions that impede weaning have been reversed/improved
- documented repeated failure to progress through a weaning protocol, even to reach modest goals (e.g. nocturnal ventilation, invasive/non-invasive)
CHEST 2005 guidelines on prolonged MV
There is no body of evidence to support a set time limit for considering mechanical ventilatory support weaning to be futile, nor when weaning attempts should cease. In the evidence-based weaning guide-lines endorsed by several authoritative bodies, a time of 3 months of mechanical ventilation was extrapolated post hoc from observational studies as being a period when most patients who could be weaned had been weaned.
Relying on a strict timeline to define futility is clearly inappropriate, as many factors enter into the decision to abandon further weaning attempts. On admission to a PMV-focused care venue, the inter-disciplinary team should immediately partner with the patient and family on goal setting and discharge planning. The decision to subsequently consider further weaning futile can then be made based on the following principles: (1) treatable conditions that impede weaning have been reversed/improved as much as possible; and (2) documented repeated failure to progress through a weaning protocol, even to reach modified goals (eg, nocturnal ventilation,invasive or noninvasive). An additional consideration would include a realization that resultant functionality and quality of life from the patient’s standpoint will be unacceptable, even if weaned.
Man thrown off horse, landed prone, horse landed on back. Presents to ED/Trauma with sensation to angle of Louis, motor – strongest to D1, weak to D5 both hands, no movement in lower extremities. HR 50, BP 80/60, Sat 98 on RA, EtCO2 52. Assume only injury is SCI (i.e. no hemorrhage)
a. What dermatome is his level.
b. Pathophysiology for hypotension.
c. 4 interventions to consider immediate management.
?what does D1 and D5 refer to?
a) angle of Louis seems to refer to C4 dermatome
b) neurogenic shock, see full description below, occurs with disruption/damage to sympathetic nerve fibers typically with traumatic SCI above T6 which results in a state of unopposed parasympathetic (i.e. vagal) stimulation leading to vasoplegia, hypotension, bradycardia, temperature dysregulation.
c)
- IVF
- atropine +/- external pacing
- vasopressors to target MAP 85-90
- C-spine stabilization +/- surgery to stabilize C spine (which may help with neurogenic shock)
Grade — Definition
A — Complete. No sensory or motor function is preserved in the sacral segments S4-S5
B — Incomplete. Sensory but not motor function is preserved below the neurological level and includes the sacral segments S4-S5
C — Incomplete. Motor function is preserved below the neurological level, and more then half of key muscles below the neurological level have a muscle grade less then 3 (Grades 0-2).
D — Incomplete. Motor function is preserved below the neurological level, and at least half of key muscles below the neurological level have a muscle grade greater than or equal to 3.
E — Normal. Sensory and motor functions are normal.
Neurogenic shock refers to hypotension, usually with bradycardia, attributed to interruption of autonomic pathways in the spinal cord causing decreased vascular resistance. Patients with TSCI may also suffer from hemodynamic shock related to blood loss and other complications. An adequate blood pressure is believed to be critical in maintaining adequate perfusion to the injured spinal cord and thereby limiting secondary ischemic injury. Albeit with few empiric supporting data, guidelines currently recommend maintaining mean arterial pressures of at least 85 to 90 mmHg and using intravenous (IV) fluids, transfusion, and pharmacologic vasopressors as needed.
While controlled hypotension may be appropriate for many trauma patients, those with SCI, like those with traumatic brain injury, are at greater risk for complications from hypotension. Thus, a higher blood pressure is needed to ensure adequate perfusion of the spinal cord. Guidelines from 2013 recommend maintaining a MAP of at least 85 to 90 mmHg for patients with SCI [40], and subsequent studies support this goal. While there is no clearly defined combination of blood products and vasopressor treatment for these patients, norepinephrine is recommended over dopamine or phenylephrine by some authorities when vasopressors are required for patients with SCI, and we concur with this approach.
Neurogenic shock is a devastating consequence of spinal cord injury (SCI), also known as vasogenic shock. Injury to the spinal cord results in sudden loss of sympathetic tone, which leads to the autonomic instability that is manifested in hypotension, bradyarrhythmia, and temperature dysregulation. Spinal cord injury is not to be confused with spinal shock, which is a reversible reduction in sensory and motor function following spinal cord injury. Neurogenic shock is associated with cervical and high thoracic spine injury.
Neurogenic shock is defined as the injury to the spinal cord with associated autonomic dysregulation. This dysregulation is due to a loss of sympathetic tone and unopposed parasympathetic response. Neurogenic shock is most commonly a consequence of traumatic spinal cord injuries.
Neurogenic shock is the clinical state manifested from primary and secondary spinal cord injury. Hemodynamic changes are seen with an injury to the spinal cord above the level of T6. The descending sympathetic tracts are disrupted most commonly from associated fracture or dislocation of vertebrae in the cervical or upper thoracic spine. Primary spinal cord injury occurs within minutes of initial insult. Primary injury is direct damage to the axons and neural membranes in the intermediolateral nucleus, lateral grey mater, and anterior root that lead to disrupted sympathetic tone. Secondary spinal cord injury occurs hours to days after the initial insult. Secondary injury is a result of vascular insult, electrolyte shifts, and edema that lead to progressive central hemorrhagic necrosis of grey matter at the injury site. At a cellular level, there is excitotoxicity from NMDA accumulation, improper homeostasis of electrolytes, mitochondrial injury, and reperfusion injury which all lead to controlled and uncontrolled apoptosis. Neurogenic shock is a combination of both primary and secondary injury that lead to loss of sympathetic tone and thus unopposed parasympathetic response driven by the Vagus nerve. Consequently, patients suffer from instability in blood pressure, heart rate, and temperature regulation.
4 clinical or investigations that portend poor prognosis following cardiac arrest
AHA Guidelines 2015 Recommendations (of note image is from European guidelines)
TIMING
The earliest time for prognostication using clinical examination in patients treated with TTM, where sedation or paralysis could be a confounder, may be 72 hours after return to normo- thermia (Class IIb, LOE C-EO).
We recommend the earliest time to prognosticate a poor neurologic outcome using clinical examination in patients not treated with TTM is 72 hours after cardiac arrest (Class I, LOE B-NR). This time until prognostication can be even longer than 72 hours after cardiac arrest if the residual effect of sedation or paralysis confounds the clinical examination (Class IIa, LOE C-LD).
Operationally, the timing for prognostication is typically 4.5 to 5 days after ROSC for patients treated with TTM. This approach minimizes the possibility of obtaining false-positive results (ie, inaccurately suggesting a poor outcome) because of drug-induced depression of neurologic function. In making this recommendation, it is recognized that in some instances, withdrawal of life support may occur appropriately before 72 hours because of underlying terminal disease, brain herniation, or other clearly nonsurvivable situations.
CLINICAL EXAM
In comatose patients who are not treated with TTM, the absence of pupillary reflex to light at 72 hours or more after cardiac arrest is a reasonable exam finding with which to predict poor neurologic outcome (FPR, 0%; 95% CI, 0%–8%; Class IIa, LOE B-NR).
In comatose patients who are treated with TTM, the absence of pupillary reflex to light at 72 hours or more after cardiac arrest is useful to predict poor neurologic outcome (FPR, 1%; 95% CI, 0%–3%; Class I, LOE B-NR).
We recommend that, given their unacceptable FPRs, the findings of either absent motor movements or extensor posturing should not be used alone for predicting a poor neurologic outcome (FPR, 10%; 95% CI, 7%–15% to FPR, 15%; 95% CI, 5%–31%; Class III: Harm, LOE B-NR). The motor examination may be a reasonable means to identify the population who need further prognostic testing to predict poor outcome (Class IIb, LOE B-NR).
We recommend that the presence of myoclonus, which is distinct from status myoclonus, should not be used to predict poor neurologic outcomes because of the high FPR (FPR, 5%; 95% CI, 3%–8% to FPR, 11%; 95% CI, 3%–26%; Class III: Harm, LOE B-NR).
In combination with other diagnostic tests at 72 or more hours after cardiac arrest, the presence of status myoclonus during the first 72 to 120 hours after cardiac arrest is a reasonable finding to help predict poor neurologic outcomes (FPR, 0%; 95% CI, 0%–4%; Class IIa, LOE B-NR).
EEG
In comatose post–cardiac arrest patients who are treated with TTM, it may be reasonable to consider persistent absence of EEG reactivity to external stimuli at 72 hours after cardiac arrest, and persistent burst suppression on EEG after rewarming, to predict a poor outcome (FPR, 0%; 95% CI, 0%–3%; Class IIb, LOE B-NR).
Intractable and persistent (more than 72 hours) status epilepticus in the absence of EEG reactivity to external stimuli may be reasonable to predict poor outcome (Class IIb, LOE B-NR).
In comatose post–cardiac arrest patients who are not treated with TTM, it may be reasonable to consider the presence of burst suppression on EEG at 72 hours or more after cardiac arrest, in combination with other predictors, to predict a poor neurologic outcome (FPR, 0%; 95% CI, 0%–11%; Class IIb, LOE B-NR).
EVOKED POTENTIALS
In patients who are comatose after resuscitation from cardiac arrest regardless of treatment with TTM, it is reasonable to consider bilateral absence of the N20 SSEP wave 24 to 72 hours after cardiac arrest or after rewarming a predictor of poor outcome (FPR, 1%; 95% CI, 0%–3%; Class IIa, LOE B-NR).
SSEP recording requires appropriate skills and experience, and utmost care should be taken to avoid electrical interference from muscle artifacts or from the intensive care unit environment. However, sedative drugs or temperature manipulation affect SSEPs less than they affect the EEG or clinical examination.
IMAGING
In patients who are comatose after resuscitation from cardiac arrest and not treated with TTM, it may be reasonable to use the presence of a marked reduction of the GWR on brain CT obtained within 2 hours after cardiac arrest to predict poor outcome (Class IIb, LOE B-NR).
It may be reasonable to consider extensive restriction of diffusion on brain MRI at 2 to 6 days after cardiac arrest in combination with other established predictors to predict a poor neurologic outcome (Class IIb, LOE B-NR).
Acquisition and interpretation of imaging studies have not been fully standardized and are subject to interobserver variability. In addition, the recommendations for brain imaging studies for prognostication are made with the assumption that images are performed in centers with expertise in this area.
BIOMARKERS
Given the possibility of high FPRs, blood levels of NSE and S-100B should not be used alone to predict a poor neurologic outcome (Class III: Harm, LOE C-LD).
When performed with other prognostic tests at 72 hours or more after cardiac arrest, it may be reasonable to consider high serum values of NSE at 48 to 72 hours after cardiac arrest to support the prognosis of a poor neurologic outcome (Class IIb, LOE B-NR), especially if repeated sampling reveals persistently high values (Class IIb, LOE C-LD).
Laboratory standards for NSE and S-100B measurement vary between centers, making comparison of absolute values difficult.
Anaphylactic Shock
a. Most important drug to give (be specific)
b. 3 other pharmacologic things to give
a) epinephrine IV or IM (IM injection is also preferred over subcutaneous or intravenous (IV) bolus because it is faster in many situations and safer (ie, lower risk of cardiovascular complications, such as severe hypertension and ventricular arrhythmias).
- IM dosing – For situations where an exact dose can be drawn up and administered, the recommended dose of epinephrine for patients of any age is 0.01 mg/kg (maximum dose of 0.5 mg - I would just give that to all adults) per single dose, injected IM into the mid-outer thigh (vastus lateralis muscle). The dose should be drawn up using a 1 mL syringe using the 1 mg/mL formulation of epinephrine
- Patients who do not respond to several IM injections of epinephrine and aggressive fluid resuscitation may not be adequately perfusing muscle tissues, as most commonly occurs in individuals presenting with profound hypotension or symptoms and signs suggestive of impending shock (dizziness, incontinence of urine and/or stool).
Such patients should receive epinephrine by slow intravenous (IV) infusion, with the rate titrated according to response and the presence of continuous electronic hemodynamic monitoring. Start the IV epinephrine infusion at 0.1 mcg/kg/minute and increase it every two to three minutes by 0.05 mcg/kg/minute until BP and perfusion improve.
- Glucagon for patients taking beta-blockers — Beta-blocker therapy, alone or in combination with angiotensin-converting enzyme inhibitors, has been associated with more severe anaphylaxis [70]. However, in a retrospective study of 789 patients presenting to the emergency department, patients taking beta-blockers were no more likely to need epinephrine or to need additional doses of epinephrine than patients not taking beta-blockers, so the clinical impact may be relatively small [71]. Nonetheless, although epinephrine should still be used at first-line therapy, even in patients taking beta-blockers, if a patient taking beta-blockers appears to be refractory to epinephrine, glucagon can be administered because it has inotropic and chronotropic effects that are not mediated through beta-receptors
b)
- glucocorticoids for rebound
- H1 blocker diphenhydramine
- H2 blocker ranitidine
- salbutamol (for epinephrine-resistant bronchospasm)
- could consider vasopressin if no longer responsive to epi (targest different receptors)
- hail mary options: methylene blue, ECMO
Stem with cardiogenic shock
a. vasopressor proven to have more adverse effects
b. Best vasopressor to give the most chronotropy
a)Initially I would have said dobutamine but technically I wouldn’t classify that as a vasopressor so I suppose epi becuase of risk of arrhythmia???
b)
I don’t think it’s possible to answer this question. The table in the AHA statement lists epi, dob, and isoproterenol as all having ++++ B1 activity and it does not give specific recommendations for bradycardia induced cardiogenic shock…
From AHA Statement on CS
We suggest that when an early invasive approach cannot be completed in a timely fashion, fibrinolysis can be considered in CS associated with STEMI. The decision to administer fibrinolysis should be individualized on the basis of perceived reperfusion benefit, bleeding risks, and the anticipated time delay to angiography.
We support guidelines that recommend an early invasive strategy with appropriate revascularization for all suitable patients with suspected ACS-associated CS, including patients with uncertain neurological status or those who have received prior fibrinolysis, regardless of the time delay from MI onset.
In summary, evidence continues to support the early revascularization of patients with CS after ACS, with either PCI or CABG used as indicated. Until the results of CULPRIT-SHOCK are available, revascularization of both the culprit and hemodynamically significant non-culprit stenoses is reasonable. We support the preferential use of radial arterial access for angiography and PCI when feasible.
We suggest that all patients with CS without serious bleeding complications be continued on dual antiplatelet therapy without interruption after PCI. In situations when oral agents cannot be administered or there are concerns about absorption, the use of an intravenous glycoprotein IIb/IIIa inhibitor or the recently available intravenous P2Y 12 inhibitor cangrelor can be considered. No high-quality data are available to support the efficacy or safety of glycoprotein IIb/IIIa inhibitors in patients with MCS.
We suggest the use of PACs in cases of diagnostic or CS management uncertainty or in patients with moderate to severe CS who are unresponsive to initial therapy.
Hemodynamic monitoring should complement (and not replace) other markers of end-organ perfusion in CS. The optimal MAP likely differs from patient to patient, and the risks of hypoperfusion with lower MAPs must be balanced (and individualized) with the potentially deleterious impact of vasoactive agents on myocardial oxygen demand, ischemia, and arrhythmia associated with higher MAP targets. We suggest that clinicians assess the adequacy of end-organ and tissue perfusion in response to individualized targets by integrating serial markers of systemic perfusion, including (but not limited to) arterial lactate, mixed or central venous oxygen saturations, urine output, creatinine, liver function tests, mental status, temperature, and other invasive hemodynamic variables.
We support guideline recommendations for the management of patients with STEMI that suggest avoidance of β-blockers in patients with signs of HF or low-output states and the avoidance of RAAS antagonists in patients with hypotension. It may be reasonable to initiate β-blockers when the patient is euvolemic and off inotropes and vasopressors for at least 24 hours. RAAS inhibitor therapy initiation can be considered when the patient has been off vasopressors for 24 hours, provided that the patient’s renal function has returned nearly to baseline levels and the risk of RAAS-associated hyperkalemia or hypotension is low. RAAS inhibitors may be started in patients with pulmonary edema and in conjunction with an inodilator.
We suggest that it is reasonable to administer statin in patients with MI-associated CS.
Norepinephrine is associated with fewer arrhythmias and may be the vasopressor of choice in many patients with CS; however, in light of the aforementioned major study limitations, the optimal first-line vasoactive medication in CS remains unclear.
