2015 Flashcards
- A 40 year old female presents with decreased LOC, with ABG with PaO2 40mmHg, PaCO2 80 mmHg and pH 7.00. What is the mechanism for hypoxemia?
hypoventilation (normal A-a gradient) A-a gradient = Alveolar oxygen pressure - arterial oxygen pressure Alveolar oxygen pressure = FiO2 (Patm-PH20) - PaCO2/0.8 ~~150-PaCO2/0.8 so for this pt: A-a grad = 50 - 40 = 10
normal A-a gradient is about 10-15 but increases with age so can be calculated with normal A-a gradient = age/4 + 4 so for this pt normal A-a grad =6
normal A-a gradient hypoxemia
- hypoventilation
- low PaO2 (low FiO2 or low Patm)
increased A-a gradient hypoxemia
- Diffusion defect (rare)
- V/Q mismatch
- Right-to-Left shunt (intrapulmonary or cardiac)
- Increased O2 extraction (CaO2-CvO2)
- Patient present with frostbite and hypothermia with temperature of 29C. What is one treatment of frostbite that requires ICU level care? What kind of imaging?
tPA infusion bone scan and CTA
- List 3 Surviving sepsis campaign guidelines for use of steroids in sepsis
Surviving Sepsis Campaign 1. We suggest against using IV hydrocortisone to treat septic shock patients if adequate fluid resuscitation and vasopressor therapy are able to restore hemodynamic stability. If this is not achievable, we suggest IV hydrocortisone at a dose of 200 mg per day (weak recommendation, low quality of evidence). CIRCI guidelines Recommendation: We suggest against corticosteroid administration in adult patients with sepsis without shock (conditional recommendation, moderate quality of evidence). Recommendation: We suggest using corticosteroids in patients with septic shock that is not responsive to fluid and moderate- to high-dose vasopressor therapy (conditional recommendation, low quality of evidence). Recommendation: If using corticosteroids for septic shock, we suggest using long course and low dose (e.g., IV hydrocortisone < 400 mg/day for at ≥ 3 days at full dose) rather than high dose and short course in adult patients with septic shock (conditional recommendation, low quality of evidence).
- Label 4 parts on a Sengstaken-Blakemore tube, list 6 steps involved in insertion of a Sengstaken-Blakemore tube; on a CXR of a Blakemore tube, list two different diagnoses related to the tube insertion (Blakemore tube is down right mainstem bronchus, patient is intubated, therefore likely ruptured ETT balloon)
o List 4 parts of a Blakemore tube o List 6 steps involved in the insertion of a Blakemore tube • Secure airway with ETT insertion • Insert Blakemore nasally or orally • Inflate balloon to 30 mL of air to verify correct radiographic placement in stomach to avoid gastric balloon insufflation in stomach leading to esophageal perforation • Once verification of gastric balloon in esophagus inflate balloon to manufacturer’s prescribed volume • If bleeding persists inflate esophageal balloon to 35 mmHg so as to have the esophageal balloon exceed the variceal pressure • Apply traction • Arrange definitive management as esophageal balloon in place for 48 hours only. • Insertion of nasogastric tube so as to suction any oropharyngeal blood that could be aspirated Equipment that is required includes: ●A tamponade tube kit (with the tube and clamps) ●A manometer (not needed for Linton tubes) ●Large-volume syringes ●A traction/pulley system to maintain constant tension on the tube ●Adequate suction Before tube placement, all equipment should be readily at hand. The balloon(s) should be inflated with air and held underwater to assess for leakage and then deflated. With the patient in the supine or left-lateral position, the tube is lubricated and carefully inserted through the mouth (preferred) or nostril until at least 50 cm of the tube has been introduced. Once the tube is placed, the ports are suctioned to remove all air. The gastric balloon is then inflated with 100 mL of air. A radiograph should then be obtained to confirm placement of the gastric balloon below the diaphragm (accidental inflation of the balloon in the esophagus or a hiatal hernia could lead to rupture). Once confirmed, the balloon is filled with an additional 350 to 400 mL of air are (for a total of 450 to 500 mL of air). Once inflated, the air inlet for the gastric balloon should be clamped. After the gastric balloon is inflated, the tube is pulled until resistance is felt, at which point the balloon is tamponading the gastroesophageal junction. The tube is then securely fastened to either a pulley device or taped to a football helmet to maintain tension on the tube (and thus continued tamponade at the gastroesophageal junction). A one to two pound weight (eg, a 500 mL intravenous fluid bag) can be used to maintain tension on the tube. This is often sufficient to stop the variceal hemorrhage. If bleeding continues despite inflation of the gastric balloon, the esophageal balloon (if present) should be inflated to 30 to 45 mmHg. While the esophageal balloon is inflated, the pressure should be checked periodically (at least once per hour). It is important not to overinflate the esophageal balloon as it puts the patient at risk for esophageal necrosis or rupture. Once the bleeding is controlled, the pressure in the esophageal balloon should be reduced by 5 mmHg to a goal pressure of 25 mmHg. If bleeding resumes, the pressure is increased by 5 mmHg. The tube can be left in place for 24 to 48 hours. The gastric balloon (along with the esophageal balloon if used) should be deflated every 12 hours to check for rebleeding. If the bleeding has ceased, the tube can be left in place with the balloons deflated. The balloons can then be reinflated if bleeding resumes. If the bleeding resumes upon deflation of the balloon(s), the balloon(s) should immediately be reinflated. As mentioned above, balloon tamponade is a temporizing measure and definitive treatment should be arranged for ongoing or recurrent bleeding.
- Table with vasopressin receptors (V1 and V2): where are these receptors and what are their functions
see image
- Patient is on CVVHDF and has poor metabolic control at 48 hours. List two things that could be changed to improve this. They didn’t mention if replacement fluid was pre or post-filter
change dialysate bath
ensure fluid replacement is post-filter
increase dialysate flow rate
Strategies to improve solute clearance from deranged physiology
- Increase filter lifespan with anticoagulation and predilution
- Rationalise planned interruptions to CRRT (eg. scans and procedures)
- Improve vascular access to minimise interruptions to CRRT
- Increase the blood flow rate
- Increase the dose of dialysis
- Increase the dialysate flow rate
- Increase the ultrafiltration rate
- Increase the replacement fluid rate
- Use of pre-dilution
- Adjustment of dialysate to modify concentration gradients
- Increasing the surface are of the filter
- Female just post-menstrual period present with shock-picture, nausea and vomiting and a sunburn-like rash, elevated CK, etc. They asked for the most likely pathogen.
List 2 immunologic processes at work.
What examination is critical?
o Staph aureus
o 2 immunologic processes at work? TSS – 1 protein Superantigen that hyperstimulates immune system, ?add immune suppression also believed to occur with superantigen stimulation of T cells (?T cell exhaustion?)
Enterotoxic A to E
both of them bypass antigen presenting cell and activate cell directly
o What examination is critical? Pelvic exam
Staphylococcal toxic shock syndrome (TSS) is a clinical illness characterized by rapid onset of fever, rash, hypotension, and multiorgan system involvement. TSS due to Staphylococcus aureus was initially described in 1978; the disease came to public attention in 1980 with the occurrence of a series of menstrual-associated cases.
Micro
Most reported cases of TSS have been due to methicillin-susceptible S. aureus (MSSA). However, as rates of infection due to methicillin-resistant S. aureus (MRSA) have increased, cases of TSS due to MRSA have also emerged [26,27]. MRSA strains are capable of producing TSS toxin-1 (TSST-1) and other exotoxins, and patients infected with these strains may develop TSS.
Immuno
Staph aureus bacteria produce TSS toxin-1 at the site of infection. The toxin then spreads through bloodstream and activates release of cytokines. TSST-1 was determined to induce massive cytokine release from both T cells and macrophages by cross-bridging major histocompatibility complex (MHC) class II molecules on macrophages with T-cell receptors (TCRs) on CD4+ T cells.
from article: Normal T-cell responses usually lead to the activation of approximately 0.0001– 0.001 % of the body’s T-cell population, whereas SAgs can activate 20–30 % of T cells and in some cases up to 70 % of a person’s total T-cell population [54]. Although immense, the SAg-mediated T-cell response is not S. aureus- or SAg-specific, as the SAg directs the response. The inflated number of activated T cells and macrophages secreting large amounts of cytokines is responsible for the clinical symptoms associated with SAgs and TSS, such as capillary leak, hypotension, rash, and fever.
Despite the massive SAg-mediated immune activation, clinical evidence suggests that the outcome of superantigenicity is actually immune suppression. It has been shown that TSS, caused by TSST-1, reactivates endogenous viruses such as herpes simplex virus, previously misleading scientists to mistakenly conclude that a virus was the causative agent of TSS.
Clinical criteria for staphylococcal toxic shock syndrome (issued by the United States Centers for Disease Control and Prevention) Not all needed
Clinical criteria
- Fever: Temperature ≥38.9°C (102.0°F)
- Rash: Diffuse macular erythroderma
- Desquamation: 1 to 2 weeks after onset of rash
- Hypotension: For adults: systolic blood pressure ≤90 mmHg; for children <16 years of age: systolic blood pressure less than 5th percentile by age
- Multisystem involvement (3 or more of the following organ systems):
- Gastrointestinal: Vomiting or diarrhea at onset of illness
- Muscular: Severe myalgia or creatine phosphokinase elevation >2 times the upper limit of normal
- Mucous membranes: Vaginal, oropharyngeal, or conjunctival hyperemia
- Renal: Blood urea nitrogen or serum creatinine >2 times the upper limit of normal or pyuria (>5 leukocytes/high-power field) in the absence of urinary tract infection
- Hepatic: Bilirubin or transaminases >2 times the upper limit of normal
- Hematologic: Platelets <100,000/microL
- Central nervous system: Disorientation or alterations in consciousness without focal neurologic signs when fever and hypotension are absent
Laboratory criteria
- Cultures (blood or cerebrospinal fluid) negative for alternative pathogens (blood cultures may be positive for Staphylococcus aureus)
- Serologic tests negative (if obtained) for Rocky Mountain spotted fever, leptospirosis, or measles
Case classification
- Probable case: A case which meets the laboratory criteria and four of the five clinical criteria
- Confirmed case: A case which meets the laboratory criteria and all five of the clinical criteria, including desquamation (unless the patient dies before desquamation occurs)
- How to differentiate hemoptysis from diffuse alveolar hemorrhage on BAL?
how to identify chronic bleeding?
List 5 causes of pulmonary parenchymal hemorrhage.
Hemosiderin-Iaden macrophages demonstrated with Prussian Blue Staining
BAL demonstrating increase hemorrhage in sequential BAL specimens
chronic bleeding? ???Lack of Prussian blue stained macrophages
- pulmonary vasculitis (granulomatosis with polyangiitis, good pasture’s, Eosinophilic granulomatosis with polyangiitis (Churg-Strauss))
- pneumonia
- PE
- TB
- lupus
- cocaine
- coagulopathy
- pulmonary AVM
- iatrogenic (?recent bronch or biopsy)
Flexible bronchoscopy with sequential bronchoalveolar lavage (BAL) is the preferred method for diagnosis of DAH and should be performed promptly to expedite the evaluation. The fiberoptic bronchoscope is wedged into a subsegmental bronchus in an area where radiographic opacities are noted. Sequential BAL is performed by instilling and retrieving three aliquots of 50 to 60 mL sterile nonbacteriostatic saline from that subsegmental bronchus. Alveolar hemorrhage is confirmed when lavage aliquots are progressively more hemorrhagic, a finding characteristic of DAH from all causes. (See “Basic principles and technique of bronchoalveolar lavage”, section on ‘Technique’.)
Hemosiderin-laden macrophages, which may be demonstrated by Prussian blue staining, are also characteristically found in BAL fluid from patients with DAH [34]. When greater than 20 percent of 200 macrophages stain positive for hemosiderin, a diagnosis of DAH is usually made. I think this also helps identify chronic bleeding on bronch…
- Patient has 40% TBSA and inhalational injury. ECG shows ST changes consistent with myocardial ischemia. List two reasons for these findings.
increased demand: metabolic demands from burn injury, catecholamine surge, tachycardia
decreased supply: ?CAD, ?ARDS/hypoxia from inhalational injury, CYANIDE, CARBON MONOXIDE
- Patient is post-Ivor Lewis esophagectomy and CT consistent with ARDS. List 4 ddx of the CT scan. They then tell you that anastomotic leak and pneumothorax are ruled out and ask for one surgical complication that absolutely must be ruled out and how to do so.
- Pulmonary contusion
- Atelectasis
- Pulmonary edema
- HAP
- aspiration pneumonitis
- ARDS
- pulmonary hemorrhage
o One surgical complication that absolutely must be ruled out and how to do so Conduit ischemia By endoscopy
The more common complications related to the esophagectomy procedure include conduit complications (eg, anastomotic leak, ischemia, stricture), nerve injury, lymphatic leak, functional disorders, and diaphragmatic hernia, which are discussed below. Other rarer complications include airway injury, tracheoesophageal injury, and splenic injury.
Conduit complications — Ischemia and denervation of the conduit are the inherent complications of creating a neoesophagus.
Anastomotic leak — The incidence of anastomotic leak ranges from 5 to 40 percent following esophageal resection and anastomosis, and the mortality associated with leak is between 2 and 12 percent.
Conduit ischemia — Ischemia of the conduit (gastric and colonic) occurs in approximately 9 percent of patients undergoing an esophagectomy [56]. This can vary from minor anastomotic breakdown to, rarely, complete loss of the conduit.
Total conduit ischemia can present as a rapidly deteriorating course with evidence of septic shock. Endoscopy can be a useful tool in such a rapidly deteriorating patient to quickly assess for total conduit ischemia [66], which mandates surgical removal and proximal esophageal diversion.
Anastomotic stricture — Anastomotic stricture occurs in 9 to 40 percent of patients following esophageal resection and reconstruction. Stricture can be due to conduit ischemia or, with later presentation, recurrent disease at the anastomosis.
recullent laryngel nerve injury?stridor post extubation
Chylothorax — The proximity of the thoracic duct to the esophagus translates into a relatively high rate of chyle leaks when compared with other thoracic operations. The diagnosis of a chyle leak is based upon an increase in chest tube output with enteral alimentation and a change in nature of the output from serosanguinous to a milky appearance. Pleural fluid triglyceride level >110 mg/dL or presence of chylomicrons is generally diagnostic of a chyle leak.
- Female patient undergoes aortobifemoral bypass and subsequently has septic shock with rising lactate. What is the most significant finding on imaging?
They asked for the most important step in management?
There is an SMA embolus and pneumatosis intestinalis.
surgical consultation (indication is shock, advanced bowel ischemia which preclude option of endovascular/IR options)
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.
- Patient in a MVC sustains cerebral contusions/Diffuse axonal injury, pelvic hematoma and initially managed as neurogenic shock. Patient now has increasing pressor requirements. They ask for what is now occurring/how to manage?
Most likely due to bleed from the pelvis
- Close pelvic ring externally with binder
- Go to IR for embolization of bleeding
- Massive transfusion protocol
Neurogenic shock — Hypotension and, in some cases, overt shock are common in patients with severe traumatic brain injury and spinal cord injury. Interruption of autonomic pathways, causing decreased vascular resistance and altered vagal tone, is thought to be responsible for distributive shock in patients with spinal cord injury. However, hypovolemia from blood loss and myocardial depression may also contribute to shock in this population.
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 (above the splanchnic sympathetic outflow). 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.
significance of T6 with autonomic dysreflexia which I presume is the same for neurogenic shock:
T6 is of particular importance in the pathogenesis of autonomic dysreflexia. The splanchnic vascular bed is one of the body’s largest reserves of circulatory volume and is controlled primarily by the greater splanchnic nerve. This important nerve derives its innervation from T5-T9. Lesions to the spinal cord at or above T6 allow the strong and uninhibited sympathetic tone to constrict the splanchnic vascular bed, causing systemic hypertension. Lesions below T6 generally allow enough descending inhibitory parasympathetic control to modulate the splanchnic tone and prevent hypertension.
- Similar to above scenario, pelvic fractures, minor TBI and patient unstable with BP 70/30 despite volume resuscitation with heart rate in 110’s. What is the next step in management prior to transport.
?pelvic binder?
Stabilize hypotension as hypotension and hypoxia are the two biggest issues for patients with TBI
Fluid and blood if required
Vasopressor
Target CPP of 60 to 70
Brain trauma foundation guidelines:
Blood pressure thresholds
Level III
• Maintaining SBP at ≥100 mm Hg for patients 50 to 69 years old or at ≥110 mm Hg or above for patients 15 to 49 or >70 years old may be considered to decrease mortality and improve outcomes.
Intracranial pressure thresholds
Level IIB • Treating ICP >22 mm Hg is recommended because values above this level are associated with increased mortality.
Level III • A combination of ICP values and clinical and brain CT findings may be used to make management decisions. *The committee is aware that the results of the RESCUEicp trial2 were released after the completion of these Guidelines. The results of this trial may affect these recommendations and may need to be considered by treating physicians and other users of these Guidelines. We intend to update these recommendations if needed. Updates will be available at https://braintrauma.org/coma/guidelines.
Cerebral perfusion pressure thresholds
Level IIB • The recommended target CPP value for survival and favorable outcomes is between 60 and 70 mm Hg. Whether 60 or 70 mm Hg is the minimum optimal CPP threshold is unclear and may depend upon the autoregulatory status of the patient.
Level III • Avoiding aggressive attempts to maintain CPP >70 mm Hg with fluids and pressors may be considered because of the risk of adult respiratory failure.
- List the three diagnostic criteria for ARDS not related to oxygenation, then list the three oxygenation criteria for classification.
Three diagnostic criteria for ARDS not related to oxygenation
- Timing – within one week of a known clinical insult or new or worsening respiratory symptoms
- Radiographic – B/L opacities not fully explained by collapse, effusions, nodules
- Hypoxia is not due cardiogenic pulmonary edema or fluid overload, need objective assessment (i.e. echo) if no risk factors present
- P:F <300 with PEEP or CPAP >/=5
Oxygenation criteria Mild 200 to 300 Moderate 100 to 200 Severe less than 100
- Female patient post-op from CABG. Easy intubation, but obese and no cuff leak. What would you do (discuss briefly)? What are risk factors for postextubation stridor?
I would probably extubate the patient despite her having a risk factor of female sex but explain my reasoning granted she doesn’t have other risk factors…
CHEST/ATS guidelines:
- We suggest performing a cuff leak test in mechanically ventilated adults who meet extubation criteria and are deemed high risk for postextubation stridor (conditional recommendation, very low certainty in the evidence).
- For adults who have failed a cuff leak test but are otherwise ready for extubation, we suggest administering systemic steroids at least 4 hours before extubation, (conditional recommendation moderate certainty in the evidence).
- Risk factors for postextubation stridor include:
- traumatic intubation
- intubation more than 6 days
- large endotracheal tube
- female sex
- reintubation after unplanned extubation.
- A repeat cuff leak test is not required after the administration of systemic steroids.
- Patient with 165/95, ST elevation in II, III, aVF, pulmonary edema, soft diastolic murmur, pain in chest radiating to neck, list 3 potential diagnoses with this patient.
Type A aortic dissection extending to aortic valve rupture and RCA dissection
RV infarct
Pericarditis
- Patient with inflammatory neck mass with tenderness, mediastinal air-fluid level. What is the diagnosis and what management does this patient need?
Retropharyngeal abscesses are among the most serious of deep space infections, since infection can extend directly into the anterior or posterior regions of the superior mediastinum, or into the entire length of the posterior mediastinum via the danger space.
The cardinal clinical features of parapharyngeal space infections are similar to the general findings of deep neck space infection (see ‘General clinical features’ above) and consist of:
- Trismus (ie, the inability to open the jaw)
- Induration and swelling below the angle of the mandible
- Medial bulging of the pharyngeal wall
- Systemic toxicity with fever and rigors
Complications – Parapharyngeal space infections are potentially life-threatening because of the possibility of involving the carotid sheath and its vital contents (eg, common carotid artery, internal jugular vein, vagus nerve), propensity for airway impingement, and bacteremic dissemination. Suppuration may also advance quickly to other spaces, particularly to the retropharyngeal and “danger” spaces, possibly reaching the mediastinum inferiorly or the base of the skull superiorly.
Treatment
Indications and methods for drainage — For patients who have a dental source of infection, we recommend early removal of that source [36]. Additional initial decisions on drainage for parapharyngeal or retropharyngeal space infections depend upon whether local suppuration has developed or whether only the initial phase of diffuse cellulitis is present. Abscess formation is often difficult to determine clinically but can be identified on imaging studies. This differentiation is important because drainage should be delayed in the cellulitis stage, whereas loculated abscesses should be drained.
Open surgical drainage has been the traditional approach to abscess management. For patients with well-defined deep neck space infections without airway compromise, ultrasound-guided needle aspiration is an effective alternative and is associated with decreased hospital stay and improved cost savings [37,38]. In retropharyngeal space infection complicated by acute necrotizing mediastinitis, surgical drainage of the mediastinum is required and may be performed by either the cervico-mediastinal or the transthoracic approach.
Abx: Ceftriaxone + Metronidazole OR Clindamycin + Levofloxacin
if concern RE ear/mastoid infection: PipTazo
*these Abx choices would be different in immunocompromised pts
my old answer but probably wrong:
(Ludwig’s angina)
- clinical presentation: Patients typically present with fever, chills, and malaise, as well as mouth pain, stiff neck, drooling, and dysphagia, and may lean forward to maximize the airway diameter [7]. They may have a muffled voice or be unable to speak at all. Trismus is usually absent unless there is spread into the parapharyngeal space. As the illness progresses, breathing may become difficult; stridor and cyanosis are considered ominous signs.
- On physical examination, patients have tender, symmetric, and “woody” induration, sometimes with palpable crepitus, in the submandibular area [7]. The mouth is held open by lingual swelling. There is typically no lymphadenopathy. The floor of the oropharynx is usually elevated and erythematous, and is tender to palpation. Occasionally, the inflammation extends to the epiglottis.
Requires antibiotics: Streptococcus (viridans, like anginosus), Peptostreptococcus, Fusobacterium, bacteroides, actinomyces
Abx: Ceftriaxone + Metronidazole
Clindamycin + levofloxacin if pen allergic
Meropenem if penicillin allergic
REMEMBER to secure the airway if necessary
- Diagnostic test for sepsis (prevalence 50%) has a sensitivity of 90% and specificity of 90%. What would happen to the PPV and NPV if the prevalence increased to 80% or decreased to 10%?
see image, with prevalence of 80% PPV = 97%, NPV=69%
with prevalence 10%, PPV=50%, NPV=99%
In biostatistics, prevalence could be considered similar to the pre-test probability. That is, before any testing, the probability of a person in the specified population having the disease is the same as the prevalence of the disease in the population. If the prevalence of a disease is 1% of the population, then we would expect approximately 1 in 100 people to have the disease before any testing.
Prevalence thus impacts the positive predictive value (PPV) and negative predictive value (NPV) of tests. As the prevalence increases, the PPV also increases but the NPV decreases. Similarly, as the prevalence decreases the PPV decreases while the NPV increases.
Osama 20. Treatment for sepsis is being studied. The company is trying to determine the needed sample size. What three things would be needed to determined the appropriate study sample size?
Effect size – how much of an effect do you expect to see (I expect my treatment will reduce mortality from 40% to 30%)
Alpha – the probability of finding a difference when one does not actually exist – if there is no difference and I do the study 100 times, alpha 5% means 5 of these studies will show a difference)
Power – the ability to detect a difference if on actually exists – if there is a difference and I do the study 100 times, a power of 80% means that only 80 of these studies will show there is a difference
…the above is if you’re assuming it’s an RCT looking to calculate sample size needed to show difference between two independent groups in a dichotomous outcome
- Table with ultrafiltration, convection, and diffusive clearance. Define the modes of clearance and give CRRT examples of each mode.
******* does ultrafiltration mean the same thing as hemofiltration? how do you make sure there isn’t any solute drag (i.e. convection)?
My answers:
ultrafiltration - movement of water across a membrane (no cells or colloids) due to a pressure difference across the membrane…?can it be only with CVVH?
convection - solutes are “dragged” by fluid that is moving across the membrane due to hydrostatic pressure gradient….I suppose this happens with CVVH as well
diffusion - solutes move from a more to less concentrated area across a membrane…occurs with CVVHD??
Ultrafiltration is the movement of water across a semi-permeable membrane because of a pressure gradient (hydrostatic, osmotic or oncotic). The increased blood pressure in the glomerulus creates a favourable driving pressure to force water across the glomerular membrane. Blood pressure within the hollow fibers is positive, while the pressure outside the hollow fibers is lower. Increased negativity can be generated outside the hollow fibers by the effluent pump by either increasing the fluid removal rate, or by increasing the replacement flow rate. The difference between the blood pressure in the hollow fibers and the surrounding pressure is the TransMembrane Pressure (TMP). The TMP determines the ultrafiltrate production.
In hemodialysis circuits, pulling large volumes of water across the semi-permeable membrane creates a convective current that “drags” additional solutes. While diffusion is effective at removing most small molecules, convection enhances the removal of small and mid-sized molecules. Thus, convection can be added to hemodialysis therapy to enhance solute removal. To prevent hypovolemia, any water removed during hemofiltration must be returned to the blood before it reaches the patient. This is called “replacement” fluid.
Ultrafiltration describes the transport of plasma water (solvent, free of cells and colloids) through a semipermeable membrane, driven by a pressure gradient between blood and dialysate/ultrafiltrate compartments. It is influenced by the intrinsic properties of the filter, such as the DKUF, and the operating parameters (e.g., TMP). When techniques are discussed, ultrafiltration may be isolated (no other mechanism is utilized in the treatment and only volume control is achieved), be used as part of hemofiltration (the ultrafiltrate is partially or completely replaced achieving volume and solute control), or combined with diffusion in treatments such as hemodialysis (HD) or hemodiafiltration (HDF).
Convection is the process whereby solutes pass through membrane pores, dragged by fluid movement (ultrafiltration) caused by a hydrostatic and/or osmotic transmembrane pressure gradient.
Diffusion is a process whereby molecules move randomly across a semipermeable membrane. Solute movement occurs from a more concentrated to a less concentrated area, until an equilibrium is reached between the two compartments. The concentration gradient (C1 – C2 = dc) is the driving force. The unidirectional solute diffusive flux (Jd) through a semipermeable membrane follows Fick’s law of diffusion, being directly proportional to the diffusion coefficient (D) of the solute and inversely proportional to the distance between the compartments (dx)
- Factors that increase the risk of contrast-induced nephrotoxicity. List 4 or 5 ways of lowering this risk.
o Factors that increase risk of contrast-induced nephrotoxicity
- CKD
- diabetic nephropathy
- CHF
- increased age >75yrs
- hypovolemia
- high osmolarity contrast media
- larger amounts of contrast media
- sepsis/acute hypotension
- previous chemo
- organ transplant
- vascular disease (HTN, CHF, CAD, PVD)
- nephrotoxic meds
Prevention strategies
- avoid dehydration
- use alternative imaging is able to answer diagnostic question
- avoid high osmolar contrast media
- avoid nephrotoxic meds 48h prior to contrast administration
- FLUID is the most important thing
see https://radiology.queensu.ca/source/Radiology/Consensus_Guidelines.pdf
- List of different pacemakers. DDD, DVI, AAI, VOO, possibly one more type. Essentially they were looking for what the nomenclature means/when you would use each one.
Five position code:
I - chamber paced
O = none
A = atrium
V = ventricle
D = dual (A+V)
II - chamber sensed
O = none
A = atrium
V = ventricle
D = dual (A+V)
III - response to sensing
O = none
T = triggered
I = inhibited
D = dual (T+I)
IV - rate modulation, aka rate responsive, rate adaptive pacing
O = none
R = rate modulation
V - multisite pacing (rarely used)
- According to the Canadian Journal of Anesthesia 2013, what would you do in the event of cannot intubate and cannot ventilate (they have already tried direct laryngoscopy and video laryngoscopy. They were looking for two things. Also, what are three predictors of difficult mask ventilation
o Cannot intubate and cannot ventilate (after calling for help)
- 1 attempt at SGD
- proceed to cricothyroidomy
Predictors of dificult BVM ventilation
- Beard
- Old
- Obese
- Toothless
- Snoring
- (Male)
- Pregnant patient being intubated and desaturates. What are two reasons for this in pregnancy?
Decrease FRC
Increase in metabolism and increase in O2 consumption
- List 5 risk factors for invasive candidiasis
- TPN
- CVC
- broad spectrum Abx
- high APACHE scores
- acute renal failure (especially if requiring hemodialysis)
- prior surgery (especially abdominal surgery)
- I think ICU admission is in and of itself a risk factor too
- burn injury
- candida colonization
immunocompromised pts
- hematologic malignancies
- recipients of solid organ or hematopoietic cell transplants
- those given chemotherapeutic agents, especially those associated with extensive GI mucosal damage
- Patient has a tunneled line for dialysis. What are three factors clinical or otherwise that make you strongly think about removing the line. The patient is on his/her third line and access has been a challenge.
- sepsis/hemodynamic instability
- presence of endocarditis/evidence of metastatic infection
- presence of suppurative thrombophlebitis
- presence of bacteremia after 72hrs of appropriate antimicrobial therapy
- subcutaneously tunnelled CVC tunnel tract infection or subcutaneous post resevoir infection\
- candida
- staph aureus
Catheter removal (in addition to administration of systemic antimicrobial therapy) is warranted in the following circumstances, given high likelihood of severe and/or progressive infection with antibiotic therapy alone:
- Sepsis
- Hemodynamic instability
- Presence of concomitant endocarditis or evidence of metastatic infection
- Presence of suppurative thrombophlebitis
- Presence of a propagating clot
- Persistent bacteremia after 72 hours of appropriate antimicrobial therapy
- Subcutaneously tunneled central venous catheter tunnel tract infection or subcutaneous port reservoir infection
In addition, catheter removal is warranted in the setting of infection with the following pathogens, given relatively high virulence and relatively low likelihood of treatment response with antibiotic therapy alone:
- S. aureus
- P. aeruginosa
- Drug-resistant gram-negative bacilli
- Candida spp
Long-term catheters should be removed from patients with CRBSI associated with any of the following conditions: severe sepsis; suppurative thrombophlebitis; endocarditis; bloodstream infection that continues despite >72 h of anti-microbial therapy to which the infecting microbes are susceptible; or infections due to S. aureus, P. aeruginosa, fungi, or mycobacteria (A-II).
This is different than for short-term catheters:
Short-term catheters should be removed from patients with CRBSI due to gram-negative bacilli, S. aureus, enterococci, fungi, and mycobacteria (A-II).
- According to quality initiatives, how do you prevent CRBSI during central line insertion?
Name 2 other quality indicators.
a) CVC insertion bundle
- perform hand hygiene before insertion
- adhere to aseptic technique
- use maximal sterile barrier precautions (mask, cap, gown, gloves, full body drape)
- choose the best insertion site to minimize infections and noninfectious complications based on individual patient characteristics (avoid femorals in obese pts)
- >0.5% chlorhexidine with alcohol
- sterile gauze dressing or sterile transparent semipermeable dressing over site
- For patients 18 years of age or older, use a chlorhexidine impregnated dressing with an FDA cleared label that specifies a clinical indication for reducing CLABSI for short term non-tunneled catheters unless the facility is demonstrating success at preventing CLABSI with baseline prevention practices
b) CVC care bundle
- Comply with hand hygiene requirements
- Bathe ICU patients over 2 months of age with a chlorhexidine preparation on a daily basis
- Scrub the access port or hub with friction immediately prior to each use with an appropriate antiseptic (chlorhexidine, povidone iodine, an iodophor, or 70% alcohol)
- Use only sterile devices to access catheters
- Immediately replace dressings that are wet, soiled, or dislodged
- Perform routine dressing changes using aseptic technique with clean or sterile gloves.
- Change gauze dressings at least every two days or semipermeable dressings at least every seven days.
- For patients 18 years of age or older, use a chlorhexidine impregnated dressing with an FDA cleared label that specifies a clinical indication for reducing CLABSI for short-term non-tunneled catheters unless the facility is demonstrating success at preventing CLABSI with baseline prevention practices.
- Change administrations sets for continuous infusions no more frequently than every 4 days, but at least every 7 days.
- If blood or blood products or fat emulsions are administered change tubing every 24 hours.
- If propofol is administered, change tubing every 6-12 hours or when the vial is changed
c)
- Catheter-related blood stream infection per 1000 catheter days
http://cmajopen.ca/content/5/2/E488.full.pdf+html
- pharmacist on rounds
- appropriate transfusion practices
- VAP bundle (HOB 30deg, SAT+SBT)
- US-guidance for CVC insertion
- pt centered care: documentation of goals of care
- maintain adequate glycemic control
- They provided definitions for Boyle’s Law, Dalton’s Law and Charles’ law and asked for an example of a complication that would occur during fixed wing patient transport based on each law.
Laplace - The larger the vessel radius, the larger the wall tension required to withstand a given internal fluid pressure
Bernoulli - an increase in the speed of a fluid occurs simultaneously with a decrease in pressure or a decrease in the fluid’s potential energy
Poiseuille - It states that the flow (Q) of fluid is related to a number of factors: the viscosity (n) of the fluid, the pressure gradient across the tubing (P), and the length (L) and diameter(r) of the tubing.
Henry - the amount of dissolved gas in a liquid is proportional to its partial pressure above the liquid. (relevant in nitrogen gas in diving I suppose)
Boyle - pressure of a given mass of an ideal gas is inversely proportional to its volume at a constant temperature.
Charles - volume of a gas proportional to temperature (i.e. when temperature of a gas increases so does volume). Charles’ law explains why the ambient temperature decreases with increased altitude.
Henry’s law -mass of gas absorbed by a liquid is directly proportional to the partial pressure of the gas above the liquid. Henry’s law has its most familiar applications in diving medicine, in which the increased pressure exerted on gases in the body at depth forces the gases into solution in the bloodstream. Rapid ascent from depth causes the gas to come out of solution within the bloodstream, resulting in decompression sickness. Henry’s law does not carry the same weight in aviation medicine because the degree of change in atmospheric pressure per unit of distance is considerably less than the degree of change in water. However, sudden decompression at altitude may result in dysbarism.
—> medical contraindication relating to Henry’s law: recent/current decompression illness or recent diving/rapid ascent from depth???
Dalton’s Law - the total barometric pressure at any given altitude equals the sum of the partial pressures of gases in the mixture (Pt = P1 + P2 + P3 … Pn). Whereas oxygen still constitutes 21% of the atmospheric pressure at altitude, Boyle’s law notes that each breath brings fewer oxygen molecules per breath to the lungs, and hypoxia results (Table 191-1). The clinical effect of Dalton’s law is manifested as a decrease in arterial oxygen tension with increasing altitude.—> medical contraindication to Dalton’s law: severe refractory hypoxemia, mayeb recent severe TBI???
Another thought: with recent extremity fracture that is casted: the hypoxic environment causes venodilation, leading to increased venous pooling and increasing the risk of swelling and compartment syndrome. For this reason, any cast (lower or upper extremity) applied for a fracture that is less than 48 hours old must be bivalved before flight.
Patients with COPD often have lower baseline oxygen saturation, particularly during an exacerbation of their disease. Even those who are asymptomatic with a baseline saturation of 93% will encounter difficulties in flight. Breathing air at 8000 ft (ie, the cabin pressure in flight) is equivalent to breathing 15% oxygen at sea level.4 This hypoxic aircraft environment will cause a decrease in your patient’s PaO2. A normal, healthy adult will desaturate to approximately 92% to 93% in flight. This COPD patient will desaturate to approximately 82% in flight and is likely to experience symptoms of hypoxia.
Boyle’s Law - the volume of a unit of gas (“unit” defined as a specific number of molecules) is inversely proportional to the pressure on it. In concrete terms, Boyle’s law means that as altitude increases and atmospheric pressure decreases, the molecules of gas grow apart, and the volume of the gas expands. With descent (increasing atmospheric pressure), the molecules are condensed, and gas volumes contract.
—> medical contraindication to Boyle’s law: simple pneumothorax can become a tension pneumothorax, but also consider other areas of trapped gas (otitis media with a blocked eustachian tube, rupture of a hollow viscus by expansion of intestinal gas, medical equipment with closed air spaces such as ventilator, ETT cuffs, IV tubing and pumps).
Boyle’s law is predominantly responsible for the presence of hypoxia at altitude as there are fewer molecules of oxygen present per volume of inhaled gas at altitude. Similarly, dispersion of molecules of water vapor within a gas volume is seen at height, and “dry air” results.
- Patient with C.difficile and septic shock. They provided a picture of pseudomembranes on endoscopy. They asked for your management and hadn’t given antibiotics yet based on the stem.
I guess first line for fulminant is PO Vanco plus IV Metronidazole
FULMINANT CDI defined as having hypotension, shock, ileus, or megacolon
- 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)
- 2 complications of IABP?
what happens if there is early deflation?
2 contraindications?
- Limb ischemia
- Mesenteric ischemia
- Stroke
- Dissection of iliacs
- Bleeding
early deflation leads to decreased benefits of the IABP:
- suboptimal diastolic augmentation
- suboptimal afterload reduction
- can lead to coronary steal/retrograde flow
- can lead to cerebral steal both from sucking blood back into aorta/lower body
- assisted systolic pressure may be equal or greater than unassisted (?)
2 contraindications:
- Aortic dissection or clinically significant aortic aneurysm
- Aortic regurgitation
- uncontrolled sepsis
- uncontrolled bleeding disorder
- 2 clinical diagnostic criteria for acute liver failure
what are 4 complications of liver transplant?
best prognosticator and what level of this prognosticator would guide you to transplantation in acetaminophen-associated liver failure?
a) severe acute liver injury with encephalopathy and impaired synthetic function (INR>/=1.5)
b) complications:
- hepatic artery thrombosis
- right heart failure
- bleeding
- acute graft dysfunction
- biliary leak/stricture
- pulmonary: acute respiratory failure, pleural effusion, atelectasis
- infections
- malignancy (non melanoma skin, non-hodgkins)
- does Mo agree with the answers from previous year?
Acute liver failure refers to the development of severe acute liver injury with encephalopathy and impaired synthetic function (INR of ≥1.5) in a patient without cirrhosis or preexisting liver disease; time course typically defined as <26wks
c)
King’s College criteria uses encephalopathy grade III or IV but I think acidosis warrants discussion here
As a general rule, the most important factors for predicting the outcome in acute liver failure are the degree of encephalopathy (table 1), the patient’s age, and the cause of the acute liver failure.
Spontaneous recovery is more likely with lower grades of encephalopathy [68]:
- Grade I to II – 65 to 70 percent
- Grade III – 40 to 50 percent
- Grade IV – <20 percent
old answer
o 4 complications of acute liver failure Encephalophathy Coagulopathy Cerebral edema Hepatorenal Syndrome Hepatopulmonary syndrome/shunt Hypoglycemia Ascites Hyperbillirubinemia o Best prognosticator and what level of this prognosticator would you guide to transplantation? Grade of encephalopathy Probability of spontaneous recovery: • Degree of encephalopathy • Age • Cause of acute liver failure
- What happens to the solubility of O2 and CO2 with decreasing temperature? How would you manage PaCO2 and pH in hypothermia (list two methods)
solubility increases as temperature decreases and therefore partial pressure decreases (think soda cans when warmed - they lose their CO2)
pH-Stat
During pH-stat acid-base management, the patient’s pH is maintained at a constant level by managing pH at the patient’s temperature. pH-stat pH management is temperature-corrected. Compared to alpha-stat, pH stat (which aims for a pCO2 of 40 and pH of 7.40 at the patient’s actual temperature) leads to higher pCO2 (respiratory acidosis), and increased cerebral blood flow. Often CO2 is deliberately added to maintain a pCO2 of 40 mm Hg during hypothermia.
Alpha-Stat
During alpha-stat acid-base management, the ionization state of histidine is maintained by managing a standardized pH (measured at 37C). Alpha-stat pH management is not temperature-corrected – as the patient’s temperature falls, the partial pressure of CO2 decreases (and solubility increases), thus a hypothermic patient with a pH of 7.40 and a pCO2 of 40 (measured at 37C) will, in reality, have a lower pCO2 (because partial pressure of CO2 is lower), and this will manifest as a relative respiratory alkalosis coupled with decreased cerebral blood flow. During alpha-stat management you have no idea what the patient’s pCO2 is, your goal is to maintain a constant dissociation state of histidine.
Arguments for using pH-stat management include increased cerebral blood flow to decrease the duration of cooling as hypothermia is induced and to potentially decrease the duration of rewarming [79]. However, cerebrovascular disease may decrease vascular reactivity in response to arterial CO2 concentration leading to impaired cooling of brain regions supplied by diseased vessels if pH-stat management is used.
for every degree C below 37…
pH increases by 0.12
pao2 drops 5
PCO2 drops by 2
- Graph of venous filling and Cardiac output versus right atrial pressure and asked for clinical context based on these (hypovolemic shock, cardiogenic and distributive shock states illustrated)
see image
- 96 yo day 4 post cardiac arrest. Neuro exam shows conjugate ipsilateral gaze to cold caloric testing, no motor response. CT head is done and is normal, EEG show burst suppression:
a. What do you say about EEG findings and prediction of neurological recovery?
b. Wife asks how can CT be normal and EEG abnormal – how do you reply to that?
c. Patient survives with normal sleep wake cycle – what is this called in medical terms and how would you explan this to the wife in non-medical terms?
EEG AHA 2015 Recommendations—Updated
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).
Imaging
some evidence that reduced grey-white ratio and diffuse edema are poor prognostic markers but no mention about “normal CT head” which I suspect means it is not sensitive in general.
2015 Recommendations—New
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.163 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.
Persistent vegetative state — Patients in a persistent vegetative state (PVS) represent a subgroup of patients who suffer severe anoxic brain injury and progress to a state of wakefulness without awareness. A vegetative state may represent a transition between coma and recovery or between coma and death. The term was first used in 1972 and is defined as [4,6,9-12]:
- No evidence of awareness of self or environment and an inability to interact with others
- No evidence of sustained, reproducible, purposeful, or voluntary behavioral responses to visual, auditory, tactile, or noxious stimuli
- No evidence of language comprehension or expression
- Intermittent wakefulness manifested by the presence of sleep-wake cycles
- Sufficiently preserved hypothalamic and brainstem autonomic function to permit survival with medical and nursing care
- Bowel and bladder incontinence
- Variably preserved cranial nerve reflexes and spinal reflexes
PVS is judged to be permanent after three months if induced nontraumatically. For traumatic brain injury, a year in this state is generally required to be considered permanent.
Minimally conscious state — The term minimally conscious state (MCS) has been proposed to describe patients who do not meet criteria for persistent vegetative state [23]. As with PVS, these patients have a severe alteration in consciousness. In contrast to PVS, they may intermittently demonstrate limited interaction with the environment by visually tracking, following simple commands, signaling yes or no (not necessarily accurately), or having intelligible verbalization or restricted purposeful behavior.
List the RIFL and AKIN criteria for AKI.
RIFL
see image in q
AKIN
A report by the AKIN proposed the following criteria for AKI [8, 9] :
- Abrupt (within 48 h) reduction in kidney function currently defined as an absolute increase in serum creatinine of 0.3 mg/dL or more (≥26.4 μmol/L) or
- A percentage increase in serum creatinine of 50% or more (1.5-fold from baseline) or
- A reduction in urine output (documented oliguria of < 0.5 mL/kg/h for >6 h)
The AKIN criteria differ from the RIFLE criteria in several ways. The RIFLE criteria are defined as changes within 7 days, while the AKIN criteria suggest using 48 hours. The AKIN classification includes less severe injury in the criteria and AKIN also avoids using the glomerular filtration rate as a marker in AKI, as there is no dependable way to measure glomerular filtration rate and estimated glomerular filtration rate are unreliable in AKI.
