2016 Flashcards
Chest CT with pulmonary infiltrates / innumerable nodules, plus picture of lesions on hands, feet, and nose. What is characteristic finding on chest CT?
DDx? (list 4possibilities) Diagnostic Test? (skin Biopsy)
TB
sarcoid
vasculitis, i.e. GPA
other infections (nocardia, fungal, mycobacterial)
malignancy
syphillis (case reports)
Various Guyton Curves shown. Label each with clinical syndrome. There was one for CHF, hypovolemic, and hyperdynamic shock.
see image
ASD: list 5 complications in a patient with sepsis and known Atrial septal defect
***not sure how these are specific to sepsis***
atrial arrhythmias
intracardiac shunting -> RV volume overload (if L to R) eventually causing pulmonary vascular injury then pulm HTN then RV failure
shunting -> if R to L could cause hypoxia (typically via Eisenmenger’s syndrome)
systemic thromboembolism
?infective endocarditis
Patient with normal LVEF but low cardiac output and shock. List 5 possible etiologies or “cardiac findings” (meaning of latter was not clear. Physical findings? unclear question)
- mitral regurgitation
- aortic regurgitation
- hypovolemia (i.e. low LVEDV to begin with causing low SV)
- right heart failure (PE?) which can still have a “normal” LVEF but the LV would be small/underfilled
- cardiac tamponade, again a small/underfilled LV which is ejecting “normal” EF but small SVs
Match the following laws with their definitions: Laplace’s, Bernoulli, Poiseuille,
Henry’s, Boyle’s
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)
ECMO - list benefits/drawbacks of VA vs VV ECMO
VA - provides cardiac and respiratory support
- higher risks with vascular access (bleeding, limb ischemia)
- always requires at least 2 catheters (VV can be one or two)
- bypasses pulmonary circulation therefore can decrease pulmonary artery pressures
- can be used in RV failure
- overall VA ECMO has higher complications that VV ECMO (highest complication is bleeding and rates are higher in VA than with VV ECMO)
additional VA ECMO only complications from uptodate:
- Pulmonary hemorrhage - Pulmonary edema and hemorrhage can occur in patients who have no left ventricular (LV) emptying during VA ECMO. Edema occurs when the left atrial (LA) pressure exceeds 25 mmHg. It is treated by venting the LA or LV
- cardiac thrombus - There is retrograde blood flow in the ascending aorta whenever the femoral artery and vein are used for VA ECMO. Stasis of the blood can occur if left ventricular output is not maintained, which may result in thrombosis
- Coronary or cerebral hypoxia – During VA ECMO, fully saturated blood infused into the femoral artery from the ECMO circuit will preferentially perfuse the lower extremities and the abdominal viscera. Blood ejected from the heart will selectively perfuse the heart, brain, and upper extremities. As a result, the oxyhemoglobin saturation of the blood perfusing the lower extremities and abdominal viscera may be substantially higher than that perfusing the heart, brain, and upper extremities. Cardiac and cerebral hypoxia could exist and be unrecognized if oxygenation is monitored using only blood from the lower extremity. To avoid this complication, arterial oxyhemoglobin saturation should be monitored in the right upper extremity. Poor arterial oxyhemoglobin saturation measured from the upper extremity is corrected by infusing some oxygenated blood into the right atrium (called VA-V access).
Malaria - Dx test and 7 complications
Dx test: thick and thin peripheral blood smear
- Clinical tools for parasite-based diagnosis include microscopy (visualization of parasites in stained blood smears) and rapid diagnostic tests (RDTs; which detect antigen or antibody). Smear examination via light microscopy is the standard tool for diagnosis of malaria; RDTs should be used if microscopy is not readily available.
- Two types of blood smears are used in malaria microscopy: thin and thick smears. Thin smear preparation maintains the integrity and morphology of erythrocytes so that parasites are visible within red blood cells. Thin smears allow identification of the infecting parasite species and can be used to measure parasite density. Thick smear preparation involves mechanical lysis of red blood cells so that malaria parasites can be visualized independent of cell structures. Thick smears allow the microscopist to review a relatively large quantity of blood and are typically used to screen for presence or absence of parasites and to estimate parasite density.
Following the bite of an infected female Anopheles mosquito, the inoculated sporozoites go to the liver within one to two hours. Individuals are generally asymptomatic for 12 to 35 days but can commence symptoms as early as 7 days (depending on parasite species), until the erythrocytic stage of the parasite life cycle (figure 1). Release of merozoites from infected red cells when they rupture causes fever and the other manifestations of malaria.
In most cases, the incubation period for P. falciparum infection is about 12 to 14 days (range 7 to 30 days); most infections due to P. falciparum become clinically apparent within one month after exposure.
Uncomplicated malaria — Malaria should be suspected in patients with any febrile illness if they have had exposure to a region where malaria is endemic [1,2,6]. The initial symptoms of malaria are nonspecific and may also include tachycardia, tachypnea, chills, malaise, fatigue, diaphoresis (sweating), headache, cough, anorexia, nausea, vomiting, abdominal pain, diarrhea, arthralgias, and myalgias [2,6]. Patients are considered to have uncomplicated malaria in the setting of symptoms of malaria and a positive parasitological test in the absence of signs of severe malaria [10].
Physical findings may include manifestations of anemia and a palpable spleen.
Laboratory evaluation may demonstrate parasitemia (usually <5000 parasites/microL of blood, <0.1 percent parasitized red blood cells [RBCs]), anemia, thrombocytopenia, elevated transaminases, mild coagulopathy, and elevated blood urea nitrogen (BUN) and creatinine.
Early in the course of malaria infection, febrile paroxysms occur at irregular intervals each day. The temperature of nonimmune individuals and children may rise above 40ºC and may occur in conjunction with tachycardia and/or delirium. Febrile convulsions may occur among children in the setting of malaria due to any species. However, generalized seizures are associated with falciparum and may herald the development of cerebral malaria.
Severe Malaria - Many of the clinical findings are the result of the parasitized (and nonparasitized) RBCs adhering to small blood vessels (“cytoadherence”) causing small infarcts, capillary leakage, and organ dysfunction; these include the following [6,14,15]:
- Altered consciousness with or without seizures
- Respiratory distress or acute respiratory distress syndrome (ARDS)
- Noncardiogenic pulmonary edema (eg, adult respiratory distress syndrome) may be observed in adults with severe falciparum malaria [35]. The pathogenesis is uncertain but may be related to sequestration of parasitized red cells in the lungs and/or cytokine-induced leakage from the pulmonary vasculature.
- Circulatory collapse
- Metabolic acidosis
- Renal failure, hemoglobinuria (“blackwater fever”)
- Hepatic failure
- Coagulopathy with or without disseminated intravascular coagulation
- Severe anemia or massive intravascular hemolysis
- Hypoglycemia (from: Diminished hepatic gluconeogenesis, Depletion of liver glycogen stores, Increase in the consumption of glucose by the host (and, to a much lesser extent, the parasite), Quinine-induced hyperinsulinemia)
Cerebral malaria is an encephalopathy that presents with impaired consciousness, delirium, and/or seizures; focal neurologic signs are unusual. The onset may be gradual or sudden following a convulsion. The severity depends on a combination of factors including parasite virulence, host immune response, and time between onset of symptoms and initiation of therapy.
Risk factors for cerebral malaria include age (children and older adults), pregnancy, poor nutritional status, HIV infection, host genetic susceptibility, and history of splenectomy.
Septicemia may complicate severe malaria, particularly in children [36]. In endemic areas, Salmonella bacteremia has been associated with P. falciparum infections [37]. Chest infections and catheter-induced urinary tract infections are common among patients who are unconscious for ≥3 days. Aspiration pneumonia may follow generalized seizures.
HIV infection — HIV and malaria often coexist. Both conditions induce cell-medicated immunodepression.
Family meeting with moribund patient. 4 strategies to approach family meeting. The meeting does not go well and the family is angry. What are 2 effects on the family?
SPIKES mnemonic
S - setting up the interview (privacy, involve significant others, sit down, connect w pt, manage time constraints/interruptions)
P - assessing the patient’s Perception, ask pt what they’ve been told or what they understand
I - obtain the pts Invitation
K - giving Knowledge and information
E - addressing the pt’s Emotion with Empathic responses
S - Strategy and Summary
Other: invite nurse, chaplain, social worker to family meeting
effects on the family
Psychological conditions are common among the family members of patients in the ICU. This was illustrated by a study of 920 family members, in which the prevalence of anxiety and depression was 69 percent and 35 percent, respectively [30]. In another report, approximately one-third of family members developed symptoms that suggested that they were at moderate to major risk of developing posttraumatic stress disorder (PTSD)
List 3 patient-centered reasons to withdrawing life sustaining therapy
- discomfort/pain associated with intervention (non-maleficence)
- limited chance for cure/positive outcome (beneficence)
- autonomy over decisions and death process
List the qSOFA criteria for sepsis
Hypotension SBP <1/=00
Altered mental status (GCS<15)
Tachypnea (RR>/=22)
The score ranges from 0 to 3 points. The presence of 2 or more qSOFA points near the onset of infection was associated with a greater risk of death or prolonged intensive care unit stay. These are outcomes that are more common in infected patients who may be septic than those with uncomplicated infection. Based upon these findings, the Third International Consensus Definitions for Sepsis recommends qSOFA as a simple prompt to identify infected patients outside the ICU who are likely to be septic.
The diagnosis of infection was left to the clinician, while the TF recommended that an acute change of more than 2 sepsis-related organ dysfunction assessment (SOFA) points would identify sepsis.
But the SOFA score requires multiple laboratory tests and may not be available in a timely manner. To facilitate simple recognition in prehospital, ward, and the emergency department, the Task Force recommended a prompt called “qSOFA” for quick sepsis-related organ dysfunction assessment score.
Pulmonary hemorrhage secondary to U/S guided endobronchial Bx.
Management (4)
endobronchial management (3)
definitive management (2)
- a) bleeding side down
- inhaled TXA (has been tested in non-massive hemoptysis)
- lung isolation via mainstem intubation
- correct coagulopathy (plts if uremic or on antiplts, Vit K/octaplex, praxbind)
- consider factor VII as rescue
- b) lung isolation via bronchial blocker
- ice cold saline via bronch
- epinephrine via bronch
- c) argon plasma coagulation
- embolization
- surgery
Post-CABG extubation questions - this was a repeat
???
Re-feeding syndrome - what are two most common labs are abnormal?
What are 4 labs that should be done to monitor?
What are 2 things to avoid when starting TPN?
a) hypophosphatemia, hypokalemia
b) PO4, K, Mg, and would probably choose Na over Ca
c) ?avoid starting feeds at full caloric needs (target 80% or 20kcal/kg/d)
?avoid feeds until given thiamine
Ebola - what are 3 components of extra PPE required not part of usual PPE?
Trained Observer - Because the sequence and actions involved in each donning and doffing step are critical to avoid exposure, a trained observer should read aloud to the healthcare worker each step in the procedure checklist and visually confirm and document that the step has been completed correctly. The trained observer has the sole responsibility of ensuring that donning and doffing processes are adhered to.
Impermeable garment:
- Single-use (disposable) impermeable gown extending to at least mid-calf.
OR
- Single-use (disposable) impermeable coverall.
Respiratory Protection: Either a PAPR (powered air purifying respirator) or disposable, NIOSH-certified N95 respirator should be worn in case a potentially aerosol-generating procedure needs to performed emergently. PAPRs with a full-face covering and head-shroud make accidental self-contamination during care more difficult (e.g., while adjusting eyeglasses); disposable N95 face piece respirators are less cumbersome and can be easier to doff safely.
Single-use (disposable) examination gloves with extended cuffs. Two pairs of gloves should be worn so that a heavily soiled outer glove can be safely removed and replaced during care. At a minimum, outer gloves should have extended cuffs.
Single-use (disposable) boot covers that extend to at least mid-calf.
Single-use (disposable) apron that covers the torso to the level of the mid-calf should be used over the gown or coveralls if patients with Ebola are vomiting or have diarrhea, and should be used routinely if the facility is using a coverall that has an exposed, unprotected zipper in the front.
SVT in asthmatic. What are two medications that can be used to Rx?
(Adenosine and Beta-blocker are CI)
non-dihydropyridine CCB (diltiazem, verapamil)
amiodarone
+/-procainamide
- Procainamide, like quinidine and disopyramide, can significantly increase the ventricular rate in patients with uncontrolled atrial fibrillation or flutter. Two factors contribute to this response:
- By slowing the atrial rate of atrial fibrillation or atrial flutter, procainamide increases the likelihood that a given impulse will pass through the AV node, thereby potentially increasing the ventricular rate.
- Procainamide has a direct vagolytic action on the AV node, increasing conduction through the AV node.
- Therefore, when administering procainamide for chemical cardioversion of atrial fibrillation, conduction through the AV node must be slowed and the ventricular response controlled (using ß-blockers, calcium channel blockers, or digitalis) before therapy with procainamide is initiated in these disorders
Drunk patient gets electrical shock from power lines. List 4 complications from electrical shock.
?rhabdomyolysis causing renal injury
cardiac arrhythmias (The overall estimate of arrhythmia following electrical injury is approximately 15 percent; most of these are benign and occur within the first few hours of hospital admission. However, acute electrical cardiac injury can result in sudden cardiac arrest due to asystole (usually with DC current or lightning) or ventricular fibrillation (AC current) prior to hospitalization. Ventricular fibrillation is the most common fatal arrhythmia.)
skin/surface burns: Superficial, partial-thickness, and full-thickness thermal burns can occur following electrical injury
weakness, decreased LOC, respiratory depression, autonomic dysfunction, memory disturbances. Damage to both the central and peripheral nervous systems can occur after electrical injury. Manifestations may include loss of consciousness, weakness or paralysis, respiratory depression, autonomic dysfunction, and memory disturbances. Sensory and motor findings due to peripheral nerve damage are common.
bone destruction: Because bone has the highest resistance of any body tissue, it generates the greatest amount of heat when exposed to an electrical current. Thus, the areas of greatest thermal injury are often the deep tissue surrounding long bones, potentially resulting in periosteal burns, destruction of bone matrix, and osteonecrosis.
compartment syndrome
electrical coagulation of small blood vessels
Pressure-time and flow-time curves shown for a patient on PCV. what is the
problem?
What are 4 mitigation strategies?
autopeep
- decrease tidal volume (i.e. Insp pressure in PCV)
- decrease I-time
- decrease RR
- ?technically you could decrease the inspiratory rise time to slightly decrease the tidal volume
treat possible bronchoconstriction?
Treatment of autoPEEP - Steps should be taken to correct auto-PEEP as soon as it is identified. Initial efforts should focus on determining and treating the underlying cause. When auto-PEEP persists despite management of its underlying cause, applied PEEP may be helpful if the patient has an expiratory flow limitation.
When a high minute ventilation is the presumed cause of auto-PEEP, the minute ventilation should be decreased by lowering the tidal volume or respiratory rate. This frequently requires a strategy of permissive hypercapnia. (See “Permissive hypercapnia during mechanical ventilation in adults”.)
When an expiratory flow limitation due to obstructive airways disease is the presumed cause of auto-PEEP, the duration of expiration should be prolonged. This can be accomplished by increasing the inspiratory flow, decreasing the tidal volume, or decreasing the respiratory rate.
Treatment with bronchodilators, steroids, and antibiotics may also be beneficial. In a study of 25 patients with COPD and acute respiratory failure, expiratory flow limitation was present in 96 percent of the patients at the initiation of mechanical ventilation [51]. The prevalence of expiratory flow limitation decreased to 47 percent at the time of extubation and 40 percent at the time of ICU discharge, indicating that expiratory flow limitation may respond to therapy.
When increased expiratory resistance is the presumed cause of auto-PEEP, the source of increased resistance should be identified and corrected. This may require sedation, pharmacologic paralysis, or replacement of the endotracheal tube or ventilator tubing.
Applied PEEP — Small amounts of applied PEEP can decrease auto-PEEP in patients who have an expiratory flow limitation [52-54]. This can be conceptualized as the applied PEEP holding open the narrowed airways during expiration, improving expiratory airflow, and allowing more complete expiration prior to the onset of the next breath. Additional benefits of using applied PEEP to offset auto-PEEP include decreased oxygen consumption and improved gas exchange. The latter is due to opening the small airways in the dependent lung zones and distributing inspired gas more homogeneously [55-57].
Applied PEEP should always be less than the measured auto-PEEP [58]. Otherwise, alveolar pressure may increase, placing the patient at increased risk for complications such as pulmonary barotrauma or hypotension (figure 5). One study even suggested that applied PEEP does not need to exceed the measured auto-PEEP for this to occur. Rather, it can occur if the applied PEEP is greater than 85 percent of the measured auto-PEEP [59]. Given the potential inaccuracy of auto-PEEP measurements, it is prudent to set applied PEEP to a level that is less than 50 percent of the measured auto-PEEP. Research has shown that mechanical ventilation with PEEP induces longitudinal atrophy by displacing the diaphragm in caudal direction and reducing the length of fibers. As a result, muscle fibers generate less force causing diaphragm weakness [60]. This may exacerbate diaphragm weakness in critically ill patients thus prolonging mechanical ventilation. This advocates for maintaining the lowest required PEEP setting.
Applied PEEP should not be used to counter auto-PEEP in patients who do not have an expiratory flow limitation. Applied PEEP may increase alveolar pressure and increase the risk of both barotrauma and hemodynamic compromise in this setting [61].
Hypoxemic respiratory failure with ARDS.
What are 2 ways to improve SpO2?
What are 3 strategies that have been proven to reduce mortality?
What are 2 strategies that can improve hypoxemia but do not improve mortality?
a) recruitment maneuvres, inhaled pulmonary vasodilators, high PEEP strategy
b) lung protective ventilation (low tidal volume), NMB, prone positioning
c) recruitment maneuvres, inhaled pulmonary vasodilators, HFO (by way of a higher mean airway pressure)
Echo image showing obviously dilated RV in patient with ARDS. What therapy can be used to mitigate this problem?
- inhaled pulmonary vasodilators: inhaled nitric oxide, inhaled epoprostenol
- prone positioning
4 hemodynamic profiles shown with CO, CI, SVR, PA pressures, wedge pressures, and CVP values given. Asked what can be added to help. There was one with LV failure, one RV failure, one with hypovolemic shock, and one with distributive shock / profound vasoplegia.
Normal values are:
cardiac output 4-8L/min
cardiac index 2.5-4L/min/m2
SVR 800-1200dynes/s/cm5
PA systolic 20-30mm Hg
PA diastolic 8-12mm Hg
PA mean 25mm Hg
wedge pressure 4-12mm Hg
CVP 2-6mm Hg
What is the oxygen delivery equation?
What is the transfusion threshold in sepsis?
a) see image
DO2=CO x [(1.34 x Hgb x SaO2) + (0.003 x PaO2)]
b) 70g/L
from guidelines: “1. We recommend that RBC transfusion occur only when hemoglobin concentration decreases to < 7.0 g/dL in adults in the absence of extenuating circumstances, such as myocardial ischemia, severe hypoxemia, or acute hemorrhage (strong recommendation, high quality of evidence).”
Toxidrome given (it was almost completely for sure anticholinergic) What are 3 things/syndromes that could match this?
What are 2 things that are characteristic of each of these possible syndromes (to differentiate them? unclear exactly what they wanted)
Anticholinergic toxidrome
- “Red as a beet” – Cutaneous vasodilation occurs as a means to dissipate heat by shunting blood to the skin, in order to compensate for the loss of sweat production.
- “Dry as a bone” (anhidrosis) – Sweat glands are innervated by muscarinic receptors, so anticholinergic medications produce dry skin.
- “Hot as a hare” (anhydrotic hyperthermia) – Interference with normal heat dissipation mechanisms (ie, sweating) frequently leads to hyperthermia.
- “Blind as a bat” (nonreactive mydriasis) – Muscarinic input contributes to both pupillary constriction and effective accommodation. Anticholinergic medications generally produce pupillary dilation and ineffective accommodation that frequently manifests as blurry vision.
- “Mad as a hatter” (delirium; hallucinations) – Blockade of muscarinic receptors in the central nervous system (CNS) accounts for these findings. Manifestations may include: anxiety, agitation, dysarthria, confusion, disorientation, visual hallucinations, bizarre behavior, delirium, psychosis (usually paranoia), coma, and seizures. Hallucinations are often described as “Alice in Wonderland-like” or “Lilliputian type,” where people appear to become larger and smaller. Patients with altered mental status often present with agitation and may appear to grab invisible objects from the air [15]. Although central and peripheral anticholinergic effects are commonly seen together, in some cases, central effects may persist after resolution of peripheral symptoms.
- “Full as a flask” – The detrusor muscle of the bladder and the urethral sphincter are both under muscarinic control; anticholinergic substances reduce detrusor contraction (thereby reducing or eliminating the desire to urinate) and prevent normal opening of the urethral sphincter (contributing to urinary retention).
Anticholinergic poisons
- antihistamines
- tricyclic antidepressants (amitriptyline)
- sleep aids (doxylamine)
- scopolamine
- tainted illicit street drugs (heroin “cut” with scopolamine)
- jimson weed
- deadly nightshade (atropa belladonna)
While systemic effects generally improve spontaneously within several hours, treatment with physostigmine may be needed for severe toxicity
b) DDx:
?sympathomimetic
?serotonin
?salicylates
Any substance or condition that produces an alteration in mental status, tachycardia, urinary retention, or seizure should be included in the differential diagnosis. A wide range of medical conditions and drugs can cause agitated delirium.
Sympathomimetic overdose and serotonin toxicity may cause agitation, tachycardia, and hyperthermia, but can usually be differentiated from anticholinergic toxicity. Sympathomimetic overdose and serotonin toxicity generally cause diaphoresis, in contradistinction to anticholinergic overdose.
In agitated, hyperthermic patients with altered mental status, salicylate overdose should also be considered.
Ischemic colon - how to manage - 4 non-operative options
- Nothing by mouth, nasogastric decompression.
- Fluid therapy to maintain adequate intravascular volume and visceral perfusion and monitored as normal urine output.
- Avoidance of vasopressors, which can exacerbate ischemia.
- Antithrombotic therapy consists of anticoagulation (unfractionated heparin, weight-based protocol) to limit thrombus propagation and help alleviate associated arteriolar vasoconstriction with or without antiplatelet therapy [32].
- Empiric broad-spectrum antibiotic therapy.
- Proton pump inhibitors [33].
- Supplemental oxygen [33].
Approach to treatment — Clinical evaluation and vascular imaging determine whether the patient is a candidate for vascular intervention and whether the occlusion is embolic or thrombotic, which has a bearing on the type of intervention offered. The goal of vascular intervention is to restore intestinal blood flow as rapidly as possible. The specific treatment chosen depends upon the clinical status of the patient and the etiology and location of the occlusion. Optimal treatment may include open, endovascular, or a combined approach. The ability to offer an endovascular approach depends upon local resources and the availability of vascular specialists. A hybrid interventional suite/operating room may be the ideal setting to manage acute mesenteric arterial occlusion, but these are generally available only at large vascular centers.
Some patients (eg, acute-on-chronic occlusion) who are hemodynamically stable and do not have clinical signs of advanced bowel ischemia can be observed while on heparin anticoagulation, if there is evidence of good collateral blood flow on vascular imaging studies. Antiplatelet therapy may be justified in this setting if the risk of progressive ischemia appears to be greater than the risk of bleeding [32,34]. The patient should have serial clinical assessment (laboratory, physical examination) with a low threshold to repeat abdominal imaging studies or, if abdominal symptoms progress, surgical or endovascular intervention.
A palliative approach may be the best option for poor-risk surgical candidates with extensive transmural infarction (eg, small bowel up to the midtransverse colon). Extensive bowel resection would be inappropriate for these patients and may also be inappropriate for a subset of patients who might otherwise be expected to tolerate the procedure but for whom lifelong parenteral nutrition would be unacceptable
Patients who are good-risk surgical candidates with indications for immediate laparotomy such as peritonitis or radiologic features of advanced bowel ischemia (free air, extensive pneumatosis) should be taken directly to the operating room for exploration. Resection of bowel should ideally be delayed until after mesenteric arterial revascularization can be performed to salvage as much bowel as possible; however, in practice, this sequence does not commonly occur. In situations where an individual with appropriate vascular expertise is not immediately available, resection of grossly necrotic or perforated bowel (leaving any questionable bowel) while awaiting intraoperative consultation is appropriate, or, alternatively, following resection, abdominal closure and transfer is also a reasonable option when required.
The traditional treatment for mesenteric embolism is open surgical embolectomy, which, in addition to expeditiously clearing the thrombus, allows direct assessment of bowel viability.
Open surgical treatment of mesenteric artery thrombosis is treated principally with mesenteric bypass. Thrombectomy alone is unlikely to offer a durable solution due to the presence of thrombogenic atherosclerotic plaques. Intraoperative retrograde superior mesenteric artery angioplasty and stenting is another option, particularly in the presence of gross contamination where bypass is more problematic.
Patients who are hemodynamically stable and who do NOT have clinical or radiologic signs of advanced intestinal ischemia may be candidates for a primary endovascular approach.
Aflutter post cardiac surgery. Adenosine is given and they show a strip. What
are pharmacological options to break it? If it persists, what must be done?
???
Rate control — Given the transient nature of the arrhythmia (see ‘Incidence and time course’ above), initial control of the ventricular response rate is an effective and relatively safe strategy in many patients who develop postoperative AF [44,128].
Rate control is most commonly achieved with beta blockers. The benefit is partly due to blockade of the augmented postoperative sympathetic state and to prevention of beta blocker withdrawal in patients on beta blockers preoperatively. Intravenous esmolol, a beta blocker with a short half-life, can be given for acute rate control if there is a concern for bradyarrhythmias, hypotension, or bronchospasm. Slowing of the ventricular rate in many AF patients receiving inotropic agents postoperatively can be achieved by lowering the dose or discontinuation of these agents.
Rhythm control — Restoration of sinus rhythm from well-tolerated postoperative AF is usually not necessary but occasionally can be beneficial. (See ‘Incidence and time course’ above.)
Restoration of sinus rhythm is indicated in symptomatic patients or in those when rate control is difficult to achieve. An attempt at the restoration of sinus rhythm can be beneficial in patients with a low ejection fraction. In addition, cardioversion in asymptomatic patients may be reasonable when well-tolerated AF occurs near the time of anticipated hospital discharge or when it does not spontaneously terminate within 24 hours, so that oral anticoagulation can be avoided; this is particularly true in patients at high risk of bleeding.
Our approach to postoperative anticoagulation — Among patients who develop AF following cardiac surgery, we suggest the following approach to anticoagulation:
- For patients with multiple episodes of AF or one episode that lasts more than 24 to 48 hours, we recommend the initiation of oral anticoagulant therapy, but only if bleeding risks are considered acceptable. As the role of direct thrombin and factor Xa inhibitors has not been established for patients with postoperative AF, we suggest that warfarin be chosen for most patients (International normalized ratio 2.0-3.0).
- We suggest continuation of anticoagulation for at least four weeks after return to sinus rhythm, particularly if the patient has risk factors for thromboembolism. Longer duration of anticoagulation is recommended by some of our experts in patients with high CHA2DS2-VASc scores (table 3), at low risk for bleeding based on the HAS-BLED score (table 4), or at high risk of AF recurrence.
- Long-term anticoagulation should be considered for patients who remain in AF or who have paroxysmal AF at four weeks.
Apixiban and ICH, last dose 2h ago.
What 4 things can be done to reverse it?
What are major complications of Apixiban reversal?
a)
- andexanet alpha
- 4 factor unactivated PCC (i.e. Octaplex if andexanet alpha is not available)
- antifibrinolytic agent (TXA)
- oral activated charcoal (Intracranial hemorrhage associated with oral non-vitamin K antagonist anticoagulants (off-label use): Oral, enteral: 50 g within 2 hours of ingestion of an oral direct thrombin inhibitor (dabigatran) or an oral direct factor Xa inhibitor (eg, apixaban, edoxaban, or rivaroxaban).
Direct factor Xa inhibitors cannot be removed by hemodialysis.
b) adverse events: thromboses (arterial and venous) but a significant proportion occured >5d after getting andexanet alpha suggesting it may have been related to pts underlying thrombotic risk
50F post-trach (decannulated) with new respiratory distress on floor. PFTs show image. What is Dx?
tracheal stenosis
from image:
A - normal
B - variable extrathoracic
C - variable intrathoracic
D - fixed upper airway obstruction (can be intra or extra-thoracic)
E - peripheral (i.e. lower airways) obstruction
CT head with acute stroke. What is shown on CT?
What 2 therapies are available?
What one test must you do before giving tPA?
tPA, endovascular clot retrieval
- Mechanical thrombectomy is indicated for patients with acute ischemic stroke due to a large artery occlusion in the anterior circulation who can be treated within 24 hours of symptom onset or the time last known to be well at stroke centers with appropriate expertise, regardless of whether they receive intravenous alteplase for the same ischemic stroke event.
test glucose
- The history, physical examination, serum glucose, oxygen saturation, and a noncontrast CT scan are sufficient in most cases to guide acute therapy (see ‘Immediate laboratory studies’ below). Other tests are considered based upon individual patient characteristics, but the absence or unavailability of any additional tests need not be a reason to delay therapy if otherwise indicated.
COPD exacerbation with image showing of pseudocolitis and septic shock, also has renal failure. CT scan shows pancolitis. What 1 management option should you proceed with?
surgical consultation
Early surgical consultation is warranted for patients with CDI who meet one or more of the following clinical indicators that have been associated with poor prognosis (table 3) [98-102]:
- Hypotension
- Fever ≥38.5°C
- Ileus or significant abdominal distention
- Peritonitis or significant abdominal tenderness
- Altered mental status
- White blood cell count ≥20,000 cells/mL
- Serum lactate levels >2.2 mmol/L
- Admission to intensive care unit
- End organ failure (eg, requiring mechanical ventilation, renal failure)
- Failure to improve after three to five days of maximal medical therapy
Antibiotics for the treatment of severe CDI include oral vancomycin or oral fidaxomicin (see image).
Antibiotics for the treatment of fulminant CDI include the combination of enteral vancomycin plus parenteral metronidazole
CT head with three arrows - name structures
internal capsule - The internal capsule is a white matter structure situated in the inferomedial part of each cerebral hemisphere of the brain. It carries information past the basal ganglia, separating the caudate nucleusand the thalamus from the putamen and the globus pallidus. The internal capsule contains both ascending and descending axons, going to and coming from the cerebral cortex. It also separates the caudate nucleus and the putamen in the dorsal striatum, a brain region involved in motor and reward pathways.
3rd ventricle
lateral ventricle
external capsule - The external capsule is a series of white matterfiber tracts in the brain. These fibers run between the most lateral (toward the side of the head) segment of the lentiform nucleus (more specifically the putamen) and the claustrum.
The white matter of the external capsule contains fibers known as corticocortical association fibers. These fibers are responsible for connecting the cerebral cortex to another cortical area.
bronchoscopy images (3) - identify the location
image in question is LUL (with lingular segments visible in middle)
image in answer is RUL bronchus
Dapsone - what is possible complication?
List 2 treatment options
a) methemoglobinemia
b) discontinue dapsone
methylene blue (or ascorbic acid if methylyne blue not available)
blood transfusion
supportive care (mechanical ventilation, vasopressors, etc)
Methemoglobin is an altered state of hemoglobin in which the ferrous (Fe++) irons of heme are oxidized to the ferric (Fe+++) state. The ferric hemes of methemoglobin are unable to reversibly bind oxygen. In addition, the oxygen affinity of any remaining globins’ ferrous hemes in the hemoglobin tetramer are increased [1]. As a result, the oxygen dissociation curve is “left-shifted”. See image.
General considerations — Offending agents in acquired methemoglobinemia should be discontinued (table 1).
- In lesser degrees of methemoglobinemia (ie, an asymptomatic patient with a methemoglobin level <20 percent), no therapy other than discontinuation of the offending agent(s) may be required.
- Patients with symptomatic and severe degrees of methemoglobinemia should be managed in the intensive care unit for stabilization of their airway, breathing, and circulation. This may require the use of oxygen supplementation, inotropic agents, and mechanical ventilation [66,67].
- Blood transfusion, especially in anemic subjects, or exchange transfusion may be helpful in patients who are in shock; hyperbaric oxygen has been used with anecdotal success in severe cases
Treatment
If the patient is symptomatic or if the methemoglobin level is >20 percent, which is often the case in deliberate or accidental overdoses or toxin ingestion, specific therapy is urgently indicated. The two treatments most often employed are methylene blue (MB) and ascorbic acid (vitamin C). While there have been no randomized trials comparing these two agents, the general experience has been that the action of a single dose of MB in this setting rapidly reduces toxic levels of methemoglobin to non-toxic levels (eg, <10 percent) within 10 to 60 minutes, whereas treatment with ascorbic acid requires multiple doses and may take 24 or more hours to reach similarly low levels and is therefore a poor alternative in emergency situations.
Accordingly, since high levels of methemoglobin constitute a medical emergency requiring urgent intervention, the more rapid and more dramatic action of MB in reducing methemoglobin levels has made MB the treatment of choice. When MB is not available or when its use is contraindicated (eg, as in glucose-6-phosphate dehydrogenase [G6PD] deficiency), ascorbic acid, and, in life-threatening situations, red cell blood exchange transfusions, are the only reasonable alternatives, although responses to these therapies are less marked and dramatic than they are to MB.
- * While methylene blue is a recognized treatment for methemoglobinemia, it also has oxidant potential and may worsen the clinical status of individuals with G6PD deficiency because it induces acute hemolysis that can further decrease oxygen delivery to the tissues. In high doses, methylene blue can paradoxically increase methemoglobinemia.
Cimetidine, used as a selective inhibitor of N-hydroxylation, may be effective in increasing patient tolerance to dapsone, chronically lowering the methemoglobin level by more than 25 percent [82,83]. Since it works slowly, cimetidine is not helpful for the management of acute symptomatic methemoglobinemia arising from the use of dapsone.
