2012 Flashcards
ICU scoring systems
a. 2 within 24 hours
b. 2 used sequentially
Within first 24hrs of admission
APACE II (Acute Physiologic and Chronic Health Evaluation)
- Based on the worst variables during the initial 24 hours in the ICU
- Predicts hospital mortality
SAPS II (Simplified Acute Physiologic Score)
- Calculates a severity score using the worst values measured during the initial 24 hours in the ICU for 17 variables.
- Predicts hospital mortality
Sequential
MPM (Mortality Prediction Model)
- Calculated from 15 variables assessed at the time of ICU admission
- Predicts mortality
SOFA (Sequential Organ Failure Assessment)
- Is calculated 24h after admission to the ICU and every 48 hours thereafter
- Predicts mortality
MODS (Multiple Organ Dysfunction Score)
- Physiologic measures of six organ systems, can be measured at any time
- Predicts ICU and hospital mortality
ENT surgeons wants leeches applied to a post-flap patient
a. What is bug transmitted with this technique? (most common)
b. What prophylactic ABX to give? (name one only)
Aeromonas
Ciprofloxacin
Aeromonas:
- Gram negative rod, distributed widely in freshwater, estuarine and marine environments
Associated diseases:
- A range of diarrheal presentations
- Wound infections: usually after aquatic injury
- Can cause cellulitis, myonecrosis with and without gas production, rhabdomyolysis
- Medicinal leeches: Aeromonas reside in the gut of the leech Hirudo medicinalis, where they assist in the enzymatic digestion of blood ingested by the leech.
- Additional reports of: respiratory infections (after near drowning), ocular infections, endocarditis, joint infections,
peritonitis, cholecystitis.
Treatment:
- Most Aeromonas produce an inducible chromosomal beta-lactamse
- Most strains are resistant to: penicillin, ampicillin
- Most are susceptible to: trimethoprim-sulfamethoxazole, fluoroquinolones, second and third generation cephalosporins,
aminoglycosides, carbapenems, tetracyclines
- Prophylactic ciproflxacin can be given if medicinal leeches are used (however, beware of some ciprofloxacin resistant
strains)
Patient with variceal bleed is transferred to you.
b. Label parts of Sengstaken-Blakemore tube
c. 6 steps of insertion (pt is already intubated and equipment checked)
1) Low threshold for securing the patient’s airway via endotracheal intubation
2) Check balloons
3) Insert Blakemore nasally or orally
4) Inflate gastric balloon to 30 mL of air to verify correct radiographic placement in stomach to avoid gastric balloon insufflation in stomach leading to esophageal perforation
5) Once verification of gastric balloon in stomach inflate balloon to manufacturer’s prescribed volume
6) If bleeding persists inflate esophageal balloon to 35 mmHg so as to have the esophageal balloon exceed the variceal pressure
7) Apply traction
8) Arrange definitive management as esophageal balloon in place for 24 hours only.
9) 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.
Chest tube
a. Label parts of a 3 bottle system
b. What’s the problem of using this system on a post pneumonectomy patient
c. Advantage of dry suction over water suction?
https://sinaiem.org/how-a-chest-tube-drainage-system-works/
- Drainage bottle: collects fluid
- Water seal is the second bottle
- Third bottle controls suction: If the tube is submerged 10 cmH20 and suction is turned on, the negative pressure will equal
10 cmH20. - As the suction machine exerts pressure, the water in the glass tube is pulled out and air is pulled in. When the air reaches the bottom of the glass tube the air bubbles through the water and ends the negative pressure. Water
refills the glass tube and the suction cycle begins again. The glass tube must always be open to air. - In a two bottle system, the first bottle collects drainage and acts as a water seal.
Post pneumonectomy: pleural leaks seal more quickly if suction is eliminated (i.e. just an underwater seal). Suction tends to prolong the duration of the leak
Wet suction control: regulation of the amount of suction by the height of a column of water in the suction control chamber - Water can evaporate from the suction control chamber which reduces the amount of suction applied to the patient as the level of water decreases.
Dry suction control: controlled by a self-compressing regulator. The setting of the suction control dial determines the
approximate amount of suction imposed regardless of the amount of source suction
ICP wave forms
a. What do P1, P2, P3 represent?
b. With ICP of 35, how do the waves change relative to each other
ICP monitoring waveform has a flow of 3 upstrokes in one wave.
P1 = (Percussion wave) represents arterial pulsation
P2 = (Tidal wave) represents intracranial compliance
P3 = (Dicrotic wave) represents aortic valve closure
In normal ICP waveform P1 should have highest upstroke, P2 in between and P3 should show lowest upstroke.
In elevated ICP, the waves have a higher amplitude and P2>P1, and the waves are more rounded out.
The vascular pulse correlates with arterial blood pressure waveform
The respiratory pulse correlates with the respiratory cycle
Lundberg A waves “or plateau waves” are steep increases in ICP (up to 50-100mmHg) lasting for 5 to 10 minutes, then they drop sharply. They are always pathological and represent intracranial hypertension indicative of early brain herniation.
Lundberg B waves are oscillations of ICP at a frequency of 0.5 to 2 waves/min and are associated with an unstable ICP.
Lundberg B waves are possibly the result of cerebral vasospasm, because during the occurrence of these waves, increased velocity in the middle cerebral artery can be demonstrated on transcranial Doppler.
Lundberg C waves are oscillations with a frequency of 4-8 waves/min. They have been documented in healthy subjects and are probably caused by interaction between the cardiac and respiratory cycles.
VV ECMO
a. 2 Physiologic reasons that CO2 is better cleared than O2?
b. How do you adjust CO2 clearance?
c. O2 levels?
VV ECMO:
- Cannulation usually of R common femoral vein for drainage and R IJ for infusion.
- The tip of the femoral catheter should be maintained near the junction of the inferior vena cava and the right atrium, while the tip of the internal jugular cannula should be maintained hear the junction of the superior vena cava and right atrium
- Double lumen cannulas also exist (Avalon by Maquet): inserted into the R IJ removes blood from both the SVC and IVC and returns into the right atrium
VA ECMO: blood is extracted from the right atrium and returned to the arterial system bypassing the heart and lungs.
Oxygenation in VV ECMO:
- Direct function of blood flow.
o The blood flow required during VV ECMO to achieve an acceptable arterial oxygenation is usually between
3-6L/min (partially depending on CO and Hb)
o The oxygenation membrane is in series with the natural lung
CO2 removal in VV ECMO:
- Primarily a function of the flow of fresh gas. CO2 elimination can be increased by increasing the gas flow rate
- CO2 is better cleared than O2 in the blood because:
o Linear nature of the CO2-Hb dissociation curve relative to the O2-Hb dissociation curve
o CO2 dissolves better in the aqueous component of the membrane (CO2 is more soluble than O2)
CXR of big heart with a ICD and PM. Then a “Postop” CXR (Pt got Impella and LVAD in new XR)
a. What’s this patients chronic condition?
b. Label items on post op CXR (Swan-Ganz and LVAD)
c. Describe the pathway of an Impella device
This patient probably has heart failure from a type of cardiomyopathy
Impella: usual percutaneous insertion via the femoral artery, up the aorta, through the aortic valve into the left ventricle
Dabigatran
a. Mechanism of action?
b. Antidote?
c. 2 ways to deal with a patient bleeding from this
Direct thrombin inhibitors:
- Argatroban
- Bivalirudin
- Dabigatran –> idarucizumab (antidote)
Direct Factor Xa inhibitors:
- Rivaroxaban
- Apixaban
- Edoxaban
Assessment of coagulation status:
- Interval since last dose: anticoagulation is fully resolved after 5 half-lives since last dose
- Dabigatran: 1/2 life = 12-17h, resolved by 2.5-3.5d, 85% renal
- Rivaroxaban: 7-17h, resolved by 1.5-3.5d, 35% renal, severe hepatic impairment could result in bio-accumulation
- Apixaban: 5-9h, resolved by 1-2d, 25% renal, severe hepatic impairment could result in bio-accumulation
- Coagulation testing:
- Dabigatran: normal thrombin clotting time (TT) is sufficient to eliminate the possibility of continued dabigatran effect (very sensitive), but can be prolonged with trivial amounts of drug
- Rivaroxaban, apixaban: anti-factor Xa specific assays. A normal anti-factor Xa activity indicates that no clinically
relevant anti-factor Xa drug effect is present, but unless the test has been calibrated for the anticoagulant, the
amount of anticoagulation effect cannot be reliably determined. - Strategies for anticoagulant reversal in serious life-threatening bleeding:
- stop dabigatran
- give idarucizumab
- give antifibrinolytic (TXA)
- activated charcoal if within 2hrs of ingestion
- +/- hemodialysis
Dabigatran – For patients with major bleeding, including life-threatening bleeding (eg, intracranial, severe gastrointestinal), we suggest administration of a specific reversal agent (idarucizumab) along with the antifibrinolytic agent (eg, tranexamic acid, epsilon-aminocaproic acid) (Grade 2C). We may also use an antifibrinolytic agent in selected patients with major bleeding that is not immediately life-threatening (eg, suspected overdose, comorbidities, worsening bleeding symptoms). We also suggest administration of oral activated charcoal if the last anticoagulant dose was within the previous two hours (Grade 2C). Hemodialysis may be used in selected patients if the potential for significant drug removal is high
- Spinal cord injury
a. Scenario of trauma pt cervical hyperextension with 0/5 arm strength, and 3/5 leg strength. Dx?
b. Goes for abdo surgery and then loses pain and temp sensation below T6. Dx?
c. What MAP should we strive for? How long do you maintain this?
An acute central cord syndrome, characterized by disproportionately greater motor impairment in upper compared with lower extremities, bladder dysfunction, and a variable degree of sensory loss below the level of injury, is described after relatively mild trauma in the setting of preexisting cervical spondylosis.
The most prominent thoracic radicular artery is the artery of Adamkiewicz, also known as the artery of the lumbar enlargement. The artery of Adamkiewicz contributes to the ASA between the T9 to T12 level in 75 percent of individuals, but may be found above and below this level.
target MAP 85-90 for first 7d after SCI
https://www.uptodate.com/contents/acute-traumatic-spinal-cord-injury/abstract/48-51
Complete cord injury — In a complete cord injury (ASIA grade A), there will be a rostral zone of spared sensory levels (eg, the C5 and higher dermatomes spared in a C5-6 fracture-dislocation), reduced sensation in the next caudal level, and no sensation in levels below, including none in the sacral segments, S4-S5. Similarly, there will be reduced muscle power in the level immediately below the injury, followed by complete paralysis in more caudal myotomes. In the acute stage, reflexes are absent, there is no response to plantar stimulation, and muscle tone is flaccid. A male with a complete TSCI may have priapism. The bulbocavernosus reflex is usually absent. Urinary retention and bladder distension occur.
Incomplete injury — In incomplete injuries (ASIA grades B through D), there are various degrees of motor function in muscles controlled by levels of the spinal cord caudal to the injury. Sensation is also partially preserved in dermatomes below the area of injury. Usually sensation is preserved to a greater extent than motor function because the sensory tracts are located in more peripheral, less vulnerable areas of the cord. The bulbocavernosus reflex and anal sensation are often
present.
Central cord syndrome — An acute central cord syndrome, characterized by disproportionately greater motor impairment in upper compared with lower extremities, bladder dysfunction, and a variable degree of sensory loss below the level of injury, is described after relatively mild trauma in the setting of preexisting cervical spondylosis. characterized by loss of pain and temperature sensation in the distribution of one or several adjacent dermatomes at the site of the spinal cord lesion caused by the disruption of crossing spinothalamic fibers in the ventral commissure. Dermatomes above and below the level of the lesion have normal pain and temperature sensation, creating the so-called “suspended sensory level.”
Vibration and proprioception are often spared.
Dorsal (posterior) cord syndrome — Dorsal cord syndrome results from the bilateral involvement of the dorsal columns, the corticospinal tracts, and descending central autonomic tracts to bladder control centers in the sacral cord. Dorsal column symptoms include gait ataxia and paresthesias. Corticospinal tract dysfunction produces weakness that, if acute, is accompanied by muscle flaccidity and hyporeflexia and, if chronic, by muscle hypertonia and hyperreflexia. Extensor plantar responses and urinary incontinence may be present
Anterior cord syndrome — Lesions affecting the anterior or ventral two-thirds of the spinal cord, sparing the dorsal columns, usually reflect injury to the anterior spinal artery (Artery of Adamkiewitz). When this occurs in TSCI, it is believed that this more often represents a direct injury to the anterior spinal cord by retropulsed disc or bone fragments rather than primary disruption of the anterior spinal artery. Ventral cord or anterior spinal artery syndrome usually includes tracts in the anterior two-thirds of the spinal cord, which include the corticospinal tracts, the spinothalamic tracts, and descending autonomic tracts to the sacral centers for bladder control. Corticospinal tract involvements produce weakness and reflex changes. A spinothalamic tract deficit produces the bilateral loss of pain and temperature sensation. Tactile, position, and
vibratory sensation are normal. Urinary incontinence is usually present
Brown-Sequard (hemi-cord) syndrome — A lateral hemisection syndrome, also known as the Brown–Sequard syndrome, involves the dorsal column, corticospinal tract, and spinothalamic tract unilaterally. This produces weakness, loss of vibration, and proprioception ipsilateral to the lesion and loss of pain and temperature on the opposite side. The unilateral involvement of descending autonomic fibers does not produce bladder symptoms. While there are many causes of this syndrome, knife or bullet injuries and demyelination are the most common. Rarer causes include spinal cord tumors, disc herniation, infarction, and infections
Conus medullaris syndrome — Lesions at vertebral level L2 often affect the conus medullaris. There is early and
prominent sphincter dysfunction with flaccid paralysis of the bladder and rectum, impotence, and saddle (S3-S5)
anesthesia. Leg muscle weakness may be mild if the lesion is very restricted and spares both the lumbar cord and the adjacent sacral and lumbar nerve roots.
Cauda equina syndrome — Though not a spinal cord syndrome, cauda equina syndrome is considered here because its location within the spinal canal subjects it to many of the same disease processes that cause myelopathy. The syndrome is caused by the loss of functions of two or more of the 18 nerve roots constituting the cauda equina. Deficits usually affect both legs but are often asymmetric. Symptoms include:
Low back pain accompanied by pain radiating into one or both legs. Radicular pain reflects involvement of dorsal nerve roots and may have localizing value
Weakness of plantar flexion of the feet with loss of ankle jerks occurs with mid cauda equina lesions, involving S1,
S2 roots. Involvement of progressively higher levels leads to corresponding weakness in other muscles
Bladder and rectal sphincter paralysis usually reflect involvement of S3-S5 nerve roots
Sensory loss of all sensory modalities occurs in the dermatomal distribution of the affected nerve roots
Transient paralysis and spinal shock — Immediately after a spinal cord injury, there may be a physiological loss of all spinal cord function caudal to the level of the injury, with flaccid paralysis, anesthesia, absent bowel and bladder control, and loss of reflex activity. In males, especially those with a cervical cord injury, priapism may develop. There may also be bradycardia and hypotension not due to causes other than the spinal cord injury. This altered physiologic state may last
several hours to several weeks and is sometimes referred to as spinal shock.
MAP goals: Albeit with little empiric supporting data, guidelines currently recommend maintaining mean arterial pressures
of at least 85 to 90 mmHg, using intravenous fluids, transfusion, and pharmacologic vasopressors as needed
- Hepatorenal syndrome
a. 3 vasopressors that help in HRS
b. List HRS criteria
norepinephrine with albumin
midodrine
vasopressin
The following definition and diagnostic criteria have been proposed for the HRS:
●Chronic or acute hepatic disease with advanced hepatic failure and portal hypertension.
●Acute kidney injury, defined as an increase in serum creatinine of 26.5 micromol/L or more within 48 hours, or an increase from baseline of 50 percent or more within seven days [30]; this definition of acute kidney injury is consistent with KDIGO criteria. However, some clinicians may prefer to use the older definition of acute or subacute kidney injury, specifically a rise in serum creatinine to above 133 micromol/L that has progressed over days to weeks. As noted above, the rise in serum creatinine with reductions in glomerular filtration rate (GFR) may be minimal due to the marked reduction in creatinine production among such patients.
●The absence of any other apparent cause for the acute kidney injury, including shock, current or recent treatment with nephrotoxic drugs, and the absence of ultrasonographic evidence of obstruction or parenchymal renal disease. Spontaneous bacterial peritonitis is complicated by acute kidney injury that may be reversible in 30 to 40 percent of patients. It can be associated with ATN, but it is also a major precipitant of the hepatorenal syndrome. Thus, ongoing infection with spontaneous bacterial peritonitis should not exclude the possibility of hepatorenal syndrome. This means that therapy for hepatorenal syndrome can commence while the bacterial infection is still being treated. In addition, hepatorenal syndrome can occur in patients with preexisting chronic kidney disease [31]. Thus, the presence of another renal diagnosis (eg, diabetic nephropathy) does not necessarily exclude hepatorenal syndrome.
In conjunction with excluding other apparent causes of renal disease, the following criteria also apply:
- Urine red cell excretion of less than 50 cells per high power field (when no urinary catheter is in place) and protein excretion less than 500 mg/day.
- Lack of improvement in renal function after volume expansion with intravenous albumin (1 g/kg of body weight per day up to 100 g/day) for at least two days and withdrawal of diuretics.
As noted above, patients diagnosed with hepatorenal syndrome are classified as type 1 hepatorenal syndrome (more severe) or type 2 hepatorenal syndrome (less severe) based upon the rapidity of the acute kidney injury and the degree of renal impairment. Type 1 hepatorenal syndrome is present if the serum creatinine increases by at least twofold to a value greater than 2.5 mg/dL (221 micromol/L) during a period of less than two weeks. Less rapidly progressive disease is classified as type 2.
In patients with hepatorenal syndrome who are admitted to the intensive care unit, we suggest initial treatment with norepinephrine in combination with albumin rather than other medical therapies (Grade 2B). Norepinephrine is given intravenously as a continuous infusion (0.5 to 3 mg/hr) with the goal of raising the mean arterial pressure by 10 mmHg, and albumin is given for at least two days as an intravenous bolus (1 g/kg per day [100 g maximum]). Intravenous vasopressin may also be effective, starting at 0.01 units/min.
Pathogenesis:
- Arterial vasodilation in the splanchnic circulation, triggered by portal hypertension, caused by increase production or activity of vasodilators, mainly in the splanchnic circulation, with nitric oxide thought be most important.
- As hepatic disease becomes more severe: rise in cardiac output and fall in vascular resistance, including that in the splanchnic circulation, causing decline in renal perfusion.
- Patients who develop HRS usually have portal hypertension, however, patients with fulminant hepatic failure from any cause can develop HRS
Clinical presentation:
- Progressive rise in serum creatinine
- Normal urine sediment
- No or minimal proteinuria (less than 500mg/day)
- A very low rate of sodium excretion (urine Na concentration <10 meq/L)
- Oliguria (not all have this, especially early in the course)
- Type 1: more serious, at least 2 fold increase in creatinine to a level > 221 μmol/L in < 2 weeks
- Type 2: renal impairment less severe than type 1. Often presents with ascites resistant to diuretics.
Diagnosis: (clinical), slightly different wording in AASLD 2007 criteria, but the same
- Chronic or acute hepatic disease with advanced hepatic failure or portal hypertension
- Serum creatinine > 133 μmol/L that progresses over days to weeks
- Absence of any other apparent cause of AKI
- Urine red cell excretion < 50 cells per HPF, protein excretion <500 mg/day
- Lack of improvement in renal function after volume expansion with intravenous albumin (1g/kg body weight,
up to 100 g/day) for at least 2 days and withdrawal of diuretics.
Treatment:
In ICU:
- Norepinephrine infusion, with albumin x 2 days at 1g/kg/day, + IV vasopressin/terlipressin
Not in ICU:
- midodrine (up to 15 mg TID) and octreotide (100-200 mcg subcut TID), and albumin x 2 days at 1g/kg/day
Not responsive to medical therapy:
- Transjugular Intrahepatic Portosystemic Shunt (TIPS)- limited data
- Liver transplant if feasible, and bridge with dialysis.
- 2 circuit related and 2 patient related complications of VV ECMO
a. Circuit:
b. Patient:
Circuit complications: - Clots - Leak - Oxygenator failure Patient complications: - DIC - Stroke - HITT From NEJM ECMO for ARDS in Adults review. Brodie 2011
15.EKG of Aflutter 2:1 block (describe rhythm)
Involves the IVC and tricuspid isthmus in the reentry circuit
Anticlockwise reentry (90%)
- Inverted flutter waves leads II, III, aVF
- Positive flutter waves in V1
Clockwise reentry (uncommon)- opposite pattern
- EKG of patient post lytic
a. What is the rhythm
b. 2 management strategies
Reperfusion arrhythmias
- Most common: accelerated idioventricular rhythm (AIVR) (but not sensitive or specific marker for successful
reperfusion)
o Also called “slow ventricular tachycardia” (AV dissociation)
o Rate of 50-100/120 bpm
o Occurs in up to 50% of pts with acute MI
- Serious ventricular arrhythmia induced by reperfusion does not appear to be a major problem (not life threatening)
- May be due to pacemaker failure, or abnormal ectopic focus in the ventricle accelerated by sympathetic stimulation and circulating catecholamines
Treatment:
- Most are transient and require no treatment.
- There is no convincing link to sustained VT or VF
- If AIVR is an escape rhythm do not attempt to suppress pacemaker focus- can cause bradycardia and asystole.
- If not well tolerated, could try atropine to increase sinus rate to inhibit AIVR in restore atrial-ventricular synchrony.
- Treat electrolyte abnormalities
- Hyperkalemia
a. 5 EKG changes (other than peaked t waves)
b. 5 management strategies
First findings: - Peaked T waves - Shortened QT interval More severe findings - Lengthening of PR interval - Lengthening of QRS duration - Flattening of P wave/disappearance of P wave - Sine wave pattern - Ventricular standstill
Management:
- Use of rapidly acting therapies when patients have ECG changes, patients with a serum potassium >6.5-7 mmol/L
Calcium: directly antagonizes the membrane actions of hyperkalemia
Insulin and glucose: drives potassium into the cells by enhancing the activity of Na-K-ATPase pump in skeletal muscle
Beta-2 adrenergic agonists: also increase the activity of Na-K-ATPase pump in skeletal muscle.
Sodium bicarbonate: raising systemic pH causes hydrogen ion release from cells as part of the buffering reaction , which is accompanied by potassium movement into the cells to maintain electroneutrality
Potassium removal:
- Loop or thiazide diuretics increase potassium loss
- Cation exchange resins: binds potassium in the gut and releases sodium (can cause intestinal necrosis)
- Dialysis
- MDR Acinetobacter
a. 2 drug classes that the bug is “intrinsically” resistant to (exact wording)
b. How does it acquire its resistance? (list 2)
c. Treatment
Multi drug resistant acinetobacter: isolate is non susceptible to at least one agent in three or more antibiotic classes
Mechanisms of antibiotic resistance:
- AmpC beta-lactamases are chromosonally encoded cephalosporinases intrinsic to all A. baumanii. Usually have low level of expression that does not cause clinically appreciable resistance, but can be affected by promotor insertion causing increased beta-lactamase production causing cephalosporin resistance.
- Acquisition of serine and metallo-beta-lactamases confer resistance to carbapenems.
- Reduced expression or mutated porin channels can hinder passage of beta-lactam antibiotics into the periplasmic space
- Overexpression of bacterial efflux pumps can decrease the concentration of beta-lactam antibiotics in the
periplasmic space. To cause clinical resistance, efflux pumps usually act in association with overexpressed AmpC beta-lactamases
- Mutations in genes gyrA and parC causes quinolone resistance
- Expression of aminoglycoside-modifying enzymes causes aminoglycoside resistance.
- Resistance from colistin is from mutation in the genes encoding PmrA and B proteins
Treatment
First line for susceptible organisms: broad spectrum cephalosporin (ceftazidine), combo of beta-lactamase/beta-lactamase
inhibitor, carbapenem
Resistant organisms:
- Polymixins: polymixin B or colistin (+/- second agent: carbapenem, tigecycline, rifampin)
- Tigecycline
19.List 6 life threatening complications of trauma IN THORAX that must be caught on primary survey
- Pneumothorax, tension pneumothorax
- Aortic transection, dissection
- Cardiac tamponade
- Airway obstruction, tracheal transection, bronchial disruption
- Massive hemothorax
- Flail chest with pulmonary contusions
20.Ciaglia technique of perc trach – what’s the most common complication?
Complications of tracheostomy Immediate Bleeding (****MOST COMMON) Tracheal tube obstruction Pneumomediastinum Pneumothorax Loss of airway Tracheal ring fracture Paratracheal placement of tracheostomy tube Injury to thyroid Cardiac or respiratory decompensation Late Infection Granulation tissue formation Tracheal tube displacement or malposition Cuff leak Tracheal stenosis TEF Tracheo vascular fistula
Benefits of Percutaneous dilational tracheostomy over operative trach:
Ciaglia technique: there is no sharp dissection involved beyond the skin incision.
Contraindications: (relative)
Uncorrectable bleeding diathesis, gross distortion of neck from hematoma, tumor, thyromegaly, previous surgical
scarring, infection of soft tissue to the neck, inability to extend the neck due to RA or cervical spine instability
Advantages of percutaneous tracheostomy vs operative:
- Requires less time
- Less expensive
- Performed sooner (do not need OR time)
- Overall less complications: decreased wound infection, less bleeding (blood vessels are compressed rather than
ligated or cauterized)
However, with percutaneous tracheostomy: increased risk of anterior tracheal injury- tracheal ring fracture and
posterior tracheal wall perforation.
Other complications:
- Subcutaneous emphysema: 1.4%
- Pneumothorax 0.8%
- Tracheostomies in general: tracheal obstruction from granulation tissue, stenosis of the trachea below the glottis
(but above the tracheal stoma), massive hemorrahge form tracheoarterial fistula
Benefits of tracheostomy:
- Decreased work of breathing: Decreased airway resistance, peak inspiratory pressures, auto-PEEP, enhanced
ventilator synchrony
- Increased patient comfort
- Enhanced patient communication
- Enhanced patient mobility and swallowing
- Improved suctioning of secretions
- CXR post op from CABG
a. 2 probs: CVC is too low, IABP too high
b. 2 complications associated with the 2 above probs
Low CVC: (should be at the level of the carina)
- Arrhythmia, myocardial perforation, cardiac tamponade from puncture of the pericardium
HIgh IAB: (should be 1-2 cm below the origin of the left subclavian artery and above the renal branches = 2-3 intercostal
space on CXR)
- Obstruction of left subclavian and carotids, causing stroke, limb ischemia
22.Pt with MI and shock. Difficult swan insertion. Name 2 ways you distinguish papillary muscle rupture vs
VSD using a Swan-Ganz catheters
- Increases or “step up” in oxygen saturation in the RV and PA on right heart catheterization
o Requires fluoroscopically guided measurement of oxygen saturation in the SVC and IVC, RA and RV and
PA. With a left to right shunt across the VSD, one will generally detect an increase in oxygen saturation of
more than 8% when going from the RA to the RV and PA - RV pressure tracing will have left sided pressures (peak > 100)
- There will be v waves in the PCWP in papillary muscle rupture
DIsorders in which pulmonary artery wedge pressure (PAW) and left ventricular end-diastolic pressure may be discordant
Conditions in which PAW>LVEDP Mitral stenosis Left atrial myxoma Pulmonary embolus Mitral valve regurgitation Pulmonary venocclusive disease
Conditions in which PAW25 mmHg) LVEDP
Aortic valve regurgitation
Conditions in which PAW does not approximate PCWP (More than 1-4 mmHg difference) Increased pulmonary vascular resistance Pulmonary hypertension Cor pulmonale Pulmonary embolus Eisenmenger's syndrome
- Pt with HIV and a variceal bleed.
a. 3 ways that make a health care worker exposure be considered high risk
b. When do you start prophylaxis? (In ideal circumstance)
c. What do you offer prophylaxis until?
Risk factors for seroconversion:
In general:
- Source has high viral load
- Large volume of bodily fluid exposure to mucous membrane or nonintact skin (i.e blood, bloody fluids, viral cultures, potentially infected body fluids: CSF, synovial, pleural, peritoneal, amniotic, pericardial fluid)
- Deep exposure (highest risk is percuteneous innoculation- needlestick or cut)
o High risk percutaneous exposure: high-risk sharps: hollow bore needles, device with blood on it, needle that was in an artery or vein of the source patient
- Fluids not considered infectious unless they contain blood: feces, nasal secretions, saliva, gastric secretions, sputum, sweat, tears, urine.
Post exposure management:
- Immediate cleansing of infected site: soap, water, alcohol based antiseptic (virucidal)
- Determine HIV status of the source
- Start PEP within 1-2 hours of exposure (benefit is diminished after 24-36 hours)
- Bloodtesting at baseline, six weeks, three months, six months following exposure with or without PEP
- If taking PEP, blood testing at two and four weeks to evaluate for drug toxicity (hepatitis, hyperglycemia,
pancytopenia, nephrolithiasis) - PEP should be continued for 4 weeks or until HIV status of source is confirmed to be negative (by Western blot)
25.Pt in community hospital with Necrotizing pneumonia. CXR with R lung abscess. Two days later, new CXR
that showed a popped abscess with pneumothorax.
a. What happened?
b. 2 things to do prior to transfer?
- Erosion of abscess through visceral pleura causing pneumothorax
Things to do before transfer:
- Decompress with chest tube, and drain empyema from abscess communication
- If intubated, use saline in ETT cuff (expansion of gas if air transported)
- Antibiotic coverage if not already done: Common pathogens that cause lung abscesses include:
o Oral anaerobes: Peptostreptococcus, Prevotella, Bacteroidies (usually not fragilis), Fusobacterium
o Non anerobes: Streptococcus milleri, Staphlococcus aureus, Klebsiella pneumoniae, Streptococcus
pyogenes, Haemophilus influenzae, Legionella, Nocardia, Actinomyces, Mycobacteria, fungi (Aspergillus,
Cryptococcus)
26.Trauma patient with a pulmonary contusions, and hemoptysis. Intubated and chest tube inserted.
Transfer via fixed wing pressurized to 8000 ft. Balloon in ETT filled with saline. Chest tube clamped.
Initially FiO2 80% and PEEP 15 with SpO2 92%. However, as PIP is 40, the PEEP is dropped to 10. Soon
afterwards, FiO2 is 100% and SpO2 still 80%. 5 differentials why.
Mechanisms of hypoxemia:
- Shunt: (blood, pus, water, atelectasis)
o Expanding pneumothorax, atelectasis and decreased tidal volume from decreased PEEP
o Worsening inflammation from contusion causing alveolar edema
o Worsening hemoptysis causing blood in alveoli - Increased deadspace:
o Overdistension causing compression of alveolar vessels - Low FiO2: less likely in this case since it’s 100%, but PaO2 decreases with increasing altitude
- Right to left shunt: from high PVR from overdistension could open a PFO
