QBank Wisdom Flashcards
Most commonly injured organ in blunt abdominal trauma
Spleen, evidence will be noticeable acutely on immediate CT scans.
What is the name for firm, necrotic, classically insensate tissue classically formed on exposed tissue following burn wounds?
Eschar!
When eschar occurs circumferrentially on an extremity, it can restrict outward expansion of the compartment as edema occurs following the burn. ==> COMPARTMENT SYNDROME (which can be alleviated by performing an escharotomy)
Clinical signs of compartment syndrome
- Deep pain out of proportion to injury
- PULSELESSNESS
- Paresthesias
- Cyanosis and pallor of affected extremities.
Indications for open reduction of a fracture
“NO CAST”
- Nonunion
- Open fracture
- Compromise (neurovascular)
- Articular fracture (involving joint)
- Salter harris III, IV, V)
- Trauma
How do you describe a fracture?
"BLT LARD": Bone Location (on bone) Type (of fracture) (open vs. closed, complete vs. incomplete, transverse vs. linear, etc.) Lengthening Angulation Rotation Displacement vs. non
ALSO, plan: open vs. closed reduction
"PLASTER OF PARIS" Plane Location Articular cartilage involvement Simple or comminuted Type (eg Colles') Extent Reason Open or closed Foreign bodies disPlacement Angulation Rotation Impaction Shortening
Bone fracture types [for Star Wars fans] GO C3PO:
Greenstick Open Complete/ Closed/ Comminuted Partial Others
What is tic douloureaux?
= Trigeminal neuralgia.
It manifests with short bursts of excrutiating, lancinating pain lasting from seconds to minutes in the distribution of V2 and V3. The etiology is most likely external compression of the trigeminal nerve.
What kinds of surgery often lead to tongue palsy?
Tongue palsy can be caused by hypoglossal nerve CNXII injury.
Surgeries that risk this injury are BELOW THE MANDIBLE (such as for submandibular salivery gland tumor resection)
Describe hoarseness as a post-op complication
Can result from injury to the recurrent laryngeal branches of the vagus nerve.
RISK FROM SURGERIES: on thyroids, parathyroids glands
Which is the only branch of the trigeminal nerve with motor innervation?
V3, the mandibular division, which exit the cranium via the foramen ovale (of skull, not <3, dummy) and follow a deep course to innervate the muscles of mastication.
Jaw asymmetry can result from a unilateral paralysis of these muscles of mastication following damage to V3 on one side.
Injury to this nerve before it reaches the muscles of mastication would require very DEEP dissection!!!
What is strabismus, and how does it come about?
Strabismus (improper alignment of the eye) can result from disorders of the extraocular muscles or of the nerves that innervate them (CNIII, CN IV, CNVI).
Brainstem lesions (as in CVAs) are most commonly responsible.
What is a risk of axillary lymphadenectomy for the treatment of breast cancer?
An injury to the long thoracic nerve, which leads to winged scapula.
How can you get an air embolism?
- Trauma patient who is on respirator
- From subclavian vein access
Can result in sudden collapse and cardiac arrest.
(?PFO necessary, ?A-line risk)
How can you get an amniotic fluid embolism?
It occurs immediately after the rupture of the membranes. Not usually seen in early pregnancy.
Classic presentation of a fat embolism
Dyspnea
Confusion
Petechiae in the upper part of body
Occurs after multiple fractures of long bones.
How can you tell a hemothorax from a pleural effusoin on CXR?
CANNOT! Both are fluid collections in the potential pleural space, and are thus indistinguishable.
Most common finding after blunt chest injury
Pulmonary contusion
CXR reveals opacities caused by hemorrhage in the involved lung segments.
What could result from traumatic tracheobronchial disruption?
Pneumothorax
Mediastinal emphysema AND/OR
SubQ emphysema
How do you identify a traumatic diaphragmatic rupture?
By herniation of abdominal contents (stomach, intestine, spleen) into thorax.
Colonic malignancy typically presents with…
Anemia
Constipation
Weight loss
(older patient group)
Complicated pyelonephritis typically presents with…
Fever
Flank pain
Sometimes dysuria
IBD usually presents with…
Prolonged episodes of diarrhea and fever.
Parasitic colitis typically presents…
acutely after travel to endemic areal, with many episodes of diarrhea (predomoinant sx) and fever.
What is paradoxical aciduria? What context is it encountered in?
You are vomiting H+, and paradoxically peeing out H+ too.
In the context of metabolic alkalosis from loss of H+, Cl-, and fluid (dehydration) from vomiting up gastric contents, where you have lost H+ and have HCO3- excess, the kidney paradoxically compensates for dehydration by excreting H+ and K+ to conserve sodium (and thus water), in an attempt to preserve intravascular volume. The renal excretion of H+ on top of the loss of gastric H+ further leads to increase pH and metabolic alkalosis.
NOTE: Normally, the kidneys would excrete bicarbonate to reduce pH; however, as the dehydration becomes more severe, kidney’s drive to retain Na+ predominates.
What are some causes of serum hypertonicity?
Hyperglycemia from DM
Mannitol
Hypernatremia
Why does hyperglycemia lead to hyperkalemia?
Hyperglycemia leads to serum hypertonicity, which leads to H2O shift from intra- to extra cellular compartments.
Loss of intracellular H2O leads to increase intracellular K+, favoring a gradient for K+ to move out of cells.
Also, as H2O exits the cell, “solvent drag” sweeps K+ along.
What are some dysrrythmias/ECG findings of HYPOkalemia?
T-wave flattening/inversion ST segment depression U-waves Prolonged QT V tachycardia
What are some dysrrythmias/ECG findings of HYPERkalemia?
Peaked T waves
Wide QRS
V-fibrillation
In wound healing, what is the order in which cells arrive to wound site?
Platelets
PMNs (neutrophils)
Macrophages
Fibroblasts
What defines the clinical syndrome of shock?
Inadequate TISSUE PERFUSION to maintain CELLULAR METABOLISM
I.e. Loss of balance between these two components such that metabolism requirements outstrip perfusion (be it O2 delivery, other nutrient delivery, or toxin/CO2 removal)
What is one of the main issues in hypovolemic shock?
Inadequate blood volume leads to decreased venous return (i.e. decreased preload), which leads to decreased cardiac output and decreased tissue perfusion.
What is a distinguishing feature of cardiogenic shock?
In cardiogenic shock, there is increased central venous pressure because of inadequate cardiac pump performance, which leads to blood backing up into the venous system.
What is neurogenic shock?
Loss of sympathetic tone leading to peripheral vasodilation can result in relative hypovolemia and decreased cardiac performance.
This can be the result of vasovagal response, cervicothoracic spinal cord injury, or spinal anesthesia.
Hypotension and vasodilation leading to maldistibutive perfusion results in deranged cellular metabolism.
Which types of shock involve decreased SVR and vasodilation?
Neurogenic and septic.
List causes of obstructive shock
Tension pneumothorax Cardiac tamponade Massive pulmonary embolism Venous air embolism Severe cardiac valvular stenosis
Which is the only type of shock in which cardiac output may be increased?
Euvolemic septic shock
What are causes of cardiac arrest?
Hs and Ts
- Hypovolemia (tx = IV fluid resuscitation, blood transfusion, control bleeding)
- Hypoxia (tx = oxygen, proper ventilation, good CPR technique, and hyperbaric oxygen if cyanide or CO poisoning)
- Hydrogen ions (acidosis - lactic, DKA, salycylate, ethanol, TCA, etc.) (tx = proper ventilation, good CPR technique, buffers like bicarb, emergent hemodyalisis)
- Hyperkalemia (tx = Ca++ administration to stabilize cardiomyocyte electrochem potentials and thus prevent fatal arrythmias; nebulized salbutamol, IV insulin usually with glucose and bicarb to drive K+ into cells; loop diuretics like furosemide to spill potassium in urine or sodium polustyrene sulfonate to bind K+ to excrete in stool; emergent hemodyalisis)
- Hypokalemia (tx = give IV K+)
- Hypothermia, core temp <35°C (tx = cardiac bypass, irrigation of body cavities with warm fluids, or warmed IV fluids)
- Hyperglycemia, such as DKA (correct acidosis)
- Hypoglycemia (tx = IV glucose)
Ts
- Tanlets or toxins (tricyclic antidepressants, phenothiazides, beta blockers, calcium channel blockers, cocaine, digoxin, aspirin, paracetamol/acetaminophen) (tx = specific antidotes, fluids for volume expansion, vasopressors, Na+ bicarb for TCAs, glucagon or Ca++ for CCBs, benzos for cocaine, or cardiopulmonary bypass)
- Tamponade (cardiac) (tx= pericardiocentesis)
- Tension pneumothorax (tx = needle decompression thoracotomy
- Thrombosis (myocardial infarction) (tx = rescucitate, MONA, antiplatelet therapy, thrombolytic therapy, or percutaneous coronary intervention)
- Thromboembolism (i.e. Hemodynamically significant pulmonary embolism) (tx = thrombolytics or thrombolectomy; prognosis is poor)
- Trauma (hard blow to the chest at precise moment in cardiac cycle, commotio cordis)
Hs and Ts of cardiac arrest, briefly
Six and SIX!
Hs: hypovolemia, hydrogen ions, hyper/hypoglycemia, hypo/hyperkalemia, hypoxia, hypothermia
Ts: tablets/toxins, tamponade, tension pneumothorax, thrombosis (MI), thromboembolism (PE), trauma
What information can you get from a pulmonary artery catheter?
- LA and LV preload pressures
- Cardiac output
- Mixed venous oxygen saturation
- Systemic vascular resistance (SVR) and pulmonary vascular resistance (PVR)
Which are the important steps in the initial management of massive hemoptysis (>600mL/day or rate >100mL/hr)?
- Establish an adequate patent airway (biggest risk is asphyxiation, not exanguination).
- Maintains adequate ventilation and gas exchange.
- Ensure hemodynamic stability.
- Place patients with bleeding lung in dependent position (lateral position).
- Bronchoscopy is the initial procedure of choice to identify/localize the bleeding site and attempt early therapeutic intervention (suctioning ability to improve visualization, balloon tamponade, electrocautery).
What are immediate causes of post-operative fever (0-2 hrs)?
Prior trauma/infection
Blood products
Malignant hyperthermia
Acute causes of post-operative fever (24hrs - 1 week)?
- Nosocomial infections
- Surgical site infections due to Group A strep or Clostridium perfringens
- Non-infectious (MI, PE, DVT)
Subacute causes of postoperative fever (1 week-1 mo)
- SSI due to organisms other than group A strep or clostridium perfringens
- C. difficile (pseudomembranous colitis)
- Drug fever
- PE/DVT
Delayed causes of post-operative fever (> 1mo)
- Viral infections (ex. from blood products)’’
- Infective endocarditis.
- SSIs due to indolent organisms
What is the pathophysiology of a febrile nonhemolytic transfusion reaction? How is it different from an acute hemolytic reaction?
The bottom line is the CYTOKINES in the transfused blood products.
In a FEBRILE, NONHEMOLYTIC transfusion reaction, when red cells and plasma are separated from whole blood, small amounts of residual plasma and/or leukocyte debris may remain in the red cell concentrate. During blood storage, these leukocytes release CYTOKINES that when transfused can cause transient fevers, chills, and malaise, WITHOUT hemolysis, within 1-6 hours of transfusion.
Manage by stopping the transfusion, rule out other serious causes of fever (such as acute hemolytic reaction ) and give antipyretics.
Acute hemolytic transfusion reaction immune-mediates because of ABO incompatibility, signs include fever, hypotension, anxiety, and tea-colored urine (with late signs of generalized bleeding (DIC) and hypotension).
Which signs usually accompany a drug fever?
“Wonder drugs!” This is a diagnosis of exclusion.
Most often accompanied by RASH and peripheral eosinophelia.
Typically occurs 1-2 weeks after medication administration.
What are the signs that characterize malignant hyperthermia?
In essence, this is a HYPERCATABOLIC state that usually develops within 1 hours of exposure to causative agents (inhaled anesthetics, succ.). Signs include:
- HIGH fever (>40C/104F).
- Muscle rigidity
- Rhabdomyolisis
- Metabolic acidosis (from increased CO2 prodution and increased O2 consumption)
- Increased RR and HR.
- Hemodynamic instability.
What is the etiology of malignant hyperthermia?
Is usually cased by the volatile INHALED ANESTHETICS and the neuromuscular paralyzing agent succinylcholine. In susceptible individuals (this is an autosomal dominant inherited susceptibility), these drugs can induce a drastic and uncontrolled increase in skeletal muscle oxidative metabolism, which overwhelms the body’s capacity to supply oxygen, remove carbon dioxide, and regulate body temperature, eventually leading to circulatory collapse and death if not treated quickly.
Which anesthetics are safe to use in a person known to be susceptible to malignant hyperthermia?
- Local anesthetic agents (the -caines, ex. lidocaine)
- Opiates (morphine, fentanyl)
- Ketamine
- Barbiturates
- Propofol
- Etomidate
- N2O (nitrous oxide)
- Benzos
The non-depolarizing muscle relaxants (the -iums, like rocuronium, cisatracurium) must be used for paralysis as opposed to succinylcholine.
How does a patient with PE present?
Pleuritic chest pain, tachypnea, dyspnea, tachycardia, and hypoxia.
What does the RQ mainly depend upon in a steady resting state?
Upon the proportions of metabolic fuels being oxidized for ATP production.
What does an RQ close to 1.0 indicate?
That carbohydrate is the major nutrient being utilized.
What does the RQ respresent?
It is the steady-state ratio of CO2 produced to O2 consumed per unit time.
RQ = CO2_eliminated/O2_consumed
It may be used to make assessments of the metabolism taking place in particular organs or in the body as a whole.
What is the normal RQ?
0.8
How does sepsis affect the RQ?
Sepsis is a hypermetabolic, hypercatabolic state wherein both body fat and protein are broken down in addition to glucose being oxidized.
Therefore, the RQ in a septic patient is typically less than 1.0.
What would the RQ tend to be in a patient being given a high-protein diet?
It would tend to be close to 0.8, since amino-acid oxidation becomes the predominant form of ATP production.
How does a high FiO2 affect the RQ?
If tissue oxygen delivery is adequate to prevent anaerobic metabolism, then the RQ will NOT be affected by the FiO2.
It is important to realize that increased O2 deliver to the tissues DOES NOT equate with increased O2 consumption by the tissues. The tissues consume only the amount of O2 that they need.
The RQ is calculated using the amount of O2 consumed (not delivered), which is determined by the difference in O2 content of the arterial and venous blood.
How is O2 consumption measured for calculation of RQ?
It is determined from the arteriovenous oxygen content difference (AVO2D).
