McNeil's notes: lytes, physiology, toxicology, hypothermia, burns, embolism, radiology, potpourrie(-stats/epi/ethics) Flashcards Preview

SF > McNeil's notes: lytes, physiology, toxicology, hypothermia, burns, embolism, radiology, potpourrie(-stats/epi/ethics) > Flashcards

Flashcards in McNeil's notes: lytes, physiology, toxicology, hypothermia, burns, embolism, radiology, potpourrie(-stats/epi/ethics) Deck (177):

Labs in diabetes insipidus show:
a. Hyponatremia.
b. Hypoglycemia.
c. High urine specific gravity.
d. Low urine osmolarity
e. Urine specific gravity

e. Urine specific gravity


1) patient post transsphenoidal resection pituitary tumour. Now has mild DI . Just complain of thirst and Na 145. Best treatment option is:
a. fluids ad lib
b. R/L at 150 cc / hour
c. D5 at 150 cc/ hr

a. fluids ad lib

DDAVP for Na > 150


The body system MOST sensitive to changes in sodium homeostasis is:
C. Respiratory
D. Musculoskeletal

Answer: CNS

The clinical features of acute hyponatremia are related to osmotic water shift leading to increased ICF volume, specifically brain cell swelling. Therefore, the symptoms are primarily neurologic, and their severity is dependent on the rapidity of onset and absolute decrease in plasma [Na+ ].

The major symptoms of hypernatremia are neurologic and include altered mental status, weakness, neuromuscular irritability, focal neurologic deficits, and occasionally coma or seizures.
- Washington Manual of Medical Therapeutics, 30th ed., Copyright © 2001


In a patient diagnosed with multiple myloma, had the following lab result, Creatinine 178, Urea 5, Na 128, K 3.5 & Albumin 22. the cause of hyponatremia is:
b. Pseudohyponatremia
c. Renal failure
d. Volume overload
e. Dehydration

Answers given:

pseudohyponatremia seem with MM and high TG, and hyperglycemia

Pseudohyponatremia is a laboratory artifact that is present when the plasma contains very high concentrations of protein (multiple myeloma, intravenous immunoglobulin infusion) or lipid (hypertriglyceridemia, hypercholesterolemia). It does not occur when a direct ion-selective electrode determines the sodium concentration, a technique that is increasingly used in clinical laboratories. In true hyponatremia, the measured osmolality is low, whereas it is normal in pseudohyponatremia.
- Kliegman: Nelson Textbook of Pediatrics, 18th ed.

Depends on the osmolality

There are two situations in which sodium can be fictitiously low as a result of the presence of substances that alter the volume of plasma water in which sodium is measured.
Pseudohyponatremia is common in the setting of hyperglycemia or the use of some other restricted solute that causes high plasma osmolality.
Pseudohyponatremia also can occur as a result of an increase in relatively high-molecular-weight substances, such as occurs with Bence-Jones proteins in multiple myeloma or in hyperlipidemia.
- Abeloff: Abeloff's Clinical Oncology, 4th ed.

Adrenal insufficiency - orthostatic hypotension and hyponatremia are common; hyperpigmentation and hyperkalemia and volume depletion occur in primary adrenal failure (disease of adrenal glands versus secondary which is caused by disorders the pituitary or hypothalamus); may become pre-renal; multiple myeloma-monoclonal malignancy of plasma cells that produce paraprotein and is characterized by replacement of bone marrow and bone destruction; often presents with bone pain, anemia and infection; labs: rouleaux/rare plasma cells/pancytopenia, monoclonal protein, heavy and light chains on SIE, decreased normal immunoglobulins, BJ proteins, hyperCa, increased Cr, increased ESR, and narrow anion gap; renal failure secondary to: myeloma kidney (light chain deposition), hypercalcemic nephropathy, pyelo, amyloid, obstruction, plasma cell infiltration, hyperuricemia, and hyperviscosity of renal blood flow; diuretics-side effects depend on class; thiazides cause hypokalemia, hypoMg, hyperlipidemia, hyperCa, hyperglycemia, hyperuremia, hyponatremia, and rarely azotemia; loop diuretics cause hypoMg, hypoCa, and hypoK; K-sparing diuretics of course cause hyperK!


65 year old male patient presents with symptomatic hyponatremia his NA is 117.What is the best way to treat his hyponatremia:
a. Slow infusion hypertonic saline
b. Rapid infusion of hypertonic saline
c. D5W
d. D5 ½ NS
e. D5 ¼ NS

a. Slow infusion hypertonic saline

Risk central pontine demyelination

Hyponatremia can be either hypovolemic, hypervolemic, and euvolemic. The treatment will usually vary depending on which of these is present. In a patient with severe hyponatremia however, (Na


Calculate the approximate sodium deficit in a 70kg man with a serum sodium of 120mmol/L.
a. 280
b. 410

this only seems to have been asked 1 year so probably low yield.

Sodium Deficit = Total Body Water * Normal Wt in kg * (Desired Na - Pt's Na) (TBW = 0.6 if male and 0.5 if female)

70*0.6 = 42kg water = 42L water
(140-120)mmol/L*42L = 840mmol needed


Post-op laryngectomy, headache, decreased LOC. AVSS, normal urine output. Sodium 118. What is the most likely diagnosis
b) Dilutional hyponatremia
c) Depletional hypokalemia

b) Dilutional hyponatremia (seems like a long surgery)

??? or could be DKA with pseudohyponatremia? depends on the question


1) Hyponatremia: when do you treatment it with Na replacement (When pt is symptomatic or if Na less than 120)



In patient with cirrhosis and ascites, hyponatremia is associated with:
a. Expanded extravascular fluid volume
b. Expanded intravascular fluid volume
c. Renal loss of Na
d. Depleted intravascular volume

Answer: Expanded intravascular fluid volume

The net effect is avid renal sodium and water retention because the patient is effectively volume depleted even though extracellular sodium stores, the plasma volume, and the cardiac output are increased. The sodium retention leads to the development of ascites unless the patient is adequately treated with dietary sodium restriction and diuretics.
- Up To Date 2007 Hyponatremia in Cirrhosis

proteins go extravascular-->intravascular hypovolemia
ADH increases as cirrhosis gets worse-->retain salt and water
lose ability to excrete water as cirrhosis worsens

end up hyponatremic with increased total body sodium. worsened by those that continue to drink alcohol. Better to be on low sodium diet.
initially would be vascular low volume but as things get worse can't pee water so would be hypervolemic hyponatremic.


Hypercalcemia causes all of the following except:
a) Polyuria
b) carpopedal spasm
c) proximal mm weakness
d) coma

b) carpopedal spasm


IV lasix is associated with all except:
All are complications of Lasix therapy EXCEPT:
a. Hyperuricemea.
b. Hyponatremia.
c. Hypercalcemia.
d. Metabolic alkalosis

c. Hypercalcemia.

actually can be used for tx of hyperCa

Loop diuretics inhibit the Na+/K+/2Cl- cotransporter in the ascending limb of the loop of Henle (see Fig. 136-1 ). They are highly protein bound and not filtered by the glomerulus. Loop diuretics are actively secreted into the proximal tubule by the organic anion pathway and reach their site of action intraluminally. They also indirectly inhibit reabsorption of calcium and magnesium by their effect on transepithelial potential difference.
- Walsh: Palliative Medicine , 1st ed.


Which of the following is the site of calcium and iron absorption in the gastrointestinal tract?
1. duodenum
2. distal ileum
3. proximal ileum
4. jejunem

1. duodenum


Which of the following will NOT cause hypercalcemia?
A. Thiazide diuretics
B. Sarcoidosis
C. Paget’s disease
D. Multiple fractures

Answer: Multiple fractures

Common question. This is always the answer

[Paget's] may also cause hypercalcemia, especially if the patient becomes bed-bound.
- Bradley: Neurology in Clinical Practice, 5th ed.

In addition to the well-known association of hypercalcemia in sarcoidosis ....
- Abeloff: Abeloff's Clinical Oncology, 4th ed.

Young, normally active patients with high bone turnover rates are subject to the development of hypercalcemia when suddenly forced into immobility, as may occur during forced bed rest after injury or major illness.
- Townsend: Sabiston Textbook of Surgery, 18th ed.


In Paget’s disease, the following abnormality is MOST likely to occur:
a. elevated serum calcium
b. elevated alkaline phosphatase
c. elevated serum phosphate

Answer: elevated alkaline phosphatase

High alk phos.normal or high calcium ,normal phos

Paget's disease can cause bone pain and deformity. An elevated bone-specific alkaline phosphatase and characteristic radiographic changes can help make the diagnosis. Joint pain caused by secondary osteoarthritis in areas of involvement of bone from Paget's disease most commonly occurs in the hip, knee, or vertebrae. Spinal stenosis from Paget's disease of the spine has been reported.
- Goldman: Cecil Medicine, 23rd ed.

Extracellular calcium homeostasis is almost invariably normal despite the massive increase in bone turnover. Hypercalciuria and more rarely hypercalcemia may occur with prolonged immobilization or fracture.


A 40 yo presents with hypocalcemia and hyperparathyroidism. What is the MOST likely diagnosis?
A. Renal Failure
B. Osteomalacia
C. Parathyroid Adenoma
D. Vitamin D Deficiency

D. Renal failure

Secondary hyperparathyroidism is caused by any condition that gives rise to chronic hypocalcemia, which in turn leads to compensatory overactivity of the parathyroid glands. Renal failure is by far the most common cause of secondary hyperparathyroidism, although several other diseases, including inadequate dietary intake of calcium, steatorrhea, and vitamin D deficiency, may also cause this disorder.
- Kumar: Robbins and Cotran Pathologic Basis of Disease, Professional Edition , 8th ed.

Uptodate 2016: Vitamin D deficiency osteomalacia is the only osteomalacia in their table that has both hypocalcemia and hyperparathyroidism

Parathyroid adenoma = hypercalcemia


All of the following are used in the treatment of hypercalcaemia except:
a. Steroid
b. Rehydration
c. Lasix
d. Calcitonin
e. None of the above

a. none of the above (although steroid is only used in granulomatous disease : lymphoma, sarcoidosis)

Other EXCEPT answers:
-Thiazide (avoid as may increase reabsorption of calcium in DCT)

1. Forced diuresis with isotonic saline and lasix (mainstay in those with normal kidneys, dialysis possible in those with RF)
2. Bisphosphonates
3. Mithramycin
4. Calcitonin
5. Corticosteroids (in sarcoidosis)
6. IV phosphates (disodium or monopotassium phosphate, use as absolute last resort)
7. Gallium nitrate
8. Chloroquine phosphate (in sarcoidosis)
9. Surgical excision of excess functioning tissue
- Morell Notes


A patient with Trousseau's sign, prolonged QT interval and hyperactive DTR. He has :

Answer given: Hypocalcemia

But more likely hypomagnesemia.
- Trousseau’s sign is seen in hypocalcemia and hypomagnesemia.
- Hyperactive DTRs are somewhat more specific for hypomagnesemia
- QT shortening is seen with hypocalcemia

Hypercalcemia can produce a number of nonspecific findings, as follows:
* Hypertension and bradycardia may be noted in patients with hypercalcemia, but this is nonspecific.
* Abdominal examination may suggest pancreatitis or the possibility of an ulcer.
* Patients with long-standing elevation of serum calcium may have proximal muscle weakness that is more prominent in the lower extremities; they also may have bony tenderness to palpation.
* Hyperreflexia and tongue fasciculations may be present.
* Anorexia or nausea may occur.
* Polyuria and dehydration are common.
* Lethargy, stupor, or even coma may be observed.

Hypercalcemia may produce ECG abnormalities related to altered trans-membrane potentials that affect conduction time. QT interval shortening is common, and, in some cases, the PR interval is prolonged. At very high levels, the QRS interval may lengthen, T waves may flatten or invert, and a variable degree of heart block may develop. Digoxin effects are amplified.

# Neuromuscular irritability
* Hyperactive deep tendon reflexes
* Muscle cramps
* Muscle fibrillation
* Trousseau and Chvostek signs
* Dysarthria and dysphagia from esophageal dysmotility
# CNS hyperexcitability
* Irritability and combativeness
* Disorientation
* Psychosis
* Ataxia, vertigo, nystagmus, and seizures (at levels


Hypomagnesemia MOST likely causes:
A. Decreased deep tendon reflexes
B. Tremor
C. Constipation
D. Muscle paralysis

B. Tremor

Tip: Hypoeverything makes you slow
EXCEPTION: hypoMg and hypoCa make you twitch

Clinical and laboratory manifestations:
a. Neuromuscular: weakness, hyperreflexia, fasciculations, tremors, convulsions, delirium, coma
b. Cardiovascular: cardiac arrhythmias
c. Hypokalemia refractory to potassium replacement
d. Hypocalcemia refractory to calcium replacement
- Ferri: Practical Guide to the Care of the Medical Patient, 7th ed.

At serum magnesium levels less than 1 mEq/L, patients have tremor, hyperactive deep-tendon reflexes, hyperreactivity to sensory stimuli, muscular fibrillations, positive Chvostek and Trousseau signs, and carpopedal spasms progressing to tetany. Mental status changes may become evident and may include irritability, disorientation, depression, and psychosis. Cardiac arrhythmias and reversible respiratory muscle failure can also occur in severe hypomagnesemia.

Clinical Manifestations of hypomagnesemia
Cardiac manifestations (7):
1. tachyarrhythmias (unstable VT)
2. digitalis toxicity enhanced as both inhibit the membrane pump
3. prolonged QT
4. T-wave flattening
5. prolonged PR interval
6. A. fib
7. Torsades de pointes
Neurologic manifestations: Changes in mental status, seizures, Tremors, Hyperreflexia
All uncommon, non-specific and have little clinical value
Tremor is the most characteristic finding with hypomagnesemia but tetany is first sign.
- Morell Notes


35 year old male patient with ulcerative colitis and chronic diarrhoea presents with hypocalcaemia, and you prescribed calcium gluconate two weeks later present with tetany. What is the most likely diagnosis:
a. Hypomagnesaemia
b. Hyponatremia
c. Hypokaemia
d. Exacerbation of ulcerative colitis
e. None compliance to medication

a. Hypomagnesaemia

Tetany associated with hypocalcemia.
Hypocalcemia in this case caused by hypomagnesemia, causing decreased PTH secretion and inhibition of PTH effect on bone.


Hypomagnesaemia is caused by all of the following except:
a. Cisplastin
b. Loop diuretics
c. Cyclosporine
d. Aminoglycosides
e. Malabsorbtion

Sources mention all answers!

I refuse to learn this list, but here it is for you keeners:

Primary nutritional disturbances
Inadequate intake, total parenteral nutrition, refeeding syndrome
Gastrointestinal disorders
Specific absorptive defects, malabsorption syndromes, prolonged diarrhea, prolonged nasogastric suction, pancreatitis
Endocrine disorders
Hyperparathyroidism, hypoparathyroidism, hyperthyroidism, primary hyperaldosteronism, Bartter's syndrome, diabetic or alcoholic ketoacidosis, administration of epinephrine, SIADH, hungry bone syndrome after parathyroidectomy
Chronic alcoholism, alcoholic withdrawal, increased renal excretion
Ethanol ingestion; idiopathic; after renal transplantation; drugs (cisplatin, aminoglycoside, amphotericin B, diuretics, pentamidine, theophylline); recovery phase of acute tubular necrosis; colony-stimulating factor therapy
-Miller: Miller's Anesthesia, 7th ed.

a Gastrointestinal and nutritional
i. Defective gastrointestinal absorption (malabsorption)
ii. Inadequate dietary intake (e.g., alcoholics)
iii. Parenteral therapy without magnesium
iv. Chronic diarrhea, villous adenoma, prolonged nasogastric suction, fistulas (small bowel, biliary)
b Excessive renal losses
i. Diuretics
ii. RTA
iii. Diuretic phase of ATN
iv. Endocrine disturbances (diabetic ketoacidosis, hyperaldosteronism, hyperthyroidism, hyperparathyroidism), SIADH, Bartter's syndrome, hypercalciuria, hypokalemia
v. Cisplatin, alcohol, cyclosporine, digoxin, pentamidine, mannitol, amphotericin B, foscarnet, methotrexate
vi. Antibiotics (gentamicin, ticarcillin, carbenicillin)
c Redistribution: hypoalbuminemia, cirrhosis, administration of insulin and glucose, theophylline, epinephrine, acute pancreatitis, cardiopulmonary bypass
d. Miscellaneous: sweating, burns, prolonged exercise, lactation, “hungry-bones” syndrome
- Ferri: Practical Guide to the Care of the Medical Patient, 7th ed.

Loop diuretics inhibit the apical membrane Na+/K+/2Cl− cotransporter of the TAL and abolish the transepithelial potential difference, thereby inhibiting paracellular Mg2+ reabsorption. Hypomagnesemia is therefore a frequent finding in patients receiving chronic loop diuretic therapy
- Brenner: Brenner and Rector's The Kidney, 8th ed


The earliest clinical sign of hypermagnesemia is:
a. stupor
b. convulsion/seizure
c. decreased DTRs
d. something else

Answer: these something elses: hypotension, nausea, vomiting, facial flushing, urinary retention, and ileus. BUT These are so common so I would say they shouldn't clinically make you think of hyperMg unless you're an internal medicine resident and listing your top 100 DDx

If those aren't there, probably decreased DTR

Causes of hypermagnesemia:
renal insufficiency, antacid overuse, adrenal insufficiency, hypothyroidism, excessive intake (e.g. tx of eclampsia).
Signs and symptoms
Clinical: nausea, vomiting, weakness, mental status changes, hyperreflexia, hyperventilation
EKG findings include AV block and prolonged QT interval
1- discontinue or remove external sources; large amounts found in antacids and cathartics
2- IV calcium gluconate for emergent symptoms
3- dialysis in renal failure patients
- Mont Reid Surgical Handbook, pg 26

Magnesium toxicity is a serious and potentially fatal condition. Mild hypermagnesemia (serum magnesium level >4 to 6 mg/dL) causes hypotension, nausea, vomiting, facial flushing, urinary retention, and ileus. Above serum magnesium levels of 8 to 12 mg/dL, flaccid skeletal muscular paralysis and hyporeflexia may ensue, together with bradyarrhythmias, respiratory depression, coma, and cardiac arrest. A low, or even negative serum anion gap may sometimes be seen.
- Goldman: Cecil Medicine, 23rd ed.


Cardiac toxicity in hyperkalemia would be BEST treated with:
A. Insulin
B. Metoprolol
C. Calcium
D. Bicarbonate

Intravenous calcium is used to stabilize the myocardium by lowering the threshold potential. It has no effect on the serum potassium level. Improvement in the ECG is usually evident within 2 to 5 minutes.
- Ferri: Practical Guide to the Care of the Medical Patient, 7th ed.


The following are clinical signs of hyperkalemia except:
a. peaked T waves
b. wide QRS
c. diarrhea
d. tetany

Answer: diarrhea

In hyperkalemia, there is a depolarizing effect on the resting membrane potential and potassium channel conductance is increased, leading to the classic electrocardiographic changes of hyperacute peaked T waves associated with rapid repolarization ( Fig. 118-2). Because of the increased potassium conductance, hyperkalemia antagonizes the normal slow depolarization of pacemaker tissue that is usually associated with a decrease in potassium conductance. Hyperkalemia, like acetylcholine, commonly results in sinus bradycardia. Heart block, loss of P waves on the electrocardiogram, and prolonged QRS intervals are all seen in cases of severe hyperkalemia, usually in excess of 6 mmol/L.
- Goldman: Cecil Medicine, 23rd ed

Neuromuscular signs and symptoms of hyperkalemia include muscle cramps, weakness, paralysis, paresthesias, tetany, and focal neurologic deficits, but these are rarely specific enough to suggest the diagnosis in themselves
- Marx: Rosen's Emergency Medicine, 7th ed.

EKG Summary:
- loss of P wave
- prolonged QRS
- hyperacute T wave


2) What are the signs of hypokalemia?
a) Depressed ST, inverted T, wide QRS
b) Depressed ST, inverted T, narrow QRS
c) Elevated ST, inverted T, wide QRS
d) Elevated ST, inverted T, narrow QRS

A) Depressed ST, inverted T, wide QRS

Low serum potassium not only hyperpolarizes most cells, leading to an increase in the resting potential, but also has effects on certain potassium channels required for repolarization. Thus, hypokalemia decreases or slows potassium conductance, the prolonged repolarization phase accounting for the characteristic electrocardiographic findings of broad, flattened T waves. U waves are also indicative of this delay in repolarization.
- Goldman: Cecil Medicine, 23rd ed.

Electrocardiographic changes in hypokalemia include broad flat T waves, ST depression, and QT prolongation; these are most marked when serum K+ is


3) Which of the following is a sign of hypokalemia:
a. U wave
b. Peaked T waves
c. ST segment elevation
d. Increased deep tendon reflexes
e. None of the above

U wave


All of the following may cause hypokalemia EXCEPT:
A. Vitamin B12
B. Ventolin
C. Insulin
D. Digoxin
E. Corticosteroids

Answer: digoxin can lead to malignant hyperkalemia (Digibind, used for digoxin toxicity, is a cause)

Etiology and classification:
a. Cellular shift (redistribution) and undetermined mechanisms
i. Alkalosis (each 0.1 increase in pH decreases serum potassium by 0.4 to 0.6 mEq/L)
ii. Insulin administration
iii. Vitamin B12 therapy for megaloblastic anemias, acute leukemias
iv. Hypokalemic periodic paralysis: rare familial disorder manifested by recurrent attacks of flaccid paralysis and hypokalemia
v. β-Adrenergic agonists (e.g., terbutaline), decongestants, bronchodilators, theophylline, caffeine
vi. Barium poisoning, toluene intoxication, verapamil intoxication, chloroquine intoxication
vii. Correction of digoxin intoxication with digoxin antibody fragments (Digibind)
b. Increased renal excretion
i. Drugs
(a) Diuretics, including carbonic anhydrase inhibitors (e.g., acetazolamide)
(b) Amphotericin B
(c) High-dose sodium penicillin, nafcillin, ampicillin, or carbenicillin
(d) Cisplatin
(e) Aminoglycosides
(f) Corticosteroids, mineralocorticoids
(g) Foscarnet sodium
ii. Renal tubular acidosis (RTA)
iii. Diabetic ketoacidosis, ureteroenterostomy
iv. Magnesium deficiency
v. Postobstruction diuresis, diuretic phase of acute tubular necrosis (ATN)
vi. Osmotic diuresis (e.g., mannitol)
vii. Bartter's syndrome: hyperplasia of juxtaglomerular cells leading to increased renin and aldosterone, metabolic alkalosis, hypokalemia, muscle weakness, and tetany (seen in young adults)
viii. Increased mineralocorticoid activity (primary or secondary aldosteronism), Cushing's syndrome, or physiologic increases in mineralocorticoid activity (dehydration)
ix. Chronic metabolic alkalosis from loss of gastric fluid (increased renal potassium secretion)
c. Gastrointestinal loss
i. Vomiting, nasogastric suction
ii. Diarrhea
iii. Laxative abuse
iv. Villous adenoma
v. Fistulas
d. Inadequate dietary intake (e.g., anorexia nervosa)
e. Cutaneous loss (excessive sweating)
f. High dietary sodium intake, excessive use of licorice
g. Hypomagnesemia
- Ferri: Practical Guide to the Care of the Medical Patient, 7th ed


What is the commonest cause of hypokalemia associated with INCREASED urine potassium?
a. prolonged thiazide diuretic use
b. spironolactone use
c. primary hyperaldosteronism

Answer: A vs C (thiazide more common than 1 hyperaldosteronism)

"The most common causes of hypokalemia due to urinary potassium losses include diuretic use, a primary increase in mineralocorticoid activity, increased distal delivery of nonreabsorbable anions, and loss of gastric secretions." uptodate 2016

The four most common causes of hypokalemia are reduced intake, gastrointestinal losses, excessive renal losses of potassium (e.g., with excess of mineralocorticoids or diuretics), and potassium shifts from the ECF to the intracellular fluid (e.g., owing to insulin administration).
- Miller: Miller's Anesthesia, 7th ed.

Renal loss of K+ is by far the most common cause of hypokalemia. With rare exceptions, hypokalemia due to increased renal wasting of potassium can be attributed to an increased activity of aldosterone or other mineralocorticoids. Increased aldosterone could be a primary disorder as in primary hyperaldosteronism or due to increased renin secretion as in secondary hyperaldosteronism.
Examples of secondary hyperaldosteronism that result in hypokalemia include renal artery stenosis, diuretic therapy, and malignant hypertension, and congenital defects in renal salt transport such as Bartter's syndrome and Gitelman's syndrome.
- McPherson & Pincus: Henry's Clinical Diagnosis and Management by Laboratory Methods, 21st ed.


Normal hemodynamic changes during pregnancy include all of the following except:
a) Hemodilution
b) increased red cell mass
c) leukocytosis
d) eosinophilia

d) eosinophilia

Turns out babies are not parasites

Increase in TBW (by 40%) – 2/3 increase in extravascular. Increase in plasma volume. Disproportionate increase in plasma volume over RBC volume – hemodilution. Despite erythrocyte production there is a physiologic fall in the HB and hematocrit readings. (likely Eosinophilia)

As a consequence of the increased minute ventilation, maternal Pao2 levels during late pregnancy range from 104 to 108 mm Hg, and maternal Paco2 ranges from 27 to 32 mm Hg.
- Townsend: Sabiston Textbook of Surgery, 18th ed.

Physiologic leukocytosis during pregnancy makes it more difficult to evaluate infectious abdominal processes, particularly late in the 3rd trimester, when the WBC is even higher.
- Gabbe: Obstetrics: Normal and Problem Pregnancies, 5th ed.


Which is not associated with pregnancy?
a. low CO2
b. metabolic acidosis
c. decreased Hct
d. leukocytosis
e. high ESR

b. metabolic acidosis

Minute ventilation begins to rise by the end of the first trimester and continues to increase until term. Progesterone mediates this response by direct stimulation of respiratory drive and by increasing sensitivity of the respiratory center to CO2.[16] This results in a mild respiratory alkalosis—Pco2 falls to approximately 27 to 32 mm Hg—and a compensatory increase in renal excretion of bicarbonate. This large increase in minute ventilation allows maintenance of high-normal Po2 despite the 20% to 33% increase in oxygen consumption in pregnancy.
- Brenner: Brenner and Rector's The Kidney, 8th ed.

Physiology maternal hyperventilation causes a compensatory metabolic acidosis with a decrease in maternal Hco3. The mother therefore has less buffering capacity for metabolic acidosis

ESR elevated in: inflammatory states (acute-phase reactant), collagen-vascular diseases, infections, myocardial infarction, neoplasms, hyperthyroidism, hypothyroidism, rouleaux formation, elderly, pregnancy
- Rakel: Textbook of Family Medicine, 7th ed.

Hematocrit is 30–50% normal
- Gabbe: Obstetrics: Normal and Problem Pregnancies, 5th ed


Resistant is proportional to:
a. Length and 1/radius to power of 4
b. Radius and 1/ length to power of 4
c. Length to power of 4 and 1/radius
d. Radius to power of 4 and 1/length

a. Length and 1/radius to power of 4


Which of the following changes in vital signs is not seen when a patient goes from standing to supine?
a) decreased heart rate
b) decreased SV
c) Decreased SVR

Standing – blood to pool in feet, less venous return, and reduced CO, compensatory increase HR/BP


What is the primary determinant of myocardial oxygen supply in a healthy person:
a) blood pH
b) sympathetic activity
c) oxygen content of the blood
d) myocardial oxygen demand

Previous answer D, but it's actually C I think

"The delivery of oxygen (DO2) to the myocardium (oxygen supply) is determined by two factors: coronary blood flow (CBF) and the oxygen content (concentration) of the arterial blood (CaO2)." - Some random website

Blood flow to coronaries based on preload (diastolic flow)

"Heart rate is the single most determinant of myocardial oxygen demand"


Which of the following are effects of thromboxane A2?
a. platelet aggregation
b. vasodilatation
c. vasoconstriction
d. bronchodilatation
e. increased vascular permeability

a. platelet aggregation

Thromboxanes are synthesised predominantly by platelets and act to promote:
• vasoconstriction
• platelet aggregation
• bronchoconstriction in lung.
They act as autocoid local hormones due to their short half lives, and they are excreted in the kidney.

TxA2 is the predominant cyclooxygenase product formed by platelets and human monocytes. It stimulates platelet aggregation and secretion and is mitogenic for and constricts vascular and bronchial smooth muscle. These biologic properties are shared by the prostaglandin endoperoxides. A single gene encodes a human thromboxane receptor, which is a member of the G protein-coupled receptor superfamily.
- Goldman: Cecil Textbook of Medicine, 21st ed., Ch 233

Thromboxane A2 (TXA2) is a thromboxane. It is produced by activated platelets and has prothrombotic properties: it stimulates activation of new platelets as well as increases platelet aggregation. This is achieved by mediating expression of the glycoprotein complex GP IIb/IIIa in the cell membrane of platelets.

Aspirin irreversibly inhibits platelet cyclooxygenase 1 (and 2) preventing the formation of prostaglandin H2, and therefore thromboxane A2.

Nonselective NSAIDS, such as ibuprofen, reversibly inhibit both cyclooxygenase1 and 2, and thus alter thromboxane A2 synthesis and platelet aggregation.

Selective NSAIDS, known as the COX-2 inhibitors (eg, Celebrex®, Vioxx®, Bextra®), inhibit cyclooxygenase 2 without affecting cyclooxygenase 1. Thus, their effects predominantly alter prostacyclin versus thromboxane A2


Which one or more of the following is primarily responsible for increasing the cardiac output in patient with acute mild to moderate normovolemic anemia?
a) Tachycardia
b) Increased contractility.
c) Increased afterload.
d) Decreased sympathetic nervous activity.
e) Decreased blood viscosity

Answer key says E. I think that's wrong
I think the answer would be B based on below: CMAJ 1997 review article conclusions

Cardiac output increases with increasing degrees of normovolemic anemia provided that blood volume is adequate

Increased cardiac output in normovolemic anemia is a result of increased stroke volume

The contribution of increased heart rate to the increase in cardiac output following normovolemic anemia is variable

Changes in blood viscosity result in many of the hemodynamic changes in normovolemic anemia

Normovolemic anemia is accompanied by increased sympathetic activity

Normovolemic anemia causes increased myocardial contractility

Normovolemic anemia causes a decrease in systemic vascular resistance

BUT also it states:
If cardiac function is normal, the increase in venous
return or left ventricular preload will be the most important determinant of the increased CO during normovolemic anemia.


Bradykinin has which of the following properties?
a) Vasoconstriction
b) Vasodilation
c) Decreased permeability of capillaries
d) Increased platelet aggregation

b) Vasodilation

Bradykinin is a potent endothelium-dependent vasodilator, causes contraction of non-vascular smooth muscle, increases vascular permeability and also is involved in the mechanism of pain. Bradykinin also causes natriuresis, contributing to a drop in blood pressure. Can also cause dry cough in patients on ACEI.

Implicated in inflammation, anaphylaxis, septic shock
Principal effects (6):
1. Stimulate production of NO (→ VD, ↓ plt aggregation)
2. Vasodilation
3.↑ capillary permeability
4. Activation of phospholipase and thus amplification of inflammatory response, e.g., ↑ PG I2 and ↓ plt aggregation
5. Pain
6. Bronchoconstriction


The endothelium creates a substance that effects blood pressure, capillary permeability, and vascular flow, what is it?
a. Nitric Oxide.
b. Bradykinin.
c. Acetylcholine.
d. Prostacyclin.
e. Norepinephrine.

a. Nitric Oxide.

Vascular actions of NO include the following:
* Direct vasodilation (flow dependent and receptor mediated)
* Indirect vasodilation by inhibiting vasoconstrictor influences (e.g., inhibits angiotensin II and sympathetic vasoconstriction)
* Anti-thrombotic effect - inhibits platelet adhesion to the vascular endothelium
* Anti-inflammatory effect - inhibits leukocyte adhesion to vascular endothelium; scavenges superoxide anion
* Anti-proliferative effect - inhibits smooth muscle hyperplasia

There are three isoforms of NOS. Two of these (cNOS) exist constitutively and the third (iNOS) is inducible. cNOS can be found in endothelium, myocardium, endocardium, skeletal muscle, platelets, and neural tissue.
Nitric oxide has the potential to be both protective and damaging in anaphylaxis (Box 59.4). It relaxes bronchial smooth muscle while dilating vascular smooth muscle. In addition to the peripheral vasodilatation, it can enhance vascular permeability. Its effect on smooth muscle thus can improve bronchospasm while worsening hypotension.
- Adkinson: Middleton's Allergy: Principles and Practice, 7th ed.


Effects of NO include all except:
a. Selective vasodilatation of pulmonary circulation with less effect on systemic circulation
b. Decrease reperfusion injury in transplanted lung
c. May have beneficial effect in ARDS
d. Increase Cyclic GMP


NO has limited improvement in oxygenation in pts with ARDS and ALI. There is no effect on mortality and s/e. It is NOT recommended.

old answer:
Nitric oxide (NO) is an endogenous substance whose primary function appears to be vascular smooth muscle relaxation. The concept of inhaled NO as a practical means by which to achieve selective and therapeutic pulmonary vasodilation is based on the presumption that NO is so rapidly inactivated in blood that diffusion into a pulmonary capillary can produce local vasodilation without systemic effects.
Available data suggest that inhalation of NO by patients with severe Acute Lung Injury reduces pulmonary artery pressures in ventilated lung areas, improves blood flow to these areas, and subsequently improves arterial oxygenation without producing systemic vasodilation.

A therapeutic potential for inhaled NO to act as a selective pulmonary vasodilator was demonstrated by Frostell and colleagues in 1991, who showed that breathing NO gas resulted in rapid and profound pulmonary vasodilation in an awake lamb model of pulmonary hypertension produced by infusion of a stable thromboxane analog ( Fig. 31-3 ).[2] Because NO binds rapidly to hemoglobin (Hb) with high affinity, the vasodilatory effect of inhaled NO is limited to the lung. This is in sharp contrast to intravenously infused vasodilators, which often cause systemic vasodilation and lead to systemic arterial hypotension. This unique ability of inhaled NO to cause highly selective pulmonary vasodilation has prompted a large number of preclinical and clinical studies.
- Miller: Miller's Anesthesia, 7th ed.

Inhaled NO has also been used to treat pulmonary hypertension associated with COPD, cardiac surgery, heart and lung transplantation, and acute lung injury.
- Mason: Murray & Nadel's Textbook of Respiratory Medicine, 4th ed.

Nitric oxide (NO) is a potent pulmonary vasodilator and has been used for a number of years to improve oxygenation in the face of acute respiratory distress syndrome (ARDS) and severe pulmonary hypertension.
- Miller: Miller's Anesthesia, 7th ed.

Most of the effects of NO on the cardiovascular system are mediated by activation of the enzyme soluble guanylate cyclase, which catalyzes formation of the second messenger cyclic guanosine monophosphate (cGMP) from guanosine 5′-triphosphate. NO stimulates soluble guanylate cyclase to synthesize cGMP, which in turn activates cGMP-dependent protein kinase and thereby leads to vascular relaxation.
- Miller: Miller's Anesthesia, 7th ed.

Endothelium-derived nitric oxide or relaxing factor (EDNO or EDRF) can be released in response to acetylcholine stimulation, hypoxia, endotoxin, cellular injury, or mechanical shear stress from circulating blood. Its vasodilatory activity has been demonstrated in large (conduit) arteries and in resistance vessels of most mammalian species, including human beings.
EDNO induces vasodilation and platelet deactivation.
- Goldman: Cecil Textbook of Medicine, 21st ed


Hypoxic pulmonary vasoconstriction is due to :
a. Increase follow in pulmonary vessels
b. Decrease PO2 in alveoli
c. Metabolic acidosis
d. All of the above
e. None of the above

Answer: decreased PO2 in alveolar gas

HYPOXIC PULMONARY VASOCONSTRICTION (HPV) is an adaptive vasomotor response to alveolar hypoxia, which redistributes blood to optimally ventilated lung segments by an active process of vasoconstriction, particularly involving the small, muscular "resistance" pulmonary arteries (PA).

HPV shunts blood from poorly oxygenated areas to better ventilated lung segments, thereby optimizing ventilation-perfusion matching, reducing shunt fraction, and optimizing systemic O2 delivery in conditions such as atelectasis and pneumonia

Although it is generally accepted the mechanism of HPV involves a direct effect of decreased oxygen tension on the pulmonary artery smooth muscle cell to increase cytosolic Ca2+ and cause contraction, the biochemistry of the oxygen sensing, the intracellular signaling pathways that link oxygen sensing to Ca2+ signaling, the relative roles of extra- and intracellular sources of Ca2+, and the role of the endothelial cell remain unresolved.
- Mason: Murray & Nadel's Textbook of Respiratory Medicine, 4th ed.

The process of active redistribution of pulmonary blood flow to maintain optimal V/Q relationship is called Hypoxic Pulmonary Vasoconstriction (HPV). Pulmonary arterial vasoconstriction occurs as the alveolar PO2 of a given lung region Falls below 70 torr. The exact mechanism by which local hypoxia is detected and cconstriction is mediated is not clear.
- Essentials of Basic Science in Surgery


A patient was just put in reverse trendlenberg position and he developed hypotension the most likely cause of hypotension is:
a. Dysfunction of baroreceptors
b. External compression of IVC
c. Decrease cardiac contractility
d. Hypovolemia
e. Dysfunction of chemoreceptors

a. Dysfunction of baroreceptors

Trendelenburg poisition = IVC dilates but is compressed by abdominal contents, and thus LESS pre-load. CO/SV increase only modestly


The loss of pedal pulses following exercise is most often related to which of the following conditions?
a. Increased venous return
b. Redistribution of blood flow
c. Proximal arterial stenosis
d. Decreased cardiac output

b. Redistribution of blood flow


Systemic diastolic BP is determined by :
a. Stroke volume
b. Peripheral vascular resistant
c. Cardiac output
d. Viscosity

b. Peripheral vascular resistant


Most normal pressure to maintain CPP at
a. 30mmHg
b. 70mmHg
c. 30mmH2O
d. 70mmH2O

b. 70mmHg

Answer: 70mmHg (80-100)

Cerebral perfusion pressure (CPP)which is equal to the Mean Arterial Pressure (MAP) minus the Intra-Cranial Pressure (ICP) is an important measurement that is used to monitor therapy in head trauma patients. The lowest acceptable CPP is 60 mmHg.
Maintaining cerebral blood flow requires using an elevated minimal CPP threshold when treating the injured brain. A CPP level of at least 70 mmHg is suggested.
- Schwartz

MAP = 1/3(Systolic-Diastolic) + Diastolic
MAP = 1/3 pulse pressyre + diastolic


Vascular injury is less likely to be present when ABI is :
a. 0.3
b. 0.5
c. 0.7
d. 0.9

d. 0.9

The Ankle Brachial Pressure Index (ABPI) is the ratio of the blood pressure in the lower legs to the blood pressure in the arms. Compared to the arm, lower blood pressure in the leg is a symptom of blocked arteries (peripheral vascular disease). The ABPI is calculated by dividing the systolic blood pressure in the arteries at the ankle and foot by the higher of the two systolic blood pressures in the arms.

above 1.2 – Abnormal - Vessel hardening from PVD- Refer routinely
1.0 - 1.2 - Normal range No treatment
0.9 - 1.0 Acceptable
0.8 - 0.9 Some arterial disease - Manage risk factors
0.5 - 0.8 Moderate arterial disease - Routine specialist referral
under 0.5- Severe arterial disease- Urgent specialist referral


What is the most reliable indicator of tissue perfusion?
a) Heart rate
b) Urine output
c) Skin color
d) Skin temperature

b) Urine output

As signs of a reduced tissue perfusion and end-organ oxygenation, a decreased urinary output (


If the end diastolic pressure is kept the same, how can you increase the CI (cardiac index)?
a) Increase SVR
b) Increase pulmonary vascular resistance
c) Increase HR
d) Decrease venous capacitance
e) Increase coronary artery blood flow

c) increase HR
This is the only one that makes a bit of sense

Cardiac index (CI) is a haemodynamic parameter that relates the cardiac output (CO) from left ventricle in one minute to body surface area (BSA)

So should increase with tachycardia

Preload refers to the passive stretch on the myocardium just prior to contraction, or the ventricular wall tension at the end of diastole. In the intact heart, preload corresponds to the end-diastolic volume or end-diastolic pressure. According to Starling's law, the higher the preload, the greater the force of ventricular contraction and the greater the stroke volume. When heart failure develops, cardiac output may be maintained within normal limits by an increase in preload. Diastolic filling increases in part due to an increase in venous return resulting from vasoconstriction and intravascular volume expansion. However, in severe heart failure, the ventricular function curve may be flat at higher end-diastolic volumes; thus cardiac output may not be augmented by an increase in filling, and a marked increase in end-diastolic pressure causes pulmonary venous congestion ( Fig. 65-3 ).

Afterload refers to the ventricular wall stress during systole or the force that the ventricle must overcome to eject its contents. According to Laplace's law, systolic wall stress is directly proportional to ventricular pressure and chamber radius and inversely proportional to ventricular wall thickness. The major determinant of left ventricular afterload is systemic vascular resistance.
Noble: Textbook of Primary Care Medicine, 3rd ed., Copyright © 2001 Mosby, Inc.


Which of the following would not be useful in improving tissue oxygenation when delivery/extraction is impaired?
a) Fluid to keep the CVP >15
b) Supplemental O2
c) Dopamine to increase cardiac output
d) Bronchodilators
e) Helium-oxygen mixture

a) fluids?
I don't really know what they mean by delivery/extraction impaired.

B, C, and D make sense! Below is the evidence for why E would make sense.

It has been recognized for some time that breathing heliox, a gas consisting of 20% oxygen and 80% helium (hence a density approximately one-third that of air), results in prompt improvement in dyspnea, work of breathing, and arterial blood gas abnormalities in patients with upper airway obstruction.[146] This benefit stems from the density dependence of the flow-related pressure drop across the upper airway in cases of severe upper airway obstruction, disorders typically producing highly turbulent flow across the narrowed airway.
- Murray & Nadel: Textbook of Respiratory Medicine, 3rd ed., Copyright © 2000


Insuflation for laporoscopy causes
a – decreased preload
b – increased cardiac output

a – decreased preload


Cardiac Index is
a – HR x SV
b – number of myocytes
c – avO2 difference x hemocrit x cardiac output
d – Cardiac output / Body surface area

d – Cardiac output / Body surface area


Tension pneumothorax is associated with all of the following except?
a. increased SV
b. increased intrapleural pressure

Answer: increased SV


Carbon dioxide is transported in the blood primarily as:
a) dissolved CO2
b) carbonic acid
c) carboxyhemoglobin
d) bicarbonate salt (HCO3)

d) bicarbonate salt (HCO3)

Transport of carbon dioxide in the blood is considerably more complex. A small portion of carbon dioxide, about 5 percent, remains unchanged and is transported dissolved in blood. The remainder is found in reversible chemical combinations in red blood cells or plasma. Some carbon dioxide binds to blood proteins, principally hemoglobin, to form a compound known as carbamate. About 88 percent of carbon dioxide in the blood is in the form of bicarbonate ion.


Asthmatic patient wheezing in the clinic what is the best way to control his asthma pre op:
a. Steroid IV
b. Steroid inhaled
c. Bronchodilators
d. All of the above
e. None of the above

Answer: Bronchodilators

A preoperative chest radiograph is necessary only for evaluation of infections or pneumothorax. Bronchodilators, inhaled and oral steroids, and antibiotics (if taken) need to be continued on the day of surgery. β-Agonists are the most useful prophylactic intervention to lower the risk for bronchospasm on induction of anesthesia. A short course of steroids (20 to 60 mg of prednisone daily for 3 to 5 days) preoperatively may be useful in any patient who is not at baseline and surgery must proceed.
- Miller: Miller's Anesthesia, 7th ed.


Elderly lady in the ICU post op, intubated. C.I. 1.6 (low), CVP of 10 (highish), PCWP > 20 (high), pulmonary artery pressure :30 (mean is 25). What is your Dx?
a. hypervolemia
b. hypovolemia
c. CHF
d. Sepsis
e. Pulmonary embolus

Answer: CHF

CI 1.6 (N=2.4-4.0),
PCWP (N=6-12),
PA Pressure (N Systolic 15–30 mm Hg Diastolic 5–12 mm Hg),
SVR of 1500 (N=900-1200)


What will decrease intrapulmonary shunting
a. increase anatomic dead space
b. alveolar collapse
c. pulm edema
d. pneumonia

Answer: increase anatomic dead space

Pulmonary shunt is a physiological condition which results when the alveoli of the lungs are perfused with blood as normal, but ventilation (the supply of air) fails to supply the perfused region.

Dead space ventilation increases when the alveolar–capillary interface is destroyed (e.g., emphysema), when blood flow is reduced (e.g., heart failure, pulmonary embolism), or when alveoli are overdistended by positive-pressure ventilation.
Intrapulmonary shunt fraction increases when the small airways are occluded (e.g., asthma, chronic bronchitis), when alveoli are filled with fluid (e.g., pulmonary edema, pneumonia) or when alveoli collapse (e.g., atelectasis), and when capillary flow is excessive (e.g., nonembolized regions of lung in pulmonary embolism).


Alveolar hypoventilation is best assessed by:
a. PaO2
b. SaO2
c. PaCO2
d. pH

Answer: PaCO2

Alveolar PAO2 =150 - 1.25 x PaCO2

Carbon dioxide retention develops when Pimax


Causes of elevated PCWP :
a. LVF
b. RVF
c. PE
d. Tricuspid regurgitation

a. LVF

B&C&D would incr CVP

PCWP as measured by a pulmonary artery catheter, is the pressure measured in a pulmonary artery distal to an occlusion of that artery. Physiologically, distinctions can be drawn among pulmonary venous pressure, pulmonary artery pressure, pulmonary wedge pressure, and left atrial pressure. it is considered the gold standard for determining the cause of acute pulmonary edema; this is likely to be present at a PWP of >20mmHg. It has also been used to diagnose severity of left ventricular failure and mitral stenosis[5]


PCWP represents
a. RA pressure
b. LA pressure
c. RV pressure

b. LA pressure

Note: it is an indirect measure of it

If a Swan-Ganz catheter is in place in the pulmonary artery, cardiac output is measured and attempts are made to maintain the cardiac index at a normal level. In many patients the pulmonary capillary wedge pressure (PCWP) provides a reasonable guide to left atrial pressure or preload.
- Schartz Ch 18


Cause of decreased alveolar ventilation in obese pt is :
a. Decreased descent of the diaphragm
b. Increased upper airway resistance
c. Decreased lung compliance

a. Decreased descent of the diaphragm

The most frequent abnormality in pulmonary function in obesity is a decrease in the expiratory reserve volume attributable to cephalad displacement of the diaphragm by adipose tissue. In severely obese individuals and in those with the OHS, total lung capacity and vital capacity may be reduced. In such patients, the residual volume may actually be increased relative to total lung capacity because of small airway closure and gas trapping. This is supported by the finding of larger total lung capacity by body box plethysmography than by helium dilution.13 Similarly, spirometry is typically normal in simple obesity, whereas severely obese individuals or those with the OHS may exhibit reductions in FEV1 and FVC, even though the ratio of these two variables is preserved or even increased


Respiratory quotient question: carbon dioxide production / oxygen consumption?
RQ carbs = 1.0
RQ protein = 0.8
RQ fat = 0.7

Ratio of the volume of carbon dioxide produced when a substance is oxidized, to the volume of oxygen used. The oxidation of carbohydrate results in an RQ of 1.0; of fat, 0.7; and of protein, 0.8.
If >0.7 – ketosis and if >1 = hyperalimentation – increased carb:fat ratio


Vital capacity is calculated as:
a. TLC – RV; also VC = IRV + TV + ERV
b. TLC - (Exp Re serve Vol + TV)
c. IC + FRC
d. IC + TV
e. none of the above

Answer: TLC – RV


Patient sustains first degree burn to face and neck, second degree burn to one arm, anterior trunk and one lower extremity. Calculate percent burn
a. 35%
b. 25%
c. 45%
d. 55%

first degree burns don't count
Second degree burns
- arm = 4.5+4.5 = 9%
- ant trunk = 18%
- lower extremity (whole) = 9+9 = 18%
- total= 45%


A patient suffers a 3rd degree burn to their torso, both legs, and half of one arm. ??assuming 70kg
The necessary fluid requirements include:
a. Crystalloid at 500 cc/hr for 8 hrs, then 1 L/hr for 16 hrs
b. Crystalloid at 750 cc/hr for 8 hrs, then 850 cc/hr for 16 hrs
c. Crystalloid at 1 L/hr for 24 hours
d. Crystalloid at 1180cc/hr for 8 hours, then 800 cc/hr for 16 hrs

Calculations don’t make sense for me…
Torso (36) + Legs (36) + ½ arm (4.5) [assuming total torso] or
Torso (18) + Legs (36) + ½ arm (4.5) [assuming ant. torso]

Total fluids in 24 = TBSA * weight in kg (assume 70) * 4 =
21420 or

Hourly rate for first 8 hrs = Total * ½ / 8 =
1338.75 or

Adding maintenance (110cc/hr] =
1438.75 or

Given these calculations, no answers are appropriate. Generally, the rate in the first 8 hours should be twice the rate in the second, unless you include maintenance. This would give D (no maintenance) but the last 16 hours should be half the rate.


80 kg female burn patient presented 30 min after 20% 3rd degree burn , what is the
fluid for the first 8hrs:
a. RL 400cc/h
b. RL 270cc/h
c. NS 400cc/h
d. NS 270cc/h


Parkland Formula
4cc x BW (kg) x % BSA burned = 24 hour replacement
½ in first 8 hours, remaining ½ over next 16 hours

4 x 80 x 20 = 6400 cc over 24hrs. 6400 x .5 = 3200 cc ( volume over next 8 hrs)
3200cc/8hrs = 400 cc/hr

use RL


A burn patient has a urine output of 45, 70, 50 cc over 3 subsequent hours. What would you do next?
a) Bolus 1L RL
b) Increase by 1/3 rate
c) Decrease by 1/3 rate
d) Monitor for another hour and reassess

Answer: Decrease by 1/3 rate (target = 0.5cc/kg/hr)


What is the BEST measure of the adequacy of burn resuscitation?
C. sBP
D. Urine output

D. Urine output


Man sustained electrical burn, has tea-colored urine, best management
a) Mannitol and bicarb.
b) Lasix and bicarb.
c) Keep urine output >0.5 cc/kg.
d) Acidify urine.

c) Keep urine output >0.5 cc/kg.

Essentially there is good evidence that making a lot of urine is good, but less good evidence that the other things can help


The rate is adjusted to maintain the desired diuresis of approximately 200 to 300 mL/hour.
The optimal fluid for the prevention of heme-induced AKI is not known
Limited data suggest that alkalinization of urine may benefit patients with severe rhabdomyolysis (so long as they are making urine, otherwise severe metabolic acidosis).

Patients with gross pigmenturia are at risk for myoglobin-induced acute tubular necrosis (Color Fig. 12-10). This situation is most common in patients who have sustained high-voltage electrical injury or deep thermal burns. In these patients, pigment must be cleared from the urine promptly. This is ideally accomplished with crystalloid loading, maintaining a brisk urine output of 2 mL/kg/h or more. Also helpful is alkalinization of the urine. This is best accomplished by administration of 0.12 to 0.5 mEq/kg/h of sodium bicarbonate intravenously as a part of the resuscitative fluid, with careful observation of the serum pH. Occasionally, osmotic diuresis using mannitol is required; however, the administration of osmotic diuretics obscures the urine output as a measure of intravascular volume status. Therefore, a pulmonary artery or central venous catheter should be placed when mannitol must be used so that cardiac filling pressures can be used to judge the adequacy of fluid administration.
- Greenfield


Young lady with face and neck first degree burns and right arm and chest/abdomen second degree burns, and high carbon monoxide, how much daily fluid in first 24 hours?

Assuming 4.5% R anterior arm, 18% chest/abdomen = 22.5%
assuming 70kg
4*70*22.5 = 7560 (6.3L)
If inhalation component, then increase the fluid requirements by 40-50%
6.3*1.5 = 9.45L

Answer: 9L (if you think is inhalational injury)

Add 2 cc/kg%TBSA for inhalational injuries
- Morell Notes

Parkland underestimates fluid req in inhalation injury


Why do you use a dry dressing over the top of a partial thickness burn?
a) Keep it dry
b) Reduce scab formation
c) Reduce the bacterial count

Answer: Reduce bacterial count

Occlusive dressings support a moist wound healing environment that is optimal for healing. A moist environment has been shown to enhance re-epithelialization and angiogenesis and to reduce pain, partly since these dressings do not need to be changed daily.
- Marx: Rosen's Emergency Medicine, 7th ed.

If the bandage is allowed to become saturated with fluid draining from the wound or to become dirty, it may promote infection.
- Auerbach: Wilderness Medicine, 5th ed.


A patient suffered a 3rd degree bum on his forearm 4 days ago. Now he presents with fever, spreading erythema, worsening arm pain, and elevated white count. The best course of management includes:
a. elevate/splint/antibiotics/secondarily debride
b. immediate eschar debridement
c. IV Abtx

Answer: immediate eschar debridement

Circumferential burns of an extremity or of the trunk pose special problems. Swelling beneath the unyielding eschar may act as a tourniquet to blood and lymph flow, and the distal extremity may become swollen and tense. More extensive swelling may compromise the arterial supply. Escharotomy may be required. To avoid permanent damage, escharotomy must be performed before arterial ischemia develops.


Burn shock is associated with:
a. Decreased SVR
b. Increased ICF
c. Increase ICP
d. Decrease ICP
e. Increase SVR

decreased cardiac output or increased SVR

Two processes lead to postburn hypovolemia: an increase in microvascular permeability in the burn wound and an increase in the osmolarity of surface burn tissue. A large intravascular to extravascular plasma shift occurs. The phase of rapid loss of intravascular fluid persists for about 24 to 36 hours.
- Goldman: Cecil Medicine, 23rd ed.

Excessive leakage of plasma, especially in the first eight hours post-burn, causes hypovolemia, hypoproteinemia, hemoconcentration, electrolyte imbalances and acid base disturbances. Plasma volume is reduced by as much as 23-27%, with a reduction in cardiac output and an increase in peripheral vascular resistance.

A marked increase in peripheral vascular resistance accompanied by a decrease in cardiac output occurs in the first 18 to 24 hours postinjury.
- Bope: Conn's Current Therapy 2010, 1st ed

Cardiovascular System (Plastic Seminar, see diagram)
➢ Dramatic effect on the cardiovascular system
➢ During the initial (emergent/ebb) phase of burn injury lasting the first 72 hours there is:
o Increased capillary permeability
o Decreased plasma volume
o Decreased cardiac output
➢ This initial burn shock may mimic hypovolemic shock because the decrease in circulating volume can result in tachycardia, hypotension, decreased cardiac output, decreased central venous pressure, decreased pulmonary artery pressures and decreased urine output
➢ The above cardiovascular responses result from Neurogenic and humoral influences (ie vasocontriction) rather than from hypovolemia

➢ The Flow Phase follows the ebb phase by approximately 24 hours
➢ During the Flow Phase burn shock is resolved and capillary integrity is re-established ==> mobilization of fluid and diuresis

➢ Several process involved in postburn vascular changes:
o Loss of intravascular volume to burn and nonburn tissue
o Increase in osmotic pressure in burn tissue can increase burn edema
o Hypoproteinemia results in cellular swelling

➢Alterations in electrolytes is common and should be monitored:
o Hyperkalemia ==> seen in initial resuscitative phase (due to release from damaged cells
o Hypokalemia can result secondarily from hemodilution
o During the acute phase alterations in Na, K, Mg, Ca, and Ph need to be monitored and corrected


A burn patient developed progressive anemia due to:
a. Ag sulfasiadine causing marrow suppression
b. Fluid redistribution
c. Hemolysis
d. Protein consumption

b. Fluid redistribution (I disagree, I think it's silver sulfadiazine that causes aplastic anemia. I think that's what they are getting to. Especially the "progressive anemia part")

McNeil's answer:

Hematologic Changes
➢ Initially laboratory values reflect hemoconcentration that reverses with fluid resuscitation
➢ Hemolysis can also occur resulting in anemia and leukocytosis
➢ Altered tissue oxygenation and sluggish blood flow can occur from a hypercoagulable state secondary to hypovolemia

> Microangiopathic hemolytic anemia
> Physical or chemical injuries
> Burn related
- Goldman: Cecil Medicine, 23rd ed.

Severe burns can also cause fragmentation hemolysis from the thermal injury.
- Bope: Conn's Current Therapy 2010, 1st ed.

Trauma (e.g., march hemoglobinuria), thermal injury from severe burns, and osmotic lysis secondary to freshwater drowning or mistaken intravenous infusion of high volumes of hypotonic fluids are additional causes of mechanical damage to otherwise normal erythrocytes.
- Goldman: Cecil Medicine, 23rd ed.

These sources don’t really mention progressive anemia.


1) A patient with an inhalational burn injury is found to have airway edema on laryngoscopy. Next step to manage includes:
a. Racemic epinephrine
b. Intubate
c. Immediate tracheostomy
d. iv steroids
e. ICU to observe

b. Intubate

Patients with extensive burns and coincident inhalation injury are best managed with intubation. Patients with generalized lower respiratory tract inhalation injury that does not affect the larynx are best managed with intubation. Patients with severe upper airway obstruction and laryngeal burns are best managed with tracheotomy to avoid the additional trauma of an endotracheal tube. Patients with severe facial burns sparing the neck, with or without inhalation injury, are often best managed with tracheotomy. Tracheotomies are best avoided in patients with significant coincident neck burns because of the adverse wound healing of burns in the presence of a tracheotomy, and the potential for pulmonary sepsis from the infected burn eschar. Obviously, these guidelines are general, and treatment should be tailored to the patient's situation and needs.
- Cummings: Otolaryngology: Head & Neck Surgery, 4th ed.

Inhalation injury to the respiratory tree is diagnosed almost exclusively by history and physical examination. Hypoxemia, hypercapnia, and increased carboxyhemoglobin levels are laboratory indicators that should prompt further clinical investigations. The most reliable test to detect early inhalation injury to the larynx, subglottis, and trachea is endoscopy, usually with a flexible bronchoscope.
- Cummings: Otolaryngology: Head & Neck Surgery, 4th ed.

Didn’t find a source that recommended routine bronch or esophagoscopy.


Most importmant indication for intubation in burn injury
a- hoursness of voice
b- carbon in sputum
c- PO2 70 %
d- carboxy Hb more than 20

?? I would think A cause it's the only one that is a sign of swelling/impending obstruction.

Clinical Indications for Intubation (Inhalation Injury)
Pao2 (mm Hg) 50 (acutely)
Pao2/Fio2 ratio


1) Silver sulfasalazine is used in burn wound. It can cause:
a. Granulocyte reduction
b. Metabolic acidosis
c. Pigmentation
d. Anemia


Know the side effects - Often asked

Silver sulfadiazine is the most commonly used. It has a broad spectrum of activity because its silver and sulfa moieties cover gram-positive, most gram-negative, and some fungal forms. Some Pseudomonas species possess plasmid-mediated resistance. Silver sulfadiazine is relatively painless on application, has high patient acceptance, and is easy to use. Occasionally, patients complain of a burning sensation after it is applied, and in a few patients, a transient leukopenia develops 3 to 5 days after its continued use. This leukopenia is generally harmless and resolves with or without cessation of treatment.
-Townsend: Sabiston Textbook of Surgery, 18th ed.

Silver sulfadiazine AKA flamazine: these are important to know
- topical proteolytic enzyme are inactivated
- skin sensitivity
- hemolytic anemia
- leukopenia
- agranulocytosis
- aplastic anemia
- hepatitis
- interstitial nephritis

McNeil seemed to think Ag sulfasalazine does not cause pigmentation changes, but I think it does. But usually more Ag nitrate


What is the agent of choice in a burn patient with sulpha allergy:
a) Silver nitrate
b) Mefanide
c) Silver sulfadiazine
d) There is no topical treatment in sulpha allergy
e) All of the above

a) silver nitrate

In real life 2016 they use aquacel ag/acticoat

Silver sulfadiazine has "sulfa" in its name..

Mafenide acetate (Sulfamylon) is another topical agent with a broad spectrum of activity owing to its sulfa moiety. It is particularly useful against resistant Pseudomonas and Enterococcus species. It also can penetrate eschar, which silver sulfadiazine cannot.
- Townsend: Sabiston Textbook of Surgery, 16th ed., Ch 20


Side effect of Silver nitrate:

broad antimicrobial
painless, no penetration of eschar
stains materials
leaching of electrolytes hyponatremia,calcemia,kalemia
- Rush Review 2006

Silver nitrate has the advantage of being painless on application and having complete antimicrobial effectiveness. Its disadvantages include staining of surfaces to a dull gray or black when the solution dries. This can become problematic in deciphering wound depth during excision of burns and in keeping the patient and surroundings clean of the black staining. The solution is hypotonic as well, and continuous use can cause electrolyte leaching, with rare methemoglobinemia as another complication. A new commercial dressing containing biologically potent silver ions (Acticoat) that are activated in the presence of moisture is available. This dressing holds promise to retain the effectiveness of silver nitrate without the problems of silver nitrate soaks.
- Townsend: Sabiston Textbook of Surgery, 18th ed.


Sulfamyon (Mafenide acetate) is used in burn wound. It can cause:
a. Granulocyte reduction
b. Metabolic acidosis
c. Pigmentation
d. Anemia

Answer: metabolic acidosis

Broad-spectrum antimicrobial; penetrates eschar; may cause pain in sensate skin; wide application may cause metabolic acidosis; mild inhibition of epithelialization.
- Townsend: Sabiston Textbook of Surgery, 18th ed

Bacteriostatic, diffuses through escar, ++pain with application, Gm-ve/Gm+ve but NO MRSA, no antifungal, PAINFUL, potent Carbonic anhydrase inhibitor and can lead to resulant hyperchloremic metabolic acidosis.
- Rush Review 2006


A Patient is admitted with 45% burn resuscitated with fluids. His pulse is 100 per minute, BP: 105/60 mmHg. Temp:38.9 C WBC:18,000 and urine output is 70 cc/hr. which is true:
a. Inadequate crystalloid resuscitation.
b. Wound infection.
c. Hyper-metabolic response to burn.
d. Inadequate colloid resuscitation.

c. Hyper-metabolic response to burn.
Should not resuscitate >1.0cc/kg/hr


The most sensitive assessment of depth of a burn to the palm of the hand
a. injection of indomethacin
b. injection of fluoroscine
c. clinical exam
d. ultrasound

c. clinical exam

1st degree→only epidermis: erythema and microscopic changes. Pain for 48-72 hrs, no scarring
2nd degree→all of epidermis, some of corium: blisters or whitish nonviable dermis. Heal 10-14 days with minimal scarring. High evaporative losses.
3rd degree→full thickness: white waxy appearance with underlying tissue darkened. No sensation


“Deeper” burns; all true except?
a. Increased pain
b. Waxy pale skin colour
e. Direct contact with flame
d. Young or elderly
e. Presence of blisters

Answer: Increased pain


What is the cause of sepsis in burn patients? (skin infection, pneumonia?)

Burn wounds are never sterile, even with the administration of topical agents or systemic antibiotics. The presence of bacteria just on the wound surface is termed colonization. Colonization may be with a single type of organism or with multiple types. Infection of the wound ( Table 113-3 ) indicates invasion of the underlying viable tissue; this process is diagnosed by eschar biopsy and quantitative culture showing greater than 105 organisms per gram of tissue. With progression, viable tissue and its blood vessels are invaded, and septicemia develops.
- Goldman: Cecil Medicine, 23rd ed.

The successful use of topical agents prevents the bacterial conversion of superficial burns to deeper injury, results in the spontaneous healing of wounds that initially appeared clinically to be of full thickness, and decreases the frequency of episodes of systemic sepsis.
- Mandell: Mandell, Douglas, and Bennett's Principles and Practice of Infectious Diseases, 7th ed.


What would you do with a 15 year old with 20% burn? (know the criteria for transfer for burns – burn on sensitive area like face, perineum and hand, greater than 10% burn, etc…)

Answer: tetanus + transfer

Criteria for transfer of care to a specialized burn unit
- Partial thickness burns > 10% total body surface area (TBSA)
- Burn of the hands, face, feet, perineum, across major joints
- Full-thickness burns in any age group
- Electrical burns (including lightening injury)
- Chemical burns
- Inhalation burns
- Burns in patients with significant co-morbid medical conditions
- Burns in patients with other traumatic injuries that have been stabilized
NCBI » Bookshelf » Surgical Treatment » Surgical Infections » Current therapy of burns


Which one is not anticholinergic?
a) Fever,
b) sweating
c) constipation
d) hallucination

Answer: sweating

The diagnosis of acute anticholinergic poisoning is suggested by the characteristic anticholinergic toxidrome. Mydriasis (excessive dilation of the pupil), dry mucous membranes, the absence of axillary sweat, flushed skin, fever, tachycardia, decreased or absent bowel sounds, and bladder distention from urinary retention constitute peripheral evidence of muscarinic blockade.[18,24-26] The patient is often alert and may be silly, agitated, violent, or incoherent. Visual hallucinations are common.[27] Central motor effects may manifest as myoclonus or choreoathetoid movements.
- Marx: Rosen's Emergency Medicine, 7th ed.

Remember common signs and symptoms with the mnemonic, "red as a beet, dry as a bone, blind as a bat, mad as a hatter, and hot as a hare." The mnemonic refers to the symptoms of flushing, dry skin and mucous membranes, mydriasis with loss of accommodation, altered mental status (AMS), and fever, respectively.


A patient undergoes a gastroscopy with diagnosis of peptic ulcer disease. Gag reflex was present and therefore the patient was given 2 sprays of benzocaine. He suddenly becomes hypoxic and his ABG is drawn, which is chocolate brown. What is the etiology?
a) methemoglobinemia
b) anemia from chronic ulcer
c) hypothermia

a) methemoglobinemia
Antidote = methylene blue

Exposure to exogenous oxidizing drugs and their metabolites (such as benzocaine, dapsone and nitrates) may accelerate the rate of formation of methemoglobin up to one-thousandfold, overwhelming the protective enzyme systems and acutely increasing methemoglobin levels.

Other classical drug causes of methemoglobi include antibiotics (trimethoprim, sulfonamides and dapsone[2]), local anesthetics (especially articaine and prilocaine[3]), and others such as aniline dyes, metoclopramide, chlorates and bromates. Ingestion of compounds containing nitrates (such as the patina chemical bismuth nitrate) can also cause methemoglobinemia.


A patient is receiving chemotherapy with doxorubicin. The medication goes interstitial during administration through a vein in the forearm. What is the MOST appropriate immediate treatment?
A. Instill leukovarin antidote immediately
B. Cold compress, elevation, and topical burn ointment
C. Topical sodium mafenide ointment
D. Debride devitalized tissues immediately

I looked this up, you should do B. Cold compress, elevation, conservative. But if there are any signs of necrosis impending, early debridement is indicated.


In snake venom, what is the component that facilitate the spread of venom in lymphatics:
a. Hirudin
b. Collagenase
c. Hyalinurinidase

Answer: Hyaluronidase

The diffusion of toxins from the site of a bite into the circulation is essential for successful envenomation. Degradation of hyaluronic acid in the extracellular matrix (ECM) by venom hyaluronidase is a key factor in this diffusion. Hyaluronidase not only increases the potency of other toxins but also damages the local tissue.

This enzyme breaks down the hyaluronic barrier and decreases the viscosity of connective tissue. It allows venom to penetrate adjacent tissues and probably is the agent most responsible for the extensive swelling or edema of the limb where the venomous bite has occurred. It is also known as the spreading factor.


Old lady brought into the ED. Received i.m. diazepam and 30 minutes later became obtunded. Tx?
a. CT
b. Watch and wait, it ill wear off
c. Give NS @ 100/cc/hr
d. Dialysis
e. Intubate

e. Intubate


Most common drug that cause liver failure
a -ASA
c- Isonazide

"Ah, c'est un mini muffin" haha

The most common cause of ALF in industrialized countries is acetaminophen poisoning.
- Piccini & Nilsson: The Osler Medical Handbook, 2nd ed.


CO poisoning, which is correct:
a. N or high PaO2, Sat O2 is low, low Pulse oxymetry
b. Low PaO2, low SatO2, N P.oxymetry
c. High PaO2 , high SatO2, high Pulse oxymetry

- PaO2 N or high - this is not a ventilation problem
- Sa02 low
- PulseOx N or high - pulse ox cannot discriminate between oxyhemoglobin and carboxyhemoglobin

CO diffuses rapidly across the pulm. Capillary and binds to iron moiety of heme (and other porphyrins) ~ 240 x affinity of oxygen. Once bound, an allosteric change that greatly diminishes the ability of the other 3 oxygen binding sites to off-load oxygen to periperal tissues. This results in a deformation and leftward shift of oxyhemoglobin dissociation curve and compounds the impairment in tissue oxygen delivery.

Diagnosis: history and physical with elevated carboxyhemoglobin levels (cooximetry of ABG). ** Cannot screen with pulse oximetry b/c does not diff. carboxyhemoglobin from oxyhemoglobin. Blood PO2 measurements tend to be normal because PO2 reflects PO2 dissolved in bld….which is not affected by CO

PaO2 levels should remain normal

The total percentage of sites actually bound with O2 is constant for a given set of conditions, and is the 'saturation of blood with oxygen'. This is called SvO2 and SaO2.

Arterial hemoglobin (SaO2)

Arterial partial pressure of oxygen (PaO2)

Alveolar partial pressure of oxygen (PAO2)


Regarding Carbon monoxide, which of the following is true:
a) carboxyhemoglobin binds to hemoglobin with less affinity than oxygen
b) the half-life of carboxyhemoglobin is 45-60 minutes in room air
c) carbon monoxide binds to the Fe in the RBC
d) irreversibly binds to hemoglobin

c) carbon monoxide binds to the Fe in the RBC (YES)

a) carboxyhemoglobin binds to hemoglobin with less affinity than oxygen (more affinity)
b) the half-life of carboxyhemoglobin is 45-60 minutes in room air (no, 5hrs)
d) irreversibly binds to hemoglobin (NO, reversible)

Hemoglobin binds CO tightly and forms a complex that is only slowly reversible.
- Marx: Rosen's Emergency Medicine, 7th ed.

Half-life of CO at room air temperature is 3-4 hours.
CO reversibly binds hemoglobin, resulting in relative functional anemia.
- eMedicine

Half life
Half-lives of COHb on room air at normal atmospheric pressure range from 249 to 320 minutes (5hrs). On 100% oxygen at atmospheric pressure, this is reduced to an average of 74 to 80 minutes.11 The exception to this is COHb generated by methylene chloride exposure, which can have a half-life of up to 13 hours due to ongoing metabolism.

Haemoglobin binds with carbon monoxide 240 times more readily than with oxygen. The presence of carbon monoxide on one of the 4 haem sites causes the oxygen on the other haem sites to bind with greater affinity. This makes it difficult for the haemoglobin to release the oxygen to the tissues and has the effect of shifting the curve to the left. With an increased level of carbon monoxide, a person can suffer from severe hypoxemia while maintaining a normal pO2.

Left = Hb retains O2, right = Hb delivers O2


All are true of carbon monoxide EXCEPT:
A. Reversibly binds hemoglobin
B. Shifts hemoglobin-O2 curve to the left
C. Intubation indicated when carboxyhemoglobin level > 20%
D. CO binds to cardiac myoglobin with higher affinity than hemoglobin

D. CO binds to cardiac myoglobin with higher affinity than hemoglobin (NO, CO binds to myoglobin with 60X higher affinity than O2, while CO binds Hg with 240X higher affinity than 02)

A. Reversibly binds hemoglobin (yes)
B. Shifts hemoglobin-O2 curve to the left (yes)
C. Intubation indicated when carboxyhemoglobin level > 20% (may be needed if patient is obtunded)

Endotracheal intubation is commonly required and is specifically indicated in the following conditions:
- Cardiac or respiratory arrest
- Respiratory insufficiency (see Box 72-1 )
- Airway protection
- The need for deep sedation or analgesia, up to and including general anesthesia
- Transient hyperventilation of patients with space-occupying intracranial lesions and evidence of increased intracranial pressure (ICP)
- Delivery of a 100% fraction of inspired oxygen (Fio2) to patients with carbon monoxide poisoning
- Facilitation of the diagnostic workup in uncooperative or intoxicated
Miller: Miller's Anesthesia, 7th ed.

Approximately 85% of carbon monoxide is bound to hemoglobin to form COHb, and the rest is dissolved in plasma or bound intracellularly, often to myoglobin. The binding affinity of normal adult hemoglobin for carbon monoxide is about 200 times that of oxygen. Fetal hemoglobin has an even higher binding affinity, which may account for potentially more severe fetal toxicity. Like hemoglobin, myoglobin has a greater affinity for carbon monoxide than it does for oxygen, and binds to carbon monoxide with approximately 60 times the affinity for oxygen.


What is the Half life of CO on 100% mask oxygen?
45-90min, 2hour, 3 hour , 4 hour

Answer: 45-90min


Patient in trauma 33 degrees and stable, closed head injury
Besides warmed iv fluids and blankets what do you do
a) Observe
b) continue current management
c) warm peritoneal lavage
d) warm pleural lavage

b) continue current management

Temperature less than 32.2, consider more invasive active internal rewarming techniques. Extracoroeal blood rewarming should be considered first and only if unavailable should lavage be considered.
Invasive methods include:
-extracorporeal blood rewarming by cardiopulmonary, arteriovenous femorofemoral, or venovenous bypass, or hemodialysis
-warm solution lavage of the stomach, colon, thoracic cavity, peritoneum (peritoneal dialysis), or bladder

Peritoneal dialysis is appropriate therapy in a severely hypothermic patient. In practice, however, it is often omitted if other measures appear to be successful. There are no universally agreed on criteria for performing peritoneal lavage in hypothermic patients who have detectable vital signs. Although theoretically less effective than other techniques that directly warm the thorax in the setting of cardiac arrest, it has been used successfully in that situation.
- Roberts: Clinical Procedures in Emergency Medicine, 5th ed.

Invasive core warming was thought to be indicated because of the risk of cardiac arrhythmia at temperatures below 30°C to 32°C (86°F to 90°F).
- Rapid Endovascular Warming for Profound Hypothermia. Annals of Emergency Medicine - Volume 51, Issue 2 (February 2008)


Patient post trauma small bowel bleeding . went to OR and had laparotomy and small bowel resection. Noticed that he was oozing from everywhere. Temp 33. INR drawn 1.2 other vitals stable
What is likely cause :
1. DIC
2. sepsis
3. hypothermia
4. preexisting congenital coagulopathy

3. hypothermia


Frostbite management:
40 degree bath
heat lamp
massage in snow

Answer: 40 degree bath

Direct cellular damage is treated by rapid thawing of all degrees of frostbite with immersion in gently circulating water warmed to between 40°and 42° C
- Auerbach: Wilderness Medicine, 5th ed.

Address life-threatening conditions first. Fluid resuscitation, especially in persons with mountain frostbite, enhances blood flow and tissue perfusion. Rapidly rewarm the affected body part, avoiding further trauma.

An appropriate warming technique is the use of a whirlpool bath or tub of water at 40-42°C. Mild antibacterial soap may be added. Avoid warmer temperatures or dry heat because of the risk of thermal injury.

If a tub is not available, use warm, wet packs at the same temperature. Avoid massaging the affected area, as this can cause further injury. Administer analgesics, such as morphine sulfate, as needed for pain.

Thawing usually takes 20-40 minutes and is complete when the distal tip of the affected area flushes. Once thawed, keep the body part on sterile sheets, elevated, and splinted when possible. A cradle may be used over an injured lower extremity to avoid pressure or trauma.

Debride clear blisters to prevent thromboxane-mediated tissue injury. Leave hemorrhagic blisters intact to reduce the risk of infection.

In patients with an associated dislocation, perform reduction as soon as thawing is complete. Manage fractures conservatively until postthaw edema has resolved.


Most arterial emboli go to where?
a) Common Femoral artery
b) Popliteal artery
c) Iliofemoral artery
d) Aortic bifurcation
e) Peroneal artery

Answer: femoral artery

26% femoral artery
25% aortic bifurcation

This is a dumb question.

Cardiac embolism is most commonly encountered in patients who have preexisting valvar heart disease, mural thrombus of the ventricle or atrium, or underlying rhythm disturbances (e.g., atrial fibrillation). The most frequent sites of lower extremity embolization are the aortic and femoral bifurcations.
- Goldman: Cecil Medicine, 23rd ed.

Emboli usually lodge at bifurcations of arteries, and therefore the most common sites are the superficial femoral artery- deep femoral artery junction, the aorta at the origin of the iliac arteries, and the popliteal artery above the trifurcation of medium arteries to the calf.
- Noble: Textbook of Primary Care Medicine, 3rd ed


All are true about acute embolic leg ischemia except:
a. Common femoral artery is the most common affected artery
b. Should be heparinized
c. Usually distal pulses are absent.

All are true.

The absence of arterial pulses on examination will alert the surgeon to both the location of the arterial occlusion and the degree of ischemia. Patients with acute arterial embolism generally have normal palpable pulses above the occlusion with a complete absence below. The pulse immediately above the occlusion (e.g., the common femoral pulse in a patient with a femoral bifurcation embolus) may be particularly prominent with a "water-hammer" quality that results from limited arterial outflow. The presence of normal arterial pulses in the contralateral extremity is most suggestive of an acute embolus because patients with acute thrombosis generally have some degree of symmetrical pulse deficit owing to long-standing atherosclerosis.
- Townsend: Sabiston Textbook of Surgery, 16th ed


An elderly gentleman presents a few days after abdominal surgery with a painful leg. Two hours after onset it is cold and mottled. The femoral and the pedal pulses are absent. The leg is swollen 2cm greater than the other side (thigh) and there is pedal edema. What is the diagnosis?
a) Femoral arterial embolism
b) Femoral arterial thrombosis
c) Calf DVT
d) Ileofemoral thrombophlebitis
e) Superficial femoral thrombophlebitis

a) Femoral arterial embolism

Acute limb ischemia. Due to timing (2h), sounds like an emboli more than an thrombosis

The site of occlusion is localized by the absence of pulses on physical exam (presence of palpable femoral pulse in the absence of a palpable popliteal pulse localizes the obstruction to the artery between, therefore the superficial femoral artery)
BUT, in addition, this patient also has swelling of the left calf with pitting edema which is more suggestive of venous thrombosis
The site of venous obstruction determines the level at which swelling is observed clinically
Femoral vein thrombosis usually is associated with swelling of the foot and calf
Ileofemoral venous thrombosis is the most extensive form of DVT and is usually associated with tenderness in the groin and swelling of the entire leg
Major DVT of the veins in the thigh or pelvis produces a characteristic presentation of pain and extensive pitting edema

The absence of arterial pulses on examination will alert the surgeon to both the location of the arterial occlusion and the degree of ischemia. Patients with acute arterial embolism generally have normal palpable pulses above the occlusion with a complete absence below. The pulse immediately above the occlusion (e.g., the common femoral pulse in a patient with a femoral bifurcation embolus) may be particularly prominent with a "water-hammer" quality that results from limited arterial outflow. The presence of normal arterial pulses in the contralateral extremity is most suggestive of an acute embolus because patients with acute thrombosis generally have some degree of symmetrical pulse deficit owing to long-standing atherosclerosis.
- Townsend: Sabiston Textbook of Surgery, 16th ed

On examination of the patient with superficial thrombophlebitis, there will be pain, tenderness, and erythema along the course of the vein, which may also be palpated as a tender cord or knot.
- Goroll: Primary Care Medicine, 4th ed., Copyright © 2000

The clinical features of venous thrombosis include leg pain, tenderness, swelling, a palpable cord, discoloration, venous distention, prominence of the superficial veins, and cyanosis. In most patients who have clinically suspected DVT, the symptoms and signs are non-specific; in more than 50% of these patients, the clinical suspicion of DVT is not confirmed by objective testing.
- Goldman: Cecil Textbook of Medicine, 21st ed., Copyright © 2000

Deep Venous Thrombosis and Thrombophlebitis
Clinical : Physical : Phlegmasia alba dolens
* Painful white inflammation was originally used to describe massive ileofemoral venous thrombosis and associated arterial spasm. The affected extremity is often pale with poor or even absent distal pulses.
* The physical findings may suggest acute arterial occlusion, but the presence of swelling, petechiae, and distended superficial veins point to this condition.


Pregnant women presents with DVT in the left iliofemoral vein. What is the most appropriate treatment?
1. warfarin
2. heparin
3. ASA
4. none of the above

Answer: heparin

Nobody likes warfarin babies

VTE in pregnancy is treated with heparin. Because of its more favorable side-effect profile, reliable pharmacokinetics, and equal efficacy in treating VTE, LMWH now represents the most commonly used anticoagulant for treatment of VTE in pregnancy.
- Hoffman: Hematology: Basic Principles and Practice, 5th ed.


The Sx with greatest risk of DVT:
a) total hip arthroplasty
b) vein stripping
c) C-section
d) Abdominal resection

a) total hip arthroplasty

Postoperative venous thrombosis varies depending on a multitude of patient factors, including the type of surgery undertaken. Without prophylaxis, general surgery operations typically have an incidence of DVT around 20%, whereas orthopedic hip surgery can occur in up to 50% of patients.

The risk for deep venous thrombosis (DVT) has been reported to be highest in critical care and spinal cord injury patients (60-80%). Following general surgery procedures, the approximate risk for deep venous thrombosis (DVT) is 15-40%. This risk nearly doubles after hip or knee replacement surgery or hip fracture surgery (40-60%).


Why do we not use ASA for DVT prophylaxis?
A. More fatal PEs and total PEs
B. More DVTs
C. More side effects
D. No ability to monitor ASA effect

See article for chest.
B. More DVT's
Previous answers: A, C

This may change in the near future..

Aspirin — Although aspirin, is highly effective in reducing major arterial thrombotic events, there is little evidence that aspirin and/or other antiplatelet agents (eg, clopidogrel) can effectively prevent venous thromboembolic events in hospitalized medical patients. Although a 1994 meta-analysis suggested that aspirin reduced the incidence of VTE by approximately 20 percent compared with placebo or no treatment [111,112], studies since then have shown either no significant benefit or inferiority when compared with other modalities such as LMW heparin [112]. Thus, we agree with others that aspirin not be used, either alone or in combination, as prophylaxis against VTE in any medical patient group [83].

The inferior efficacy of aspirin compared to other methods of VTE prophylaxis has been demonstrated in clinical trials. Among 205 patients undergoing hip or knee arthroplasty, who were randomized to receive aspirin or the LMWH ardeparin, the relative reduction in the risk of VTE with the use of LMWH over aspirin was 63% (p 95%, respectively (p


1) With regards to indications for IVC filter in all are true except:
a. Streptokinase allergy
b. C/I to anticoagulation
c. Complication of anticoagulation
d. Failed trail of anticoagulation
e. Free floating ilio-femoral thromus

a. Streptokinase allergy

DVT or PE with contraindication to anticoagulation therapy
DVT or PE in a patient with a complication of anticoagulation therapy
Failure of anticoagulation therapy
Free-floating iliofemoral or caval thrombus
- Patients with DVT who are about to undergo surgery
- Patients with chronic pulmonary hypertension and a marginal cardiopulmonary reserve
- Trauma patients: Patients with severe trauma are prone to develop DVT and PE


DVT risk factors. All except

Can probably deduce this one rather easily.

The following risk factors for DVT have been identified in many different epidemiologic studies:

* General
o Age
o Immobilization longer than 3 days
o Pregnancy and the postpartum period
o Major surgery in previous 4 weeks
o Long plane or car trips (>4 h) in previous 4 weeks
* Medical
o Cancer
o Previous DVT
o Stroke
o Acute myocardial infarction (AMI)
o Congestive heart failure (CHF)
o Sepsis
o Nephrotic syndrome
o Ulcerative colitis
* Trauma
o Multiple trauma
o CNS/spinal cord injury
o Burns
o Lower extremity fractures
* Vasculitis
o Systemic lupus erythematosus (SLE) and the lupus anticoagulant
o Behçet syndrome
o Homocystinuria
* Hematologic
o Polycythemia rubra vera
o Thrombocytosis
o Inherited disorders of coagulation/fibrinolysis
o Antithrombin III deficiency
o Protein C deficiency
o Protein S deficiency
o Prothrombin 20210A mutation
o Factor V Leiden
o Dysfibrinogenemias and disorders of plasminogen activation
* Drugs/medications
o Intravenous drug abuse
o Oral contraceptives
o Estrogens
o Heparin-induced thrombocytopenia



Which of the following BEST explains why patients with a PE don’t develop ischemic lung segments?
A. The lungs are well ventilated
B. The lungs have a double blood supply
C. The PA carries only deoxygenated blood
D. A PE is rapidly eliminated by the body thus restoring blood flow

Answer: The lungs have a double blood supply


Picture showing normal CXR and EKG (S1,Q3,T3) for patient having chest pain post total hip replacement. What is the most appropriate initial
a. Angiogram
b. Infused chest CT
c. Lung scan
d. Echo.

b. Infused chest CT

I guess that is a CT-PA?


What is the most common source of PE?
a) Iliofemoral vein
b) Saphenous vein
c) Tibial vein
d) Inferior vena cava

Answer: Iliofemoral vein

Venous thrombi occurred in the segment in 79% of cases, including the inferior vena cava in 21%

The majority of PE originates from an existing DVT in the legs, and the iliofemoral venous system is the site from which most clinically significant pulmonary emboli arise. PE develops in about 50% of patients with proximal DVT. Rare causes of PE include a fat embolus associated with fractures of long bones and air embolism, often associated with operative procedures and central lines.
- Townsend: Sabiston Textbook of Surgery, 18th ed.


Commonest sign of PE is :
a. Rales.
b. Tachypnea.
c. High PCO2.

b. Tachypnea.

Answer: Tachypnea

In patients with recognized PE, the incidence of physical signs has been reported as follows:
96% have tachypnea (respiratory rate >16/min), 58% develop rales, 53% have an accentuated second heart sound, 44% have tachycardia (heart rate >100/min), 43% have fever (temperature >37.8°C), 36% have diaphoresis, 34% have an S 3 or S 4 gallop, 32% have clinical signs and symptoms suggesting thrombophlebitis, 24% have lower extremity edema, 23% have a cardiac murmur
19% have cyanosis

Pulmonary embolism (PE) is a potentially fatal entity. Typical symptoms include dyspnea (80%), tachypnea (>16 respirations per minute, 80%) pleuritic chest pain (70%), rales (60%), fever (45%), tachycardia (40%), and hemoptysis (20%).
- Mettler: Essentials of Radiology, 2nd ed.


All of the following increase the risk of pulmonary embolism EXCEPT:
a. Chest trauma
b. Surgery within last 3 months
c. Cancer
d. History of DVT
e. Decreased mobility

a. Chest trauma


All of the following except one accurately leads to the diagnosis of pulmonary embolus:
a) Increased PCWP
b) Increased CVP
c) Increased PAP
d) Increased JVP
e) Decreased pC02

a) Increased PCWP

Answer: Increased PCWP

Diagnosis: Massive pulmonary embolism
PCWP: Normal or ↓
CO: ↓↓
Comments: Usual finding is elevated right-sided pressures.
- Piccini & Nilsson: The Osler Medical Handbook, 2nd ed


All of the following are indicative of a PE except:
a. hypoxia resistant to FiO2
b. hypercapnia
c. tachypnea
d. hemoptysis
e. nonspecific ST changes on EKG

b. hypercapnia

Cause they hyperventilate

As well, hypoxia or hypercapnia is suggestive but not diagnostic of pulmonary embolism.
- Townsend: Sabiston Textbook of Surgery, 18th ed.

An elevated PaCO2 is distinctly unusual in pulmonary embolic disease.
- Goldberg et al. Hypercapnia complicating massive pulmonary embolism. Crit Care Med. 1984 Aug;12(8):686-8.


What are the finding in PE?

Pulmonary embolism (PE) is a potentially fatal entity. Typical symptoms include dyspnea (80%), tachypnea (>16 respirations per minute, 80%) pleuritic chest pain (70%), rales (60%), fever (45%), tachycardia (40%), and hemoptysis (20%). Patients who initially have no dyspnea, pleuritic chest pain, or tachypnea are unlikely to have a PE. A low-grade fever may occur with PE, but a high-grade fever and leukocytosis suggest a pneumonia. About 35% of patients with PE will also have clinically evident phlebitis. The converse is more important, however; that is, about two thirds of patients with PE will not show evidence of phlebitis.
The chest x-ray findings in a patient with PEs are relatively nonspecific, and the major reason for ordering a chest x-ray is to exclude other causes of the patient’s symptoms. Occasionally a small pleural effusion, atelectasis, or an elevated hemidiaphragm may be present. If infarction of a portion of the lung is a result of the embolism, a wedge-shaped infiltrate may be noted.
After a chest x-ray, the next study to be performed is a nuclear medicine ventilation/perfusion (V/Q) lung scan or a contrasted CT scan. In the nuclear medicine study, ventilation is assessed by having the patient inhale and then exhale a radioactive gas or an aerosol containing radioactive particles ( Fig. 5–18 A). Perfusion is assessed by intravenously injecting a number of biodegradable radioactive particles that are unable to pass through the pulmonary capillary bed. These are trapped in the capillary bed, and because they give off radiation, images of the lungs can be obtained in various projections ( Fig. 5–18 B). The V/Q lung scans are then compared. You are looking for a defect on the perfusion scan that is not seen on the ventilation scan (a mismatch). The reason is that a PE generally does not interfere much with ventilation. Abnormalities such as tumors and bullae would cause both a ventilation abnormality and a perfusion abnormality (a matched defect).
- Mettler: Essentials of Radiology, 2nd ed.


When is streptokinase therapy indicated?
a) Pulmonary embolism with shock
b) Multiple pulmonary emboli
c) Lobar pulmonary emboli
d) Pulmonary infarction

a) Pulmonary embolism with shock

Answer: Pulmonary embolism with shock

In patients with a serious hemodynamic and hypoxic response to pulmonary embolism (cardiogenic shock or hemodynamic instability) who do respond to resuscitation, heparin is initiated as standard therapy. In addition, thrombolytics (streptokinase or urokinase) may be given.
- Townsend: Sabiston Textbook of Surgery, 18th ed.

[T]hrombolysis is reserved in most centers for patients with massive pulmonary embolism causing cardiovascular collapse.
- Hoffman: Hematology: Basic Principles and Practice, 5th ed.


Fat embolism associated with all but:
a. DM
b. Liposuction
c. Hypothyroid
d. Sickle cell
e. Long bone fractures

C. Hypothyroidism
Other answers: COPD, hyperthyroidism

Access Medicine
Traumatic fat embolism
Long bone fracture (especially femur)
Other fractures
Orthopedic surgery
Blunt trauma to fatty organs (e.g., liver)
Bone marrow biopsy
Nontraumatic fat embolism
Diabetes mellitus
Lipid infusions
Sickle cell crisis
Cardiopulmonary bypass
Decompression sickness
Corticosteroid therapy
Alcoholic fatty liver
Acute fatty liver of pregnancy
Cyclosporine infusion


Fat embolism can cause all except :
a. Lipiduria
b. Skin rash
c. CXR infiltrate
d. CNS symptoms

All are true

Pulmonary fat embolus is the second most common etiology of ACS. Definitive diagnosis requires bronchoscopy; however, the classic presentation of severe long bone pain followed several days later by fever, leukocytosis, and a new infiltrate is highly suggestive of pulmonary fat embolus.
- Mason: Murray & Nadel's Textbook of Respiratory Medicine, 4th ed.

The diagnosis is made from the clinical and radiographic findings in the setting of risk factors such as surgery and trauma.
- Goldman: Cecil Medicine, 23rd ed.

Radiographic abnormalities may not be detected for several days after the onset of symptoms.
- Long: Principles and Practice of Pediatric Infectious Diseases, 3rd ed.

Neurologic- Central nervous system dysfunction initially manifests as agitated delirium but may progress to stupor, seizures, or coma and is frequently unresponsive to correction of hypoxia.

Dermatologic- Alert clinicians may notice reddish-brown nonpalpable petechiae developing over the upper body, particularly in the axillae, within 24-36 hours of insult or injury. These petechiae occur in only 20-50% of patients and resolve quickly, but they are virtually diagnostic in the right clinical setting. Subconjunctival and oral hemorrhages and petechiae also appear.

Fat globules are found in blood, sputum, urine, and cerebrospinal fluid. The urine or sputum can be stained for fat using a saturated alcoholic solution of Sudan III.
- Browner: Skeletal Trauma, 4th ed


How long after a trauma do changes on chest X-ray appear with fat embolism syndrome?
a) 48 hrs
b) 4 days
c) 1 week
d) 2-3 weeks

a) 48 hrs
Radiographic abnormalities may not be detected for several days after the onset of symptoms.
- Long: Principles and Practice of Pediatric Infectious Diseases, 3rd ed

Chest radiography: Serial radiographs reveal increasing diffuse bilateral pulmonary infiltrates within 24-48 hours of onset of clinical findings.


After femur fracture suffered 24 hours ago and splinted, a patient develops decreased SaO2, confusion, petechiae, and CXR infiltrates. The next best course of action includes:
a. ICU for monitoring
b. ORIF of femur fracture
c. Diuresis
d. Anti-coagulate with IV heparin

A. ICU for monitoring.

Management of fat embolism syndrome is primarily supportive, usually in an intensive care unit.
- Marx: Rosen's Emergency Medicine, 7th ed.

If the question was prevention, then it would be ORIF or early immobilization of the fracture:

Other interventions that have been shown to reduce the incidence and/or severity of FES are early immobilization of fractures, operative correction rather than conservative management (ie, traction alone), and limitation of the intraosseous pressure during orthopedic procedures. - Uptodate 2016


The incidence of fat embolism syndrome increase in all of the following except:
a. Increase fatty acid in blood
b. Respiratory problem due to fat globule
c. Decrease fatty acid in blood
d. Long bone fractures
e. Increase body weight

Answer: Decrease fatty acid in blood

I don't really know what B. means


The incidence of fat embolism syndrome is increased in all of the following EXCEPT?
a) Delayed fixation of a fracture (>24hrs)
b) Pelvic fracture
c) Multiple long bone fractures
d) Prolonged mobility at a fracture site
e) Increased age

e) Increased age


Clinical signs are evident hours to days after trauma involving multiple long bone fractures or femoral, tibial, and pelvic fractures. Although fat globule embolization may occur in nearly 100% of traumatized patients, the incidence of FES ranges from 1 to 17% in traumatized individuals. [25] In patients with isolated long bone fractures, the incidence is between 2 to 5%. In the multiply injured patient with long bone fractures or pelvic fractures, the incidence is as high as 15%. [75] Marrow fat from the fracture site after musculoskeletal trauma can enter into the pulmonary vasculature.
Early fixation has resulted in a reduction of FES and ARDS in several studies. [30] [47] [65] [76] [84] Johnson and associates [44] reported a 17% incidence of ARDS with early fracture stabilization compared with 75% with delayed fixation. Both clinical and experimental studies suggest that the method of fracture fixation plays a minor role in the development of pulmonary complications. [73] ARDS occurs several days after the primary insult and can be lessened with early fixation, debridement of necrotic soft tissue and hematoma, and maintenance of the upright position. Early debridement and reassessment with frequent dressing changes can prevent secondary infection and subsequent bacterial translocation. Avoidance of protein malnutrition, in addition, can protect against gut translocation and systemic infection. Earlier range of motion and muscle strengthening can result in decrease in length of hospitalization, rehabilitative time, and long-term disability.
- Townsend: Sabiston Textbook of Surgery, 16th ed., 2001

The incidence of the fat embolism syndrome depends on the bone involved, whether fractures are isolated or multiple, the age of the patient and the gender.
- Stein PD, Yaekoub AY, Matta F, Kleerekoper M. Fat embolism syndrome. Am J Med Sci. 2008 Dec;336(6):472-7.


What colour is fat on MRI:
a) dark on T1 and T2
b) light on T1 and T2
c) dark on T1 and light on T2
d) light on T1 and dark on T2

d) light on T1 and dark on T2

A fairly constant rule is that fat has a high signal (bright) on T1-weighted images, and fluid has a high signal on T2-weighted images. Structures with little water or fat, such as cortical bone, tendons, and ligaments, remain dark in all types of sequences.
- Canale & Beaty: Campbell's Operative Orthopaedics, 11th ed.

Although many MRI techniques exist, the two basic types of images are T1 and T2. T1 images show fat as a white or bright signal, whereas water (or cerebrospinal fluid [CSF]) is dark. On a T2 image, fat is dark, and blood, edema, and CSF appear white.
- Mettler: Essentials of Radiology, 2nd ed.


PET scan diagnose certain tumors depends on:
a. Enhanced blood supply
b. Abnormal glucose metabolism
c. Rapid growth

Answer: Abnormal glucose metabolism

PET scanning with the tracer (18F) fluorodeoxyglucose (FDG, FDG-PET) is widely used in clinical oncology. This tracer is a glucose analog that is taken up by glucose-using cells and phosphorylated by hexokinase (whose mitochondrial form is greatly elevated in rapidly-growing malignant tumours). A typical dose of FDG used in an oncological scan is 200-400 MBq for an adult human. Because the oxygen atom which is replaced by 18F to generate FDG is required for the next step in glucose metabolism in all cells, no further reactions occur in FDG. Furthermore, most tissues (with the notable exception of liver and kidneys) cannot remove the phosphate added by hexokinase. This means that FDG is trapped in any cell which takes it up, until it decays, since phosphorylated sugars (due to their ionic charge) cannot exit from the cell. This results in intense radiolabeling of tissues with high glucose uptake, such as the brain, the liver, and most cancers. As a result, FDG-PET can be used for diagnosis, staging, and monitoring treatment of cancers, particularly in Hodgkin's disease, non Hodgkin's lymphoma, and lung cancer. Many other types of solid tumors will be found to be very highly labeled on a case-by-case basis-- a fact which becomes especially useful in searching for tumor metastasis, or for recurrence after a known highly-active primary tumor is removed. Because individual PET scans are more expensive than "conventional" imaging with CT and MRI, expansion of FDG-PET in cost-constrained health services will depend on proper Health Technology Assessment; this problem is a difficult one because structural and functional imaging often cannot be directly compared, as they provide different information. Oncology scans using FDG make up over 90% of all PET scans in current practice.


The most common x-ray finding of aortic rupture is:
a. Widen mediastinum
b. Tracheal deviation
c. Pleural cap
d. Loss of aortic knob

Answer: Widen mediastinum

increase in the width of the superior mediastinum is the most sensitive sign and is found in 50% to 92% of aortic ruptures ( Figure 42-17 ).[92] Specificity of this radiologic sign is 10%. Mediastinal widening may be caused by venous bleeding from a clavicle, thoracic spine, or sternal fracture; pulmonary contusions; a previous mediastinal mass; a misplaced CVP catheter; or magnification caused by the anteroposterior and supine position of a portable chest radiograph. The sign is not pathognomonic for aortic rupture.
- Rosen


CT scan is better than MRI in visualization of:
a. Soft tissue
b. Tumor
c. Bone cortex
d. Bone marrow

Answer: Bone cortex


A patient is having an abdominal CT with IV contrast. You should avoid which of the following medications?
A. Metformin
B. Glyburide
C. Synthroid
D. Insulin

A. Metformin

Metformin (Glucophage)
oral diabetic agent
patients with renal insufficiency may develop lactic acidosis
withhold drug for 48 hrs after contrast administration in all patients taking this drug


Female with NIDDM on metformin and glyburide, well hydrated, goes for contrast enhanced X-ray. Receives 1cc/kg of low osmolarity radio contrast. What will be the most likely outcome?
a) Metabolic acidosis.
b) Anaphylaxis.
c) Renal failure.
d) Nothing

d) Nothing

Factors associated with elevated risk include chronic renal insufficiency (baseline creatinine >1.5), diabetic nephropathy, multiple myeloma–associated nephropathy, dehydration, age older than 60 years, recent surgery, and larger doses of contrast medium. The risk factors appear additive. Iodinated contrast agents given to patients receiving metformin (dimethyl-biguanide) can rarely result in lactic acidosis. Accordingly, this agent is held for 2 days before and then re-started 2 days after administration of the contrast agent if the renal function is stable. Maintenance of adequate hydration before, during, and after contrast injection is absolutely critical and is best accomplished by continuous intravenous (IV) administration of isotonic sodium chloride or sodium bicarbonate.[9] Although controversial, the selective administration of N-acetylcysteine, a thiol-containing antioxidant, at a dose of 600 mg for 2 days before and after the procedure in individuals with evidence of renal impairment may offer the potential of renal preservation.[10]
- Townsend: Sabiston Textbook of Surgery, 18th ed.

Given that it is a RARE occurance, most likely outcome is nothing.


Which of following is a risk factor for anaphylactoid reaction with administration of IV contrast?
a) Previous allergy
b) Asthma
c) shellfish allergy
d) on beta blocker
e) cv disease
f) iodine allergy

Answer: Asthma
?or previous allergy if they were anaphylactic before??

Intravenous radiocontrast media
IV administered radiocontrast media causes an anaphylactoid reaction that is clinically similar to true anaphylaxis and is treated in the same way. The reaction is not related to prior exposure. Shellfish or iodine allergy is not a contraindication to use of IV contrast and does not mandate a pretreatment regimen.
The term iodine allergy is a misnomer. Iodine is an essential trace element present throughout the body. No one is allergic to iodine. Patients who report iodine allergy usually have had either a prior contrast reaction, a shellfish allergy, or a contact reaction to povidone-iodine (Betadine). Manage these patients as indicated earlier.
Pretreatment with antihistamines or corticosteroids and use of LMW agents lead to lower rates of anaphylactoid reactions to IV contrast. Consider these measures for patients who have prior history of reaction, since rate of recurrence is estimated at 17-60%. Some institutions use only LMW agents. Patients who are atopic and/or asthmatic also are at increased risk of reaction. In addition, allergic reaction is more difficult to treat in those taking beta-blockers.


With regards to allergy to IV contrast. there is a risk of prophylaxis in:
a. Asthma
b. 1st exposure
c. Dehydration
d. All of the above
e. None of the above

In another large randomized trial, isotonic saline significantly reduced the incidence of contrast nephropathy following coronary angiography compared with half-normal saline with a particular benefit noted in diabetic patients and those receiving large contrast loads.[568] In a smaller single trial, hydration with sodium bicarbonate before contrast exposure was more effective than hydration with isotonic saline for the prevention of contrast nephropathy.[569] In aggregate, the key message from these studies is that the avoidance of hypovolaemia is the key intervention in preventing contrast nephropathy.
- Brenner: Brenner and Rector's The Kidney, 8th ed.

Not sure what the question is asking, but hyderation is important. Answer key says B.


Which of the following best describes the pathophysiology of pigment induced renal failure?
a) direct toxic effect of myoglobin on renal tubular cells
b) free Fe from myoglobin and hemoglobin causing free radical release
c) precipitation of hemoglobin or myoglobin as hematin
d) conversion of pigment to toxic metabolites

a) direct toxic effect of myoglobin on renal tubular cells

Answer: Direct toxic effect to renal cells vs. Reduced cortical flow, causing medullary ischemia

The primary pathways by which contrast agents cause nephropathy are by renal ischemia (by reducing blood flow or increasing oxygen demand) and, possibly, by direct toxicity to tubular epithelial cells.
A number of experimental observations suggest that contrast agents are directly toxic to kidney cells, causing proximal cell vacuolization, interstitial inflammation, cellular necrosis, and enzymuria.8,17 Furthermore, suspensions of proximal tubular segments exposed to contrast media showed abnormalities in several markers of cellular injury, that were potentiated by hypoxia and were more pronounced with high-osmolar agents than with low osmolar agents.
- Rudnick. Contrast-induced nephropathy: How it develops, how to prevent it. Cleveland Clinic Journal of Medicine January 2006 vol. 73 1 75-80

Three core elements in the pathophysiology of CIN are (1) direct toxicity of iodinated contrast material to nephrons, (2) microshowers of atheroemboli to the kidneys, and (3) contrast material– and atheroemboli-induced intrarenal vasoconstriction.
- Libby: Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine, 8th ed.

The nephrotoxicity of contrast dyes (see Chapter 79 ) probably involves microvascular obstruction by crenated red cells as well as direct tubular toxicity by release of free oxygen radicals.
- Miller: Miller's Anesthesia, 7th ed.

Radiographic Contrast Nephropathy
Free radical–induced apoptosis and alteration in renal hemodynamics are the two pathogenic mechanisms that underlie CN. Experimental data show a biphasic response to contrast media, with an initial increase in renal blood flow followed by a sustained decrease in GFR.
- Piccini & Nilsson: The Osler Medical Handbook, 2nd ed.


What is the best way to prevent radiocontrast induced renal failure?
a) Give mannitol and lasix
b) Hydrate
c) Give lasix only
d) Give the contrast quickly
e) Give half strength contrast

b) Hydrate

In another large randomized trial, isotonic saline significantly reduced the incidence of contrast nephropathy following coronary angiography compared with half-normal saline with a particular benefit noted in diabetic patients and those receiving large contrast loads.[568] In a smaller single trial, hydration with sodium bicarbonate before contrast exposure was more effective than hydration with isotonic saline for the prevention of contrast nephropathy.[569] In aggregate, the key message from these studies is that the avoidance of hypovolaemia is the key intervention in preventing contrast nephropathy.
- Brenner: Brenner and Rector's The Kidney, 8th ed.


Patient complaining of severe pain after extravasation of 250cc of gadallinum (MRI contrast) into subcutaneous tissue:
a. Elevate the arm and give steroid
b. Open and debridement
c. Observation.
d. Measure compartment pressure

Answer given: Open and debridement (???)

Causes necrosis if sub cut

Extravasation injuries: Extravasation injuries are treated by elevating the affected extremity and applying cold compresses. A plastic surgeon should be consulted if the patient's pain gradually increases over 2-4 hours, if skin blistering or ulceration develops, or if the circulation or sensation changes at or distal to the level of the extravasation. No specific treatment is unequivocally effective; therefore, most extravasation injuries are conservatively treated with supportive measures.


Which of the following is the LEAST consistent with child abuse?
A. Multiple bruises on anterior shins
B. Long bone spiral fractures in toddler
C. Retinal hemorrhages
D. Femur fracture in non-walking infant
E. Sharply demarcated burns

A. Multiple bruises on anterior shins


1) Which phase trial type looks at morbidity and efficacy?
a. Phase I
b. Phase II
c. Phase III
d. PhaseIV
e. Phase V

b. Phase II

Phase 1: Assessing the safety (pharmacovigilance), tolerability, pharmacokinetics, and pharmacodynamics of a drug. Dose ranging, dose escalating.
Phase 2: dosing requirements and efficacy, toxicity (morbidity)
Phase 3: randomized controlled multicenter trials on large patient groups: definitive assessment of how effective the drug is, in comparison with current 'gold standard' treatment
Phase 4: Post Marketing Surveillance Trial


In response to the concept of a “learning curve” in surgical training, all of the following are correct EXCEPT:
a) One should get consent if a “novice” is doing the procedure
b) 3D simulation exercises do decrease the learning curve
c) The tradition of “see one, do one, teach one” is an effective way of addressing the learning curve
d) Applies to surgical specialists as well as residents

c) The tradition of “see one, do one, teach one” is an effective way of addressing the learning curve


Canadian health act includes all except:
a. Accessibility.
b. Autonomy.
c. Universality.
d. Portability

b. Autonomy.

There are five main principles in the Canada Health Act:
- Public Administration: All administration of provincial health insurance must be carried out by a public authority on a non-profit basis. They also must be accountable to the province or territory, and their records and accounts are subject to audits.
- Comprehensiveness: All necessary health services, including hospitals, physicians and surgical dentists, must be insured.
- Universality: All insured residents are entitled to the same level of health care.
- Portability: A resident that moves to a different province or territory is still entitled to coverage from their home province during a minimum waiting period. This also applies to residents which leave the country.
- Accessibility: All insured persons have reasonable access to health care facilities. In addition, all physicians, hospitals, etc, must be provided reasonable compensation for the services they provide.


Which laser does NOT use visible wavelength (390-750)
a. krypton 676.4 nm
b. argon 488 nm
c. pulse dye 585 nm
d. helium-neon 632 nm
e. CO2

Answer: CO2

A typical human eye will respond to wavelengths from about 390 to 750 nm.

Ar lasers produce blue-green light in the visible range of the electromagnetic spectrum, with primary wavelengths of 0.488 and 0.514 µm.

Nd:YAG lasers produce light with a wavelength of 1.064 µm (1064 nm) in the near infrared (invisible) range of the electromagnetic spectrum.

The CO2 laser produces a beam of infrared light with the principal wavelength bands centering around 9.4 and 10.6 micrometers. (10600nm)

The KTP laser emits light at 532 nm and is therefore comparable with the Ar laser.

The management of hemangiomas and port-wine stains with lasers has benefited from the application of the flash lamp pumped dye laser. The dye was initially selected for maximum absorption by the oxyhemoglobin at 577 nm. Tan and others showed that at 585 nm, hemoglobin absorption is maximal with minimal scattering and absorption by melanin and other pigments.

A helium-neon laser, usually called a HeNe laser, is a type of small gas laser. HeNe lasers have many industrial and scientific uses, and are often used in laboratory demonstrations of optics. Its usual operation wavelength is 632.8 nm.

Krypton : 676.4 nm

a. krypton (visible)
b. argon (visible)
c. pulse dye (visible)
d. helium-neon (visible)
e. CO2 (invisible)


A man positive for an X linked recessive condition marries a woman with no family history for the condition. Which of the following is true?
a) All the children will have the disease
b) All the sons and daughters will be carriers
c) All the sons will be normal and all the daughters will have the disease
d) All the sons will be normal and all the daughters will be carriers
e) All the sons and half the daughters will be carriers

d) All the sons will be normal and all the daughters will be carriers


What is the chance that an obese patient can lose weight with diet change alone?
A – 10
B – 25
C – 50
D – 75

??probably 10%??


Sympathetic supply to the eyelids originate from:
a. stellate ganglion
b. cervical sympathetic trunk
c. thoracic sympathetic trunk

Answer: cervical sympathetic trunk

The superior tarsal muscle (also known as Müller's muscle) is a smooth muscle adjoining the levator palpebrae superioris (CN III) muscle that helps to raise the upper eyelid.
The superior tarsal muscle receives its innervation from the sympathetic nervous system on fibers carried along with the ophthalmic artery through the cavernous sinus. These postganglionic sympathetic fibers originate in the superior cervical ganglion.


Injury of the ulnar nerve at the level of the wrist will lead to the inability to:
a) Abduct the thumb
b) Cross the index and second fingers
c) Flex the middle finger at the carpometacarpal joint
d) Extend the fingers

Answer: Cross the index and second fingers


In regards to the sensory branch of the median nerve:
a) it travels with the motor branch
b) it travels thru the carpal tunnel
c) it branches off distal to the transverse palmar ligament
d) it branches off 5 cm proximal to the wrist crease

d) it branches off 5 cm proximal to the wrist crease

Palmar cutaneous branch of median nerve arises just proximal to flexor retinaculum. It passes superficial to flexor retinaculum to supply skin of the lateral part of the palm.
- Moore’s Anatomy

The palmar cutaneous branch of the median nerve arises 5 cm proximal to wrist joint and runs down along the ulnar side of the tendon of the FCR before crossing flexor rectinaculum.
- Hoppenfeld Surgical exposure in orthopedics


If you were to perform a saphenous vein cutdown, where would you make your incision?
A. Antero-superior to the medial malleolus
B. Postero-superior to the medial malleolus
C. Antero-superior to the lateral malleolus
D. Postero-superior to the medial malleolus

Answer: Antero-superior to the medial malleolus

The greater, or long, saphenous vein, which is the longest vein in the body, originates at the ankle as a continuation of the medial marginal vein of the foot and ends at the femoral vein within the femoral triangle. At the ankle, it crosses 1 cm anterior to the medial malleolus and continues up the anteromedial aspect of the lower leg.

The vein crosses 1 cm anterior to the medial malleolus and continues up the anteromedial aspect of the leg.
The vein's superficial, predictable, and isolated location has made the distal saphenous vein the classic pediatric cutdown site.
- Roberts: Clinical Procedures in Emergency Medicine, 5th ed.

The greater saphenous vein originates from the medial aspect of the dorsal venous arch and ascends anterior to the medial malleolus.


Vertebral artery originates from
a) subclavian artery
b) aorta

a) subclavian artery

Vertebral arteries – 1st branch off the subclavian artery, they pass through foramen in the transverse processes of the cervical vertebrae and enter the skull in the foramen magnum. The Vertebral arteries unite within the skull to form the basilar artery. Basilar artery bifurcates into 2 posterior cerebral arteries.
- Mont Reid Surgical Handbook


Which nerve is in the carotid sheath
a) vagus
b) phrenic

a) vagus

Carotid Sheath Contents
-Internal Jugular Vein
- Common Carotid Artery and Internal Carotid Artery
- CN 10 (vagus), CN 12 (Hypoglossal)
- Ansa cervicalis (nerves off the Cervical Plexus, includes HYPOGLOSSAL nerve)
- Deep Cervical Lymph Nodes

Carotid sheath extends from the base of the skull to the root of the neck; formed by the fascial extensions of the cervical fascia, which fuse with the prevertebral fascia; inferior part of the sheath contains: common carotid arteries medially, internal jugular vein laterally, vagus nerve (CNX) posteriorly, and ansa cervicalis.


Which of the following structures does the left recurrent laryngeal nerve loop around?
a) Subclavian artery
b) Subclavian vein
c) Ligamentum arteriosum
d) Carotid artery
e) Pulmonary artery

Answer: Ligamentum arteriosum

On the left side, it arises on the left of the arch of the aorta, and winds below the aorta at the point where the ligamentum arteriosum is attached, and then ascends to the side of the trachea.

The left recurrent laryngeal nerve comes from the left vagus nerve, loops posteriorly around the arch of the aorta, and ascends in the tracheoesophageal groove posterior to the left lobe of the thyroid, where it enters the larynx and innervates the musculature in a similar fashion as the right nerve.


How do the sympathetic nerve fibers leave the spinal cord?
a) Gray rami communicantes
b) White rami communicantes
c) Dorsal root ganglia
d) Anterior nerve root
e) Posterior columns

d) Anterior nerve root ?
Sympathetic nerves originate inside the vertebral column, toward the middle of the spinal cord in the intermediolateral cell column (or lateral horn), beginning at the first thoracic segment of the spinal cord and are thought to extend to the second or third lumbar segments. Because its cells begin in the thoracic and lumbar regions of the spinal cord, the SNS is said to have a thoracolumbar outflow. Axons of these nerves leave the spinal cord through the anterior rootlet/root. They pass near the spinal (sensory) ganglion, where they enter the anterior rami of the spinal nerves. However, unlike somatic innervation, they quickly separate out through white rami connectors (so called from the shiny white sheaths of myelin around each axon) which connect to the either the paravertebral (which lie near the vertebral column) or prevertebral (which lie near the aortic bifurcation) ganglia extending alongside the spinal column.


Which nerve is the motor supply to tongue?
a. VII
b. V
c. XI
d. IX
e. XII

Answer: Hypoglossal (XII)


Of the cranial nerves listed below, which is responsible for taste sensation in the ant. 2/3 of the tongue
a. trigeminal nerve
b. facial
c. glossopharygeal nerve
d. vagus n.
e. hypoglossal n.

Answer: facial

The facial nerve is the seventh (VII) of twelve paired cranial nerves. It emerges from the brainstem between the pons and the medulla, and controls the muscles of facial expression, and taste to the anterior two-thirds of the tongue.


Peroneal nerve injury causes which of the following deficits:
a) weakness of tibialis posterior
b) loss of sensation of sole of foot
c) loss of sensation in 1st web space
d) weakness in plantar flexion
e) loss of ankle reflex

c) loss of sensation in 1st web space

The peroneal nerve supplies extensor and peroneal leg compartments and the dorsum of the foot
o sensory function:
o deep peroneal - skin of 1st web space
o superficial peroneal - skin on dorsum of foot, medial great toe, 2nd to 4th web space
o skin over peronei and extensor muscles in lower 1/3 of leg
o motor function:
o deep peroneal - extensor digitourm longus, tibialis anterior, extensor hallucis longus, peroneus tertius, extensor digitorum brevis
o superficial peroneal - peroneus longus and brevis
- Grant’s anatomy


A young ♂ patient is involved in an MVA. He is unconscious on presentation with unknown neurological status preoperatively. He had a vertical shear pelvic fracture with right SI joint dislocation repaired through an anterior approach. Post-operatively, the patient is noted to have decreased sensation in the 1st dorsal webspace of the right foot, with decreased right extensor hallucis longus power. What is the MOST likely cause of his deficit?
A. Injury to deep peroneal nerve at time of accident
B. L5 nerve root injury at time of accident
C. Injury to sciatic nerve at time of accident
D. Injury to sciatic nerve at time of surgery
E. Saphenous nerve injury at time of surgery

B. L5 nerve root injury at time of accident


Woman with sudden back pain and numbness of anterior thigh would likely have what motor deficit?
a-Hip flexion
b-Hip Extension
c-Knee flexion
d-Ankle dorsiflexion

a-Hip flexion

Knee extension is the same but not a choice


Following removal of a failed orthotopic kidney transplant, the patient complains of numbness on the right anterior thigh. Which nerve was most likely injured?
a) Femoral nerve
b) Sciatic nerve
c) Lateral femoral cutaneous nerve
d) Ilio-hypogastric nerve
e) Ilio-inguinal nerve

Femoral neuropathy: a complication of renal transplantation. (1981 article)

Femoral neuropathy occurred in 3 patients after renal transplantation. This appeared to be due to compression of the femoral nerve by medial and inferior blades of the self-retaining retractors used during renal transplantation surgery. The condition resulted in weakness of quadriceps muscles, loss of patellar reflex, and sensory deficit on the side of transplantation surgery. The rate of recovery from neurologic deficits appeared to depend on the level of transplant renal function.


A patient suffering a L4/L5 disc herniation would likely have:
a. Reduced patella reflex
b. Reduced toe flexion
c. Thigh parasthesia
d. Reduced toe extension

d. Reduced toe extension

Level L4-L5
Weakness extension of big toe
Altered Reflex big toe
Sensory Loss back of thigh
Pain lateral calf

The majority of disc herniations, being posterolateral, compress the root that exits at the intervertebral foramen below the level of the involved disc (L5 root in L4/5/ posterolateral disc herniation).
L5 radiculopathy may present with pain, and paresthesia/numbness along the posterolateral aspect of the leg down to the great toe; weakness of extensor hallusis longus and dorsiflexion may be noted.
For herniated disc, ipsilateral positive straight leg raise is 72-97% sensitive but unspecific (11-66%) while crossed straight leg raise is less sensitive (23-42%) but more specific (85-100%). Ankle dorsiflexor weakness is 20-49% sensitive for lumbar disc herniation, 70-90% of patients with dorsiflexor weakness had HNP at L4/L5 level.
- Spine 1996;21:10S-18S


In a patient suffering a C5/6 disc herniation, which would you expect?
a. Decreased wrist flexion
b. Reduced wrist extension
c. Weakened finger abduction
d. Loss of 3rd finger sensation
e. Shoulder weakness

b. Reduced wrist extension

C5-6 disc = C6 nerve root

Technically this would affect your shoulder abduction as well via axillary nerve, and biceps via mskcut nerve if you look at your brachial plexus. But this is a question written by ortho/neurosurgeons who just look at the ASIA exam instead of the anatomy of it, and C6 = wrist extension on it

Involvement of C6 is associated with pain at the tip of the shoulder radiating into the upper part of the arm, lateral side of the forearm, and thumb. Paresthesias are felt in the thumb and index finger. The brachioradialis and biceps reflexes are attenuated or lost. Weakness may occur in the muscles of the C6 myotome supplied by several different nerves, including the biceps (musculocutaneous nerve), deltoid (axillary nerve), and pronator teres (anterior interosseous branch of the median nerve)
- Bradley: Neurology in Clinical Practice, 5th ed.


Female with a displaced mid-humeral shaft # would be unable to do what?
a. Wrist extension
b. Wrist flexion
c. Finger abduction
d. Elbow flexion

a. Wrist extension

Radial nerve loops around the humerus

Fracture, Humerus
Assessment of the radial nerve
- The radial nerve's primary motor function is to innervate the dorsal extrinsic muscles in the forearm. Motor testing should include extension of the wrist and metacarpophalangeal (MCP) joints as well as abduction and extension of the thumb. Proximal injury of the radial nerve causes wrist drop.
- On examination, the fingers are in flexion at the MCP joints and the thumb is adducted.
Rarely, the median or ulnar nerves are affected.


3 months after a distal radius fracture treated surgically a patient comes with thumb and index finger numbness. Which nerve is responsible?
A – Ulnar
B – Median
C – Palmar cutaneous
D – Radial

B – Median

FCR approach to the distal radius is close to the median nerve


1) A patient has a C8 lesion. Which of the following is the patient MOST UNlikely able to perform?
A. Wrist extension
B. Finger abduction
C. Elbow extension
D. Elbow flexion
E. Finger extension

finger flexion is probably the more correct answer, but otherwise finger abduction

An examination of the upper extremities must include, at a minimum, the muscle groups that are designated by their respective nerve root innervation. These are C5, elbow flexion; C6, wrist extension; C7, finger extension; C8, finger flexion; and T1, finger abduction.
- Browner: Skeletal Trauma, 4th ed.


A 25 year old ♂ jumps into a pool and sustains an injury at C7-8 with jumped facets and an anterior cord syndrome. Which of the following is the MOST likely presentation?
A. Intact proprioception in feet
B. Intact great toe flexion
C. Intact great toe extension
D. Intact light touch lower extremities
E. Intact bladder control

A. Intact proprioception in feet

Sensory afferents give rise to two major ascending pathways: the anterolateral system (nociceptive, serving thermal sensation primarily) and posterior columns (serving large-fiber modalities primarily, including touch, vibration, and proprioception)
- Bradley: Neurology in Clinical Practice, 5th ed.

Anterior cord syndrome is characterized by diminished motor function and pain and temperature sensation below the level of the injury. Position, vibratory, and crude touch sensation are maintained. Prognosis for recovery is poor.
- Schwartz

The anterior spinal artery syndrome involves the bilateral loss of motor function, pain, and temperature sensation below the level of the lesion, with sparing of position–vibratory and light touch sensation. This incomplete lesion develops when the anterior spinal artery is occluded. This renders the cord ischemic within the anterior spinal artery distribution, affecting the anterior and lateral columns bilaterally.
- Greenfield


Sensory level at umbilicus what is the cord injury at
a – T6
b – T8
c – T10
d – T12

c – T10


Which of the following is the most appropriate type of central catheter for a patient requiring long-term home parenteral nutrition?
a. Tunnelled, single-lumen catheter.
b. Tunnelled, double-lumen catheter.
c. Single lumen catheter with implanted port.
d. Double-lumen implanted port.
e. Peripherally inserted ventral venous catheter.

a. Tunnelled, single-lumen catheter.

As the number of lumens increases, infection rates will rise proportionally, thus arguing in favor of single-lumen catheters when the device is intended solely for TPN administration.
The principle underlying tunneled catheters is that the subcutaneous tract forms a barrier to bacterial encroachment and colonization, thus discouraging a so-called tunnel or tract infection, although a competing mode of infection for these or any other catheters, with resultant bacteremia, is by an intraluminal route. Tunneled catheters are desirable when frequent access is required, or perhaps if a high incidence of infection is anticipated, because they are easily removed.
Particularly if accessed frequently, the portacath may have a higher rate of infection and overall rate of failure than tunneled catheters in the setting of TPN, as opposed to other common scenarios such as when used for chemotherapy.
- Townsend: Sabiston Textbook of Surgery, 18th ed.


What is the best and safest way to put a catheter into the SVC for a patient requiring long term TPN?
a) Cephalic
b) Basilic
c) Internal jugular
d) External jugular

Answer: Basilic

At best, a PICC line in the outpatient setting has a lifetime of 4 to 6 weeks before malfunctioning or becoming infected. Therefore, for long-term TPN administration, a more permanent solution is needed.
Particularly if accessed frequently, the portacath may have a higher rate of infection and overall rate of failure than tunneled catheters in the setting of TPN, as opposed to other common scenarios such as when used for chemotherapy.
- Townsend: Sabiston Textbook of Surgery, 18th ed.

The basilic vein is preferred over the brachial and cephalic veins because there is less chance of injury to the brachial artery and nerve. The cephalic vein has the highest rate of thrombus and phlebitis.
- Walsh: Palliative Medicine , 1st ed.

Retrospective analysis of pts with PICC. Greater incidence of venous thrombosis cephalic (57%) vs. basilic (14%)
- JVIR 11:1309-1314 (2000)


Which central line access site has the least complications?
a. Internal jugular
b. External jugular
c. Femoral
d. Subclavian
e. Brachiocephalic


Depends on the complication:
hemo/pneumothorax higher in subclavian
infection lowest in subclavian, highest in femoral
thrombosis lowest in IJ
arterial puncture highest in femoral, lowest in subclav

Pneumothorax is the most frequently reported complication, occurring in up to 6% of subclavian venipunctures.
Femoral venous catheterization may be related to a greater risk of infection than subclavian catheterization. Merrer and associates[113] reported overall infectious complications from femoral versus subclavian catheters to be 19.8% and 4.5%, respectively.
Although both approaches to the SV are relatively safe ( Fig. 22–18 ), the infraclavicular SV approach is more likely to be associated with complications.
- Roberts: Clinical Procedures in Emergency Medicine, 5th ed.


A patient with a coagulopathy requires a central line. Which of the following venous sites is contraindicated?
a. Internal jugular
b. External jugular
c. Subclavian
d. Femoral

c. Subclavian

Subclavian most difficult to compress.


Air embolism occurs what is your management?

How do you manage an air embolism during central line placement?
a) Reverse Trendelenburg
b) Aspirate from the right heart
c) Right lateral decubitus position
d) left lateral decubitus

d) left lateral decubitus

A patient with venous air embolization should be immediately placed into the left lateral decubitus position (Durant’s maneuver), Trendelenburg position, or left lateral decubitus head down position

The best approaches to air embolism are prevention and early detection. Treatment consists of measures designed to restore blood flow and to promote reabsorption of the intravascular air. Measures designed to restore flow include patient positioning (Trendelenburg position with the left side down), removal of air through central venous catheters or direct needle aspiration, and closed-chest cardiac massage. Measures designed to increase absorption include the use of 100% oxygen and the institution of hyperbaric oxygen therapy as early as possible.
- Mason: Murray & Nadel's Textbook of Respiratory Medicine, 4th ed.

“Immediately place the patient in the left lateral decubitus (Durant maneuver) and Trendelenburg position. This helps to prevent air from traveling through the right side of the heart into the pulmonary arteries, leading to right ventricular outflow obstruction (air lock). Direct removal of air from the venous circulation by aspiration from a central venous catheter in the right atrium may be attempted.”
– eMedicine: Venous Air Embolism: Treatment & Medication


A patient on TPN for the last 14 days through a left subclavian line, suddenly develops dyspnea, cyanosis, hypoxia and a cardiac murmur. You would:
a. Remove the line and heparinize.
b. Trendelenberg position and turn the patient to his side.
c. Chest tube.
d. Observe

b. Trendelenberg position and turn the patient to his side.

Answer: Trendelenberg position and turn the patient to his side.

Air embolism⎯a rare but often lethal complication of subclavian vein catheterization⎯is characterized by sudden, severe respiratory distress (tachypnea), hypotension, and a cogwheel murmur. To prevent air embolism, the subclavian line should be inserted only with the patient tilted into a head-down position. It is also critical that the line not be disconnected when the patient is upright. This is easier to ensure if Luer-Lok connections are used. Treatment of air embolism involves placing the patient with left side down, head down, and feet (Durant position) elevated and aspirating blood and air through the subclavian catheter.


Of the sites listed below, which is the best for the insertion of a central venous catheter for the delivery of TPN?
a) right subclavian vein
b) right internal jugular
c) right external jugular
d) right femoral vein

Answer given: right subclavian vein

Catheter Choice and Rationale
In choosing a catheter for TPN administration, the first consideration should be the anticipated duration of therapy. In the inpatient setting, the traditional percutaneous central line, introduced via the subclavian or internal jugular vein and often containing multiple lumens (e.g., the so-called triple-lumen catheter), is most common. As the number of lumens increases, infection rates will rise proportionally, thus arguing in favor of single-lumen catheters when the device is intended solely for TPN administration. A more recent trend is to use peripherally inserted central catheters (PICCs) introduced via the basilic vein, both in the inpatient setting and also for longer-term outpatient therapy. When evaluated in controlled trials, PICC lines show similar rates of line sepsis as traditional central catheters but have an increased incidence of local complications such as leakage, thrombophlebitis, and malpositioning. At best, a PICC line in the outpatient setting has a lifetime of 4 to 6 weeks before malfunctioning or becoming infected. Therefore, for long-term TPN administration, a more permanent solution is needed. The devices available consist of either subcutaneously tunneled central catheters (Hickman, Broviac, Groshong) or self-contained implantable chambers that connect to the central venous system (portacath).
- Townsend: Sabiston Textbook of Surgery, 18th ed.


All true about catheter related infection except :
a. Regular change of catheters every 7 days decrease risk of infection
b. Femoral > subclavian risk of infection
c. Chlorexidine-Sulphadiazine coated catheters decrease risk of infection
d. Common organisms include coagulase negative and coagulase positive staph.

Answer: Regular change of catheters every 7 days decrease risk of infection

- regular changing catheters is the old way of thinking, this increases infection risk
- only silver coated catheters decrease risk of infection

A report by Darouiche and colleagues[6] indicated that catheters with minocycline and rifampin on the external and luminal surfaces had a lower infection rate than those with chlorhexidine and silver sulfadiazine on the external surface only. This finding indicates that the antibiotic combination may be important but also that the intraluminal route remains important in central catheter–related bloodstream infections.
Infections are most often caused by skin flora. The most common bacteria are Staphylococcus epidermidis and Staphylococcus aureus.
- Townsend: Sabiston Textbook of Surgery, 18th ed.

Risk Factors for Device-Associated Bacteremia
Location of catheter (central > peripheral; jugular > femoral > subclavian; lower extremity sites > upper extremity sites)
- Mandell: Mandell, Douglas, and Bennett's Principles and Practice of Infectious Diseases, 7th ed.

Routine replacement of lines makes no difference in preventing infection
- NEJM 1992;327:1062-1068


IO should be placed:
a – 1 finger below Tibial tubercle and 45degrees toward knee
b – 1 finger below tibial tubercle and 45 degrees away from the knee
c – at tibia tubercle and 45 degrees toward knee
d – at tibial tubercle and 45 degrees away from the knee

Answer: 1 finger below tibial tubercle and 45 degrees away from the knee


The heat generated by electrocautery is:
Answer choices are various combinations of proportional or inversely proportional to the amperage and resistance

Proportional to resistance
Proportional to amperage

Resistivity is the intrinsic property of a material to resist the passage of electricity: the higher the resistivity, the poorer a conductor and vice versa. When an electric current is passed through a poor conductor energy is lost in the form of heat and the temperature of the material increases. The amount of heat produced depends upon the current (amperes) and the resistance of the tissue (ohms). The heating power developed may be expressed as: Power = Current x Current x Resistance.
- Sabiston


What is the most significant factor in preventing diathermy injuries:
a. strength of current
b. distance of the ground from cathode
c. contact surface area of the ground
d. fat content of the patient
e. waveform of current

The heating power developed may be expressed as: Power = Current x Current x Resistance.
- Sabiston


Which of the following is TRUE regarding bi-polar cautery?
A. Confines tissue damage to between tines
B. Low frequency current for coagulation
C. Will not work in a wet environment
D. Causes extensive tissue damage

A. Confines tissue damage to between tines


Commonest side effect of electocautery is:
a. PVC
b. Pacemaker dysfunction
c. Cutaneous burn

c. Cutaneous burn


Which suture material is used in AAA graft operation

Answer: Non-absorbable,monofilament (least reactive, less likelihood of infection)


Which properties of a suture material will incite the LEAST amount of inflammatory reaction?
A. Monofilament, absorbable
B. Monofilament, non absorbable
C. Polyfilament
D. Braided

B. Monofilament, non absorbable


Which is the best suture that you can use in infected wound:
a. Nonabsorb, monofilament
b. Absorb, polyfilament
c. Nonabsorb, polyfilament
d. Absorb, monofilament

a. Nonabsorb, monofilament


How many sizes of suture between “number 2” and 2-0:
a. 0
b. 1
c. 2
d. 3
e. 4


#1, 0, 1-0, 2-0


how many suture size between 2.0 and #2:
a. 1 size
b. 2 sizes
c. 3 sizes
d. 4 sizes

Suture sizes are defined by the United States Pharmacopeia (U.S.P.). Sutures were originally manufactured ranging in size from #1 to #6, with #1 being the smallest. A #4 suture would be roughly the diameter of a tennis racquet string. The manufacturing techniques, derived at the beginning from the production of musical strings, did not allow thinner diameters. As the procedures improved, #0 was added to the suture diameters, and later, thinner and thinner threads were manufactured, which were identified as #00 (#2-0 or #2/0) to #000000 (#6-0 or #6/0).


What material retains the least strength at 2 months:
a. Silk (“non-absorable”, mutifilament)
b. Prolene (non-absorable, multifilament)
c. Monofilament nylon (non-absorable, monofilament)
d. Stainless Steel (non-absorable, steel)
e. PDS (absorbable, monofilament)

Answer: silk

Sutures that are rapidly degraded in tissues are termed absorbable; those that maintain their tensile strength for longer than 60 days are considered nonabsorbable (see Table 37-1) . Plain gut may be digested by white blood cell lysozymes in 10 to 40 days; chromic gut will last 15 to 60 days. Remnants of both types of sutures, however, have been seen in wounds more than 2 years after their placement. [40] [43] [46] A newer type of catgut (Ethicon) is rapidly absorbed within 10 to 14 days but with less inflammation than that caused by chromic catgut. [47] Vicryl is absorbed from the wound site within 60 to 90 days, [40] [43] and Dexon, within 120 to 210 days. [48] [49] When placed in the oral cavity, plain gut disappears after 3 to 5 days, chromic gut after 7 to 10 days, and polyglycolic acid after 16 to 20 days. [50] In contrast, SQ silk may not be completely absorbed for as long as 2 years. [43] The rate of absorption of synthetic absorbable sutures is independent of suture size. [48]
Sutures may lose strength and function before they are completely absorbed in tissues. Braided synthetic absorbable sutures lose nearly all of their strength after about 21 days. In contrast, monofilament absorbable sutures (modified polyglycolic acid [Maxon, Davis & Geck] and polydioxanone [PDS, Ethicon]) retain 60% of their strength after 28 days. [51] [52] Gut sutures treated with chromium salts (chromic gut) have a prolonged tensile strength; however, all gut sutures retain tensile strength erratically. [40] [43] Of the absorbable types of sutures, a wet and knotted polyglycolic acid suture is stronger than a plain or chromic gut suture subjected to the same conditions. [41] [53]
Polypropylene remains unchanged in tissue for longer than 2 years after implantation. [54] In comparison testing, Hermann found that sutures made of natural fibers such as silk, cotton, and gut were the weakest; sutures made of Dacron, nylon, polyethylene, and polypropylene were intermediate in tensile strength; and metallic sutures were the strongest. [41] Kaplan and Hentz used the comparison of suture strength versus wound strength as a measure of the usefulness of a suture. They stated that catgut is stronger than the soft tissue of a wound for no more than 7 days; chromic catgut, Dexon, and Vicryl are stronger for 10 to 21 days; and nylon, wire, and silk are stronger for 20 to 30 days. [55]
Among absorbable sutures, polyglycolic acid and polyglactin sutures are least reactive, followed by chromic gut. Nonabsorbable polypropylene is less reactive than nylon or Dacron. [41] [56] [57] Significant tissue reaction is associated with catgut, silk, and cotton sutures; highly reactive materials should be avoided in contaminated wounds. Adams found absorbable polyglycolic acid sutures to be less reactive than those of nonabsorbable silk. [58]
Multifilament sutures provoke more inflammation and are more likely to produce infection than monofilament sutures if left in place for prolonged periods. [59] [60] Monofilament sutures elicit less tissue reaction than do multifilament sutures, and multifilament materials tend to wick up fluid by capillary action.
- Roberts Clinial procedures in emergency medicine


Which is a non-absorbable, monofilament suture?
a) Nylon
b) Silk
c) Vicryl
d) Monocryl

Answer: Nylon (can be monofilament or braided)

- Polypropylene (Prolene* & Surgilene+)
- Nylon (Ethilon* & Dermalon+)
- Polyester (Mersilene*)
- Silk
- Nylon (Surgilon* & Nurolon+)
Braided & Coated
- Polyester & Polybuterate (Ethibond*)
- Polyester & Silicone (Tichron+)
- Polyester & Teflon (Tevdek#)
- Silk & Beeswax
Multifilament Sheathed
- Multistrand Nylon & Polyethylene Sheath (Supramid$)


which will last longer:
a. Vicryl
b. Dexon
c. Chromic
d. PDS

d. PDS

Absorption: 10 ds., effective strength: 4 – 10 ds
Absorption of chromic: 20 ds., effective strength: 10 – 14 ds.
Absorption: 60 – 90 ds., effective strength: 14 – 21 d
Absorption: 60 – 90 days, effective strength: 20 – 30 days.
Absorption: 180 days, effective strength: 40 – 60 days