Surgical Intensive Care

Question 1

A patient needs renal replacement therapy.

Who gets CRRT, who gets HD?

Answer 1

CRRT: Patients who have poor cardiovascular stability and cannot tolerate large fluid shifts over a short period of time.

HD: Patients who are cardiovascularly stable or who arrive with toxic ingestion.

Basically, CRRT is easier on hemodynamics, but less effective at reducing electrolyte concentrations and reversing uremia.

Question 2

Tracheobronchomalacia diagnosis and ventilator management

Answer 2

>90% obstruction with exhalation during provocation maneuver

Definitive management is with tracheobronchoplasty, however ventilation with PEEP can also keep the tracheal cartilage open in order to ventilate.

Question 3

Etiology of critical illness neuromyopathy

Answer 3

Two components:

1. Use-dependence. If you aren’t using your muscles or nerves, they will become less efficient/weaker.
2. Perfusion – poorly perfused muscle/nerve will not function as well.

Question 4

Looking for edema in ICU patients

Answer 4

You want to look in the dependent positions, so posterior hip and pre-sacral regions are optimal in ICU patients lying supine.

Question 5

If a patient has an S3 on exam, their PCWP is at least. . .

Answer 5

. . . 18 mmHg

Question 6

Measuring SVR with a Swan-Ganz catheter

Answer 6

Calculated using MAP, CVP, and cardiac output (flow)

F = dP / R

R = dP / F

SVR = [MAP - CVP] / CO

Question 7

Pulmonary, cardiovascular, and neuro assessment of readiness to extubate

Answer 7

Pulmonary: RSBI < 105, Inspiratory pressure < 25 cm H2O

Cardiovascular: PEEP < 5 cm H2O

Neuro: Mental status adequate

Question 8

How to test pulmonary compliance with a ventilator

Answer 8

Set mode to volume control. For the volume, use lung-protective ventilation (6 mL/kg idela body weight)

Compliance = TV / (P_pleateau - PEEP)

Compliance > 60 is normal.

Question 9

Special nutrition formulations for:

Hypoxic repsiratory failure

Renal failure

Cirrhosis

Answer 9

Hypoxic respiratory: Low RQ diet (less carb, more fat)

Renal failure: Low K, low Phos diet

Cirrhosis: High calorie, branched chain amino acid diet

Question 10

Assessing a patient’s nutritional requirements (3 elements)

Answer 10

1. Pre-morbid state (is the patient malnourished?)
2. Stress level (very sick, or relatively stable?)
3. Risks of the intervention (infection)

Question 11

How many calories does the patient need?

Answer 11

Calories = BMR x Stress Factor x Ideal body weight

If they have sepsis, SF = 1.7. If they have large burns, SF= 2.0.

Usually for an inpatient, 17 x 1.5 x IBW = 25 x IBW, so:

25 kCal/kg_IBW/day

Question 12

Respiratory quotient

Answer 12

RQ = CO₂ production / O₂ consumption

For most people, this is 0.8

Question 13

Why does muscle wasting occur, metabolically, in patients without exogenous glucose?

Answer 13

Gluconeogenesis requires pyruvate, which can only come from fermented glucose or amino acid skeletons – not from fats.

Ergo, when glucose stores run out, amino acids start to be pulled for pyruvate to participate in gluconeogenesis.

Question 14

Nutritional composition of a typical tube feed

Answer 14

• Macronutrients:
  
  • 30% carbohydrates (for protein-sparing effect)
  • 40% protein (2g/kg/day if sick, 4 if really sick)
  • 30% fat (cell membrane synthesis)
• Micronutrients and other:
  
  • Fluid (minimal)
  • Electrolytes
  • Vitamins
  • Minerals
  • Additives (insulin, famotidine)

Question 15

RQ of carbohydrates

Answer 15

1.0

Question 16

RQ of fatty acids

Answer 16

0.6

Question 17

What is the biggest risk of small bowel feeding over gastric feeding?

Answer 17

The small bowel can’t control the rate of digestion.

The pylorus is the filter for metabolic demand on the small bowel. Once stuff is in the bowel, the bowel must increase its metabolic demand to digest and absorb the nutrients.

In a patient with enteric hypoperfusion, this is effectively exercising an ischemic gut, and may result in enteric infarction.

Question 18

Patient in the ICU has a high anion gap metabolic acidosis that is not fully explained by their lactate level.

What is the next best step?

Answer 18

Check the beta-hydroxybuyrate

They may be in DKA – especially nowadays with so many diabetics on SGLT2 inhibitors or other antihyperglycemics that keep glucose normal even when absolute insulin levels are low.

Question 19

When is a Swan Ganz helpful?

Answer 19

1. Acute aortic insufficiency, to assess hemodynamics and to use the pacing port for acute heart pacing.
2. Mixed shock, to assess relative contributions from different etiologies and optimize cardiac output

Question 20

Spontaneous breath vs Ventilator breath

Answer 20

Spontaneous breath: Intrathoracic pressure decreases, increasing venous return to the R heart.

Ventilator breath: Intrathoracic pressure increases, decreasing venous return to the R heart but increasing pulmonary venous return to the L heart.

Question 21

Delta down

Answer 21

After a period of apnea, deliver a large-volume breath (8-15mL/kg) and measure the change in systolic blood pressures.

Δ_Down = P_{peak, apnea} - P_{peak, post-breath}

Higher delta down predicts better fluid responsiveness.

Question 22

Types of amiodarone-induced thyroid abnormalities

Answer 22

Amiodarone-induced thyrotoxicosis type I: Thyrotoxicosis in individuals with preexisting thyroid disease. Treated with methimazole or PTU.

Amiodarone-induced thyrotoxicosis type II: Thyrotoxiosis resulting from amiodarone-induced thyroiditis and destruction of glandular tissue. Best treated with glucocorticoids. May be followed by a hypothyroid period.

Amiodarone-induced hypothyroidism: Due to Wolff-Chaikoff effect from high iodine levels in amiodarone. Women and those with Hx of Hashimoto’s are at increased risk.

Note: Due to the long halflife of amiodarine (50-100 days), these effects may persist long after discontinuation of the medicaiton.

Question 23

Adrenal insufficiency in sepsis

Answer 23

While this is a well-documented phenomenon, and steroids have been shown to help some patients, conventional AI testing (Cosyntropin stimulation, etc) has not been shown to be helpful in determining who will benefit from corticosteroids.

So, we just give corticosteroids to anyone who has hypotension resistant to fluids and pressors, as well as those with baseline corticosteroid therapy (stress dosing). In other words, those with clinical adrenal insufficiency.

Question 24

CYP inhibitors and inducers on corticosteroids

Answer 24

Paradoxically, both can decrease the level of circulating corticosteroids:

CYP inducers can increase cortisol catabolism

CYP inhibitors can reduce cortisol synthesis

Question 25

Lots of patients in the ICU have hypotension and require sedation.

So, why don’t we use etomidate?

Answer 25

Because these patients are also at risk for adrenal insufficiency, which could be devastating if they are already hypotensive.

Etomidate’s one major complication is that it can cause adrenal insufficiency via dose-depedent inhibition of enzymes involved in cortisol synthesis. Even single-dose etomidate may produce clinically significant adrenal insufficiency in septic patients, and etomidate has been shown to increase all-cause mortality in the ICU.

For these reasons, ketamine is the preferred rapid-sequence induction agent in critically ill ICU patients.

Question 26

Sleep-wake cycle problems in critically ill patients

Answer 26

1. Many either have or are receiving high levels of cortisol. Cortisol is known to inhibit sleep.
2. Septic patients have continuous, non-fluctuating secretion of melatonin.

Both of these serve to derange the sleep-wake cycle and increase the risk and severity of delirium.

Question 27

In whom is the Hgb goal > 10g/dL instead of >7 g/dL?

Answer 27

1. Patients with active hemorrhage
2. Patients with significant lactic acidosis
3. Patients with coronary ischemia

Question 28

Management of euthyroid sick syndrome

Answer 28

Really nothing.

Characterized by a decrease in T3 followed by a decrease in T4 within 24-48 hours, due to inhibition of T4 to T3 conversion and increased rT3. TSH remains normal to low.

While it may be an adaptive mechanism, it is associated with increased mortality despite an absence of hyper- or hypo-thyroid symptoms.

No treatments have been shown to be effective. So, we do nothing but prognosticate.

Question 29

Vasopressin and sepsis

Answer 29

In sepsis, the V1 receptor may be downregulated.

This results in relative vasopressin deficiency, and these patients may benefit from low-dose exogenous vasopressin.

Clinically, this just makes vasopressin our 2nd-line vasopressor in patients with septic shock (after norepinephrine).

Question 30

pO2 / FiO2

Answer 30

P/F < 300 indicates acute lung injury (ALI)

P/F < 200 suggests ARDS, particularly when there is new bilateral alveolar infiltrate on CXR

Question 31

Multiorgan dysfunction syndrome

Answer 31

All in the name. Basically, organ dysfunction begets organ dysfunction. Macrophage cytokine release in the setting of organ dysfunction is thought to be the instigating factor of the syndrome.

Biggest risk factor is circulatory failure within the first 24 hours of admission.

MODS takes days to weeks to develop following the initial insult.

Question 32

Anesthetics that preserve respiratory drive

Answer 32

Ketamine: Also increases sympathetic outflow (and ICP). NDMAR antagoist.

Dexmetomadine: Also decreases sympathetic outflow. Centrally acting alpha-2 agonist.

Question 33

It is generally advisable to withhold enteral feeding from patients in the ICU until. . .

Answer 33

. . . these patients are fully resuscitated and have adequate blood pressures

Question 34

In a previously healthy patient with no evidence of malnutrition, how long can you go before it is no longer justifiable to withhold parenteral nutrition?

Answer 34

7-10 days

Question 35

Traditional markers of malnutrition (albumin, prealbumin, transferrin, retinol-binding protein) . . .

Answer 35

. . . change with acute phase response and cannot be used in the ICU

Question 36

Enteral nutrition should be initiated for a new ICU patient. . .

Answer 36

. . . within 24-48 hours of admission OR as soon as fluid resuscitation is complete and the patient is hemodynamically stable

Question 37

Why do we tend to prefer small bowel feeding in the ICU?

Answer 37

To reduce the risk of aspiration, particularly in patients with severe brain injury (the lack of vagal input results in gastroparesis).

Question 38

“Trickle” feeds

Answer 38

Prevent mucosal atrophy in ICU patients, but do not improve immunologic function and infectious outcomes

Question 39

What is an acceptable gastric residual volume (in the absence of other signs of intolerance)?

Answer 39

< 500 mL

Fluid of less than this amount is not associated with increased risk of aspiration or pneumonia

Question 40

Enteral lipids should generally consist of. . .

Answer 40

. . . an anti-inflammatory, anti-oxidant lipid profile

This includes omega-3 oils and borage oil, which have been shown to reduce the ICU length of stay, duration of MV, and overall mortality.

Question 41

Don’t miss complications of aortic dissection

Answer 41

Acute cardiac tamponade

Acute aortic regurgitation (especially bad i/s/o aortic dissection therapy)

Acute RCA coronary syndrome (contraindication to intravascular inervention)

Acute limb ischemia, anterior circulation stroke, mesenteric and renal involvement/embolism

Question 42

Impulse control in aortic dissection

Answer 42

Reduce the amount of time that the vessel is experiencing high pressure

1. HR control – reduce the frequency of systolic pressure exposure
2. Pressure control – reduce the magnitude of systolic pressure

Start with a beta blocker (to avoid reflex tachycardia – often esmolol), then afterload reducer (dihydropyridine CCB, hydralazine, nitroprusside, etc).

Question 43

Initial IV nutrition regimen

Answer 43

30 kcal/day, 1g protein/kg body weight