Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / @xirurgi_2025 / @xirurgi_2025 - 1039 - файл
.pdf
112 PART III PERIOPERATIVE CARE
https://t.me/medicina_free
9. What is tonicity (effective osmolality)?
Tonicity is the ability of solutes to generate an increase in osmotic pressure, when they are restricted
to a compartment, causing water to move from an intracellular compartment to an extracellular one
to establish osmotic equilibrium. These solutes are termed effective osmoles. Sodium, glucose, mannitol, and sorbitol are effective osmoles. An increase in tonicity is the main stimulus for thirst and the
release of ADH to help water regulation.
10. What are some causes of hypovolemia?
Volume depletion can be secondary to renal losses because of diuretic use, adrenal insufficiency,
osmotic diuresis, and Diabetes Inspidus (DI). Third spacing is common in soft tissue injuries, infections, pancreatitis, and intestinal obstruction. Fluid can also be lost through the skin and lungs in
cases of high fever, sweating, increased respiratory rate, and hyperventilation.
11. What are signs of a hypovolemic fluid status?
Patients will typically develop oliguria with acute renal failure secondary to prerenal azotemia, ortho-
static hypotension, tachycardia, decreased Central Venous Pressure (CVP), and pulmonary capillary
wedge pressure. Central nervous system findings can include mental status changes and sleepiness.
These patients may also develop weakness, dry mucous membranes and hypothermia, and will
exhibit poor skin turgor.
12. How is hypovolemia diagnosed?
Urine output will decrease, serum sodium will be elevated, BUN/Cr ratio will be greater than 20:1, and
hematocrit will increase 3% for each liter of deficit.
13. How is hypovolemia treated?
Crystalloid therapy is the gold standard except in cases of severe blood loss; 2 L of isotonic crystalloid
fluid should initially be bolused. It is important to note that in these patients, close monitoring of vitals
is imperative. Urine output should be maintained at 1 cc/kg/hr. Colloid therapy is more expensive and
has not shown any benefit over crystalloid therapy. In cases of severe hemorrhagic hypovolemia or
shock, blood transfusion should be used. Patients with cardiac history should be cautioned in replenishing their fluid deficiency.
14. What are clinical signs of hypervolemia, and when does volume excess occur?
Peripheral edema, pulmonary rales secondary to edema, low albumin, elevated CVP, and jugular
venous distention are all signs of volume excess. These patients will often exhibit weight gain.
Typically volume excess occurs when water and sodium intake/retention are greater than renal and
extrarenal losses. The etiology of hypervolemia includes liver disease, congestive heart failure, acute
renal failure, and nephrotic syndrome.
15. What is edema?
Edema is a condition of volume excess that occurs in the interstitial or extracellular space and is not
evident until 3 to 4 L of fluid have accumulated.
16. Which commonly used parenteral fluid most closely resembles ECF? How
does its composition differ from 5% dextrose in half-normal saline (D5-1⁄2 NS)
(Table 10-1)?
Table 10-1. Commonly Used Parenteral Fluids
Electrolyte Content (mEq/L)
SODIUM POTASSIUM CALCIUM MAGNESIUM CHLORIDE HCO
Lactated
130 4 3 – 109 28
Ringer’s
ECF 142 4 5 3 103 27 280-310
D5-1⁄2 NS 77 – – – 77 – 407
3
(as
lactate)
OSMOLARITY
(IN OSM)
273
CHAPTER 10 FLUID AND ELECTROLYTES 113
2 mEq/L × 0.6 × (body weight in kg) × 1000
2 × 0.6 ×(70)× 1000
513
https://t.me/medicina_free
17. What is the most common electrolyte disorder in hospitalized patients? What are
general considerations?
Hyponatremia is the most common electrolyte disorder in hospitalized patients. It is defined as having a
serum sodium concentration <130 mEq/L. It is usually caused by a water imbalance because of increased
water intake or a decrease in excretion by the kidney. The most common type is a hypoosmolar form in
which the serum osmolarity is reduced to <280 mOsm/kg. Two other types must be ruled out. One is an isotonic form, in which the serum osmolality is normal (280 to 295 mOsm/kg) and is caused by hyperproteinemia, hyperlipemia, and posttransurethral resection (TUR) prostatectomy. The other is a hyperosmolar form
with a serum osmolality >295 mOsm/kg caused by hyperglycemia, mannitol, and radiocontrast agents.
18. How is the concentration of sodium maintained?
Sodium is restricted to the extracellular space and is the main osmotic cation in the extracellular fluid.
When sodium intake is increased, there is a concurrent increase in the extracellular fluid volume. This
will then increase sodium excretion through the renal system.
19. What is hypoosmolar hyponatremia?
Hypoosmolar hyponatremia can occur with normal TBW (euvolemic hyponatremia), excess TBW (hypervol-
emic hyponatremia), and low TBW (hypovolemic hyponatremia). The most common cause of hyponatremia
with euvolemia is SIADH. Other causes of this can be drugs (nonsteroidal antiinflammatory drugs, Diabinese, Tegretol, cytotoxin), diuretics, pulmonary infection, meningitis, and oat cell carcinoma. Hypervolemic hyponatremia is a depletion of the effective circulating volume with no restriction of water intake
[Congestive Heart Failure (CHF), hepatic cirrhosis, nephritic syndrome]. Hypovolemic hyponatremia can
be nonrenal in origin (vomiting, diarrhea, sweating) when the urine sodium concentration is <10 mEq/L, or
renal (diuretics, a salt-losing renal disease or adrenal insufficiency) when the urine sodium concentration is
>20 mEq/L. Rapid correction can lead to irreversible central nervous system (CNS) damage.
20. How is hyponatremia diagnosed?
Hyponatremia is caused by too much water; however, the etiology and diagnosis is found when serum
osmolality is calculated. A normal serum osmolality is isotonic hyponatremia and is typically caused by
hyperlipidemia and hyperproteinemia. A high serum osmolality is hypertonic hyponatremia and is caused by
hyperglycemia. When serum osmolality is low, hypotonic hyponatremia is the diagnosis; however, it needs
to be further classified based on volume status. In the hypotonic hyponatremic setting, the patients who are
hypovolemic are losing salt, the euvolemic patients can have SIADH, hypothyroidism, or psychogenic polydipsia, and the hypervolemic patients are typically in renal failure, congestive heart failure, or liver failure.
21. What are symptoms of hyponatremia?
The most common are neurologic symptoms that are caused by an increase in ICF volume leading
to headaches, hyperactive deep tendon reflexes, weakness, and irritability. Other symptoms include
hypertension, nausea, vomiting, ileus, and oliguria.
22. What are the critical levels of hyponatremia, and how can this condition be
corrected?
Symptoms usually occur during an acute, sudden decrease of sodium levels to <130 mEq/L or during
a chronic, gradual decrease to <120 mEq/L. Treat the underlying cause or restrict free water intake
first. Treat only acutely hyponatremic and profoundly symptomatic patients, and raise serum sodium
levels by 2 mEq/L/hr but no higher than 125 mEq/L, with 3% NaCl.
513 mEq/L
For example, for a 70-kg patient:
23. What is hypernatremia?
A sodium greater than 145 and diagnosed based on volume status. A hypovolemic hypernatremia is from
renal failure and renal losses; an isovolemic hypernatremia is related to diabetes insipidus; and hypervolemic hypernatremia is secondary to Cushing’s syndrome, exogenous glucocorticoids, and can be iatrogenic.
= mL / hr of 3% NaCl
= 160 mL/hr of 3% NaCl
114 PART III PERIOPERATIVE CARE
https://t.me/medicina_free
24. Discuss the symptoms of hypernatremia.
Again, neurologic symptoms are the most common with altered mental status, restlessness, focal
neurologic deficits, and seizures all possible.
25. How is hypernatremia treated?
The hypovolemic patients should be given isotonic fluid gradually by calculating their water deficit:
Water deficit = 0.6 × (body weight in kg) × [(Na/140)−1]
In addition, underlying disorders should be addressed such as diabetes insipidus in isovolemic
patients, and hypervolemic patients can be treated with diuretics.
26. When can D5W be used, and why?
One liter of D5W contains 1 L of free water and 50 g of glucose. Because it contains no sodium, it is
used in patients with hypernatremia. Free water will distribute evenly between the ICFV and the ECFV,
and the glucose will move into the cell. Pure water is not given because it can cause hemolysis. It
is not used in diabetics because it can cause hyperglycemia; so in nondiabetics, it is used to give
medications. It should not be used in patients with depletion of ECFV because it is a hypotonic solution
and its use could cause hyponatremia. It can be used in patients with ECFV overload as a KVO (keep
vein open) solution.
27. When is a hypotonic saline solution used?
A hypotonic saline solution such as 0.45% saline is used to expand the ECFV in someone who is
volume depleted and to correct hypertonicity in someone who is hyperglycemic or hypernatremic.
28. What are the risks of rapid correction of hyponatremia or hypernatremia?
Rapid correction of hyponatremia with hypertonic solution may lead to permanent brain damage, sei-
zures, and pontine myelinolysis. Rapid expansion of the ECF compartment can also worsen preexisting
conditions, such as CHF. Rapid correction of hypernatremia and a severe decrease in serum osmolarity can cause convulsions, coma, and death.
29. What is the difference between SIADH and DI?
SIADH has an increase in ADH secretion, which causes water retention and hyponatremia. In DI, ADH
secretion is decreased, leading to a large volume of dilute urine. Central DI has no ADH release leading
to the kidneys being unable to concentrate urine. Nephrogenic DI has a normal amount of circulating ADH, but water is unable to be absorbed by the collecting tubules. Hypernatremia arises in both
central and nephrogenic DI.
30. What is central DI?
In the absence or lack of ADH, the kidney is unable to concentrate urine. This can lead to excessive
loss of water from the kidney and hypernatremia. This is manifested by polyuria and polydipsia.
31. What is nephrogenic DI?
In this syndrome, there are adequate levels of circulating ADH; however, water is not absorbed
because the permeability of collecting tubules is not increased. This results in hypernatremia because
of excessive water loss.
32. What are normal levels of potassium?
Levels between 3.5 and 5 are considered normal, with most of the potassium being found
intracellularly.
33. What causes hypokalemia?
GI losses including vomiting, diarrhea, laxatives, and renal losses from diuretics, renal disease,
magnesium deficiency, and excess of glucocorticoids. Other causes of hypokalemia are secondary to
redistribution, such as with insulin excess or a metabolic alkalosis.
34. Discuss symptoms of hypokalemia.
Arrhythmias secondary to hypokalemia as the cardiac cycle will be prolonged. Polyuria, polydipsia,
and nausea/vomiting or altered mental status, as well. On ECG, the T wave will flatten and a U wave
may be present.
35. How is hypokalemia treated?
Any underlying cause should immediately be addressed. Oral potassium replacement is the safest
method for replacement. For every dose of 10 mEq of KCl, the potassium should increase by
0.1 mEq/L. IV forms are available, but serum potassium needs very close monitoring in these patients.
CHAPTER 10 FLUID AND ELECTROLYTES 115
https://t.me/medicina_free
36. What causes hyperkalemia?
A redistribution of potassium from intracellular to extracellular in cases of insulin deficiency, hemolysis,
GI bleeding, and acidosis. Renal failure, blood transfusion, spironolactone, and ACE inhibitors can all
increase potassium levels. Renal failure with oliguria is the most common cause of true hyperkalemia.
37. What ECG changes are noted in hyperkalemic patients?
Peaked T waves, prolonged PR interval, and QRS widening are seen on ECG. The patient may enter
ventricular fibrillation when potassium levels are high enough.
38. How is hyperkalemia treated?
The goal is to shift the potassium back from extracellular to intracellular sources. In severe cases of
hyperkalemia, IV calcium is given to stabilize the myocardium and decrease the excitability. Sodium
bicarbonate will shift potassium intracellularly and insulin will also push potassium intracellularly. When
giving insulin, it is important to also provide the patient with glucose to prevent hypoglycemia. Removing potassium is possible with Kayexalate and dialysis.
39. How is calcium maintained by the body?
Maintenance is hormonal and based on Parathyroid Hormone (PTH), calcitonin, and vitamin D. All of
these hormones act on the gut, kidney, and bones. PTH increases plasma calcium and decreases
plasma phosphate, calcitonin decreases plasma calcium and decreases plasma phosphate, and
vitamin D increases plasma calcium and increases plasma phosphate.
40. How is calcium found in plasma?
There is a protein-bound form that is bound to albumin, and a free, ionized form. An increase in pH will
increase calcium-albumin binding. Hypoalbuminemia is the most common cause of hypocalcemia. For
every 1 g/dL decrease in albumin below 4 g/dL, the total serum calcium is corrected by adding 0.8 mg/dL.
The free ionized form is the physiologically active calcium and is independent of albumin levels.
41. What are the causes and symptoms of hypocalcemia?
Hypocalcemia is defined by an ionized calcium level below 2 or a serum calcium lower than 9. Hypo-
calcemia is commonly caused by renal failure and hypoalbuminemia (most common). Other causes
include a vitamin D deficiency, hypoparathyroidism, pancreatitis, and rhabdomyolysis. Increased
neuromuscular irritability is common with perioral numbness, hyperactive deep tendon reflexes,
grand mal seizures, and cardiac arrhythmias. Chvostek’s sign and Trousseau’s sign are both seen
in hypocalcemia. Chvostek’s sign is twitching of the facial muscles when the facial nerve is tapped.
Trousseau’s sign causes carpal spasm after occluding forearm blood flow for 3 minutes. Patients with
a chronic hypocalcemia may exhibit no symptoms.
42. What are clinical features of hypercalcemia?
Stones, bones, groans, and psychiatric overtones is a mnemonic for this problem. Patients have
kidney stones, bone aches with brown tumors, muscle pain, gout, constipation, and can have signs of
depression, anxiety, and lethargy. A shortened QT interval is seen on ECG.
43. What are some of the signs that should alert you to a patient having an acid–base
disorder?
A patient who has a change in mental status; tachypnea; Kussmaul breathing; cyanosis; respiratory
failure; severe fluid loss from vomiting, diarrhea, or shock; and a history of an endocrine disorder,
renal problems, or drug ingestion should be suspected of having an acid–base problem.
44. What is metabolic acidosis?
Decreased blood pH with a decreased bicarbonate; there are two types: an anion gap metabolic
acidosis (gap >12) and a nonanion gap acidosis.
45. What is the significance of an anion gap?
A normal anion gap typically ranges from 8 to 12 mmol/L. It is significant in the presence of metabolic
acidosis. A normal anion gap acidosis is due to a drop in bicarbonate, whereas an anion gap acidosis
is due to an increase in anions.
Anion Gap = [Na+] + [K+] − [Cl−] − [HCO3−]
46. What is the etiology of metabolic acidosis?
MUDPILES is a common mnemonic for the etiology of anion gap metabolic acidosis.
Methanol ingestion
Uremia
116 PART III PERIOPERATIVE CARE
https://t.me/medicina_free
Diabetic ketoacidosis
Paraldehyde ingestion
Isoniazid ingestion
Lactic acidosis
Ethylene glycol ingestion
Salicylate ingestion
Nonanion gap acidosis occurs secondary to GI and renal losses.
47. What are signs of metabolic acidosis, and how is it treated?
Decreased tissue perfusion, decreased cardiac output, altered mental status, arrhythmias, hyperka-
lemia, and a compensatory hyperventilation. Treatment relies on determining the underlying cause of
the acidosis and treating the etiology. Sodium bicarbonate has been shown to be ineffective and is
only used in cases of rapid deterioration.
48. What is metabolic alkalosis?
The pH levels increased secondary to an increase in bicarbonate. The etiology is based on extracellu-
lar fluid volumes. An expansion of the ECF with a metabolic alkalosis is common in adrenal disorders.
ECF contraction in the face of a metabolic alkalosis points the etiology toward renal and GI losses.
Again, the treatment of metabolic alkalosis relies on treating the underlying disorder.
49. What are the signs, symptoms, and treatment of respiratory acidosis?
Respiratory acidosis is a decreased blood pH with PaCO2 >40. Signs and symptoms include confusion,
headaches, CNS depression, and fatigue. Commonly this is secondary to COPD and hypoventilation.
Acute respiratory acidosis will have no renal compensation; however, chronic respiratory acidosis will
show renal compensation with an increase in plasma bicarbonate. These patients are treated with
supplemental oxygen and possible mechanical ventilation in severe cases.
50. What is respiratory alkalosis?
This is an increased blood pH with a decrease in PaCO2 secondary to hyperventilation. The etiology of
this phenomenon includes pregnancy, sepsis, anxiety, asthma, and pulmonary embolism.
51. What are signs, symptoms, and treatment of respiratory alkalosis?
Signs include perioral numbness, anxiety, arrhythmias, and decreased cerebral blood flow. Severe
cases can cause tetany. The treatment includes inhaling carbon dioxide and treatment of the underlying disorder.
52. What is a desirable parenteral fluid level in a sickle cell crisis patient who weighs
150 lb?
1⁄2 NS will create an osmotic gradient to distribute water intracellularly.
53. What is the maintenance fluid requirement of a healthy 72-kg adult who is re-
Maintenance fluid should be replaced with lactated Ringer’s solution or D5-1⁄2 NS with 20 mEq KCl/L
54. How will the same situation be managed in a patient with end-stage renal
Intravenous (IV) fluids will be restricted to minimal level, usually 30 mL/hr of D5-1⁄2 NS regardless of
55. What is the drug therapy for an unconscious patient who develops DI after exten-
Unconscious patients may receive 5 U of the ADH analogue desmopressin (1-deamino-8-D-arginine
This is thought to cause cellular swelling and reduce sickling of red blood cells.
kg = lb − 10/2 = 150 − 10/2 = 70 kg
“4, 2, 1 method”: 40 mL first 10 kg/hr + 20 mL second 10 kg/hr + 10 mL for each additional
10 kg/hr. Therefore the 70-kg patient will receive 110 mL/hr of 1⁄2 NS.
stricted from oral intake (NPO) while awaiting surgery?
in the following amount:
40 mL/hr for the first 10 kg of body weight + 20 mL/hr for second 10 kg + 10 mL/hr for each additional 10 kg
Therefore for a 72-kg patient, the fluid requirement is:
40 mL/hr + 20 mL/hr + 52 mL/hr = 112 mL/hr (for practical purposes, 115 mL/hr)
disease?
weight. Potassium usually will be avoided.
sive panfacial and cranial fractures? How does therapy differ for a patient who is
conscious and alert?
vasopressin; DDAVP) subcutaneously every 4 hours along with slow replacement of free water.
CHAPTER 10 FLUID AND ELECTROLYTES 117
(3.5 g/dL − albumin level) × 0.8 + calcium level (mg/dL)
(3.5 − 2.0) × 0.8 + 7.5 = 8.7 mg/dL of corrected calcium level
2 × 6(kg
24 hours
https://t.me/medicina_free
Patients who are alert and have sufficient oral intake of water may receive 2 to 4 mg of intranasal
DDAVP twice a day.
56. How is the true serum calcium level calculated in a patient with a lab calcium
concentration of 7.5 mg/dL and an albumin level of 2.0 g/dL? What other lab value
might be helpful?
Most serum calcium is bound to albumin, and therefore hypoalbuminemia will give a false reading
of hypocalcemia. The minimal normal albumin level is 3.5 g/L, and the corrected calcium level is
calculated as:
The measurement of ionized calcium (iCa) in serum will give a true level of available calcium in serum.
57. An 11-month-old infant who underwent palatoplasty had minimal blood loss but
is refusing any type of feeding and will be temporarily started on parenteral fluids.
She weighs 22 lb. What is her TBW? What is her minimal acceptable urine output?
What maintenance parenteral fluids should be prescribed?
TBW in infants represents 75% to 80% of the kilogram body mass (in comparison to 50% to 60% in
adults). Adequate urinary output in children younger than age one is 2.0 mL/kg/hr (in comparison to
0.5 to 1.0 mL/kg/hr in adults).
Maintenance IV fluids would be D5-1⁄4 NS + 20 mEq KCl/L in the amount of 40 mL/hr. The amount
of fluids is calculated the same way as in adults. The sodium and potassium intake requirements for
infants are 3 mEq/kg/day and 2 mEq/kg/day, respectively.
58. A young, healthy woman who was hospitalized and treated for Ludwig’s angina
is unable to have any oral intake and is currently running a fever of 39.4° C. She
weighs 60 kg, and her electrolytes are within normal limits. How should her parenteral fluids be managed?
Add 2 to 2.5 mL/kg/day per each degree above 37.0° C to the appropriate maintenance fluid require-
ment to compensate for insensible losses due to fever. This patient’s baseline would be 100 mL/hr of
lactated Ringer’s solution, and 12 mL/hr would be added according to the formula:
)
× 2.4 (° C) = 12 mL / hr
59. A patient has hyposmolar, hypervolemic hyponatremia 24 hours after surgery.
What is the initial treatment?
Restrict oral fluid intake (usually to about 1000 mL/24 hours). This patient most likely has been over-
hydrated with hypotonic IV fluid. If the sodium level is not in the range that needs emergent correction,
the patient will mobilize the fluid, and the sodium level will be corrected slowly on its own.
60. A trauma patient who has undergone repair of maxillofacial fractures develops oliguria with a serum osmolarity of 1000 mOsm/dL. What is the most likely
diagnosis?
SIADH, probably due to trauma.
61. A patient who has been on IV antibiotics for 7 days develops diarrhea. The patient
is hemodynamically stable. What is the most appropriate fluid to administer
initially?
This patient is suffering from insult to normal intestinal function. Thus the patient is losing sodium,
potassium, and, to a lesser extent, other ions (e.g., calcium, magnesium). Lactated Ringer’s solution
is the best fluid for this situation because it contains sodium, potassium, calcium, lactic acid, and
sodium bicarbonate, which resemble the fluid lost from the small intestine.
62. A patient with a history of CHF is on loop diuretics and digoxin. He is admitted
for maxillofacial surgery. Perioperatively, what is the most important electrolyte to
check and adjust?
Potassium. Loop diuretics (e.g., furosemide) are potassium-wasting drugs. Digoxin is an inotrope,
which blocks Na/K channels. The serum potassium level of patients who take digoxin and loop diuretics should be safely above 4.0 mEq/L to prevent arrhythmia. This patient has the potential to develop
118 PART III PERIOPERATIVE CARE
https://t.me/medicina_free
hypokalemia because of the loop diuretic. Thus paying close attention to the serum potassium level is
critical for prevention of cardiac dysfunction.
63. A patient manifests signs and symptoms of muscle twitching and prolonged QT
on ECG. What electrolyte should be checked?
Calcium. Hypocalcemia increases excitation of the neuromuscular system, causing cramps and tetany.
Chvostek’s sign and Trousseau’s sign (carpopedal spasm following occlusion of arterial blood supply
to the arm for 3 minutes) are clinically important indications of hypocalcemia. Prolonged QT may lead
to arrhythmias and subsequent heart failure if not treated.
64. A trauma patient develops polyuria with low osmolarity on day 1 of hospital admission. What is the most likely diagnosis, and what is the initial management?
DI is the most likely diagnosis. The initial management would be IV 1⁄2 NS and DDAVP. In DI, ADH is
not adequately released from the posterior pituitary. In this patient, trauma to the stalk in the pituitary
gland is probably the cause. Therefore the patient is losing free water. The patient requires IV fluid
to keep him hemodynamically stable and prevent hyperosmolar hypovolemic hypernatremia. This is
best accomplished with a hypotonic solution, such as 1⁄2 or 1⁄4 NS. The patient also needs exogenous
replacement of ADH. Thus DDAVP needs to be administered intravenously to prevent free water loss.
65. After a motor vehicle accident, a patient is on a ventilator, receives appropriate
fluid, has a Foley catheter, and has no oral intake. What is the source of his insensible fluid loss?
Perspiration. Sensible losses are through the kidneys and feces. Insensible losses are through the skin
and lungs. When a patient is on a closed-system ventilator, there is really no insensible loss through
the lungs. Thus the only insensible loss that needs to be replaced is the evaporated sweat.
66. A patient who has a past medical history significant for chronic renal failure is
put on a regular diet. The next day, the patient develops flaccid muscles and
decreased urine output. His magnesium is normal. Which electrolyte is the most
likely cause?
Potassium. Hyperkalemia is characterized by flaccid muscles, fatigue, and ECG abnormalities in
severe cases. Considering the patient’s history, he might have hypermagnesemia or hyperkalemia,
but the magnesium is reported as normal. Therefore the potassium level must be checked and treated
accordingly.
67. Twenty-four hours after an elderly patient underwent oral maxillofacial surgery,
she develops tonic-clonic seizures. Her lab results indicate that her serum sodium
is 119 mEq/L and her serum osmolarity is 250 Osm. The patient is euvolemic with
stable vital signs. What is the appropriate fluid management of the patient?
Fluid restriction and very slow replacement with hypertonic saline solution (usually 3% NaCl). Many
conditions can cause hypotonic, euvolemic hyponatremia. This patient is symptomatic (seizure),
which should be treated first (e.g., with Valium). Sodium must be replaced very slowly to prevent CNS
damage.
NUTRITIONAL SUPPORT
https://t.me/medicina_free
Hani F. Braidy, Vincent B. Ziccardi
1. When is enteral feeding/nutrition indicated?
• Inability to ingest food normally because of maxillofacial trauma
• Protein-energy malnutrition
• Normal functioning bowel
2. What are the indications for nutritional support?
• Inadequate intake for more than 5 days
• Malnourished patients undergoing surgery
• Major trauma (burn victims, blunt or penetrating injury, etc.)
3. What are the causes of malnutrition?
• Neglect (e.g., severe alcoholics, extreme of ages)
• Digestive problems
• Inadequate food intake
• Chronic illness
• Dysphagia
• Stress and trauma
• Vomiting
4. What is the definition of malnutrition according to the World Health Organization
(WHO)?
According to the WHO, malnutrition is “the cellular imbalance between supply of nutrients and energy
and the body’s demand for them to ensure growth, maintenance, and specific functions.”
5. What are the two forms of protein-energy malnutrition?
Marasmus and kwashiorkor.
6. What is marasmus?
Marasmus is a form of protein malnutrition in the presence of inadequate total calorie intake. It is
endemic in third-world countries and characterized by decreased weight, decreased body fat, loss of
muscle mass, hypothermia, apathy, and dehydration.
7. What is kwashiorkor?
Kwashiorkor is a form of protein malnutrition in the presence of near-normal total calorie intake. It is
endemic in third-world countries and characterized by hypoalbuminemia, edema, muscle wasting,
immunosuppression, fatty liver, and distension of the abdomen. Patients with marasmus undergoing
major surgery or stress may suffer subsequently from kwashiorkor.
8. What vitamin deficiency is commonly found in chronic alcoholics, and what are
the common symptoms associated with it?
Thiamin (vitamin B1) deficiency is commonly found in severe alcoholics. The following symptoms and
clinical pictures are classically described:
• Beriberi: fatigue, weakness, depression, right- or left-sided congestive heart failure, peripheral
vasodilation, neuropathy
• Wernicke-Korsakoff’s syndrome: symptoms of beriberi in addition to ophthalmoplegia, gait distur-
bance, nystagmus, confusion, amnesia, dementia
9. If a patient is at risk for aspiration, which short-term feeding route is indicated?
If a patient is at risk for aspiration, the nasoduodenal and nasojejunal (postpyloric) routes are best.
The technique of nasoduodenal feeding can overcome problems of gastric retention. There are fewer
problems with gastroesophageal reflux and subsequent risk of tracheobronchial aspiration. The
technique of nasojejunal feeding bypasses an obstructive lesion or motor abnormalities involving the
gastrointestinal (GI) tract proximal to the jejunum.
119
CHAPTER 11
120 PART III PERIOPERATIVE CARE
https://t.me/medicina_free
10. What route of administration is indicated for long-term enteral feeding?
For long-term enteral feeding, enterostomies are the preferred access route. Percutaneous endoscopic
gastrostomy (PEG) involves placement of a 16- to 18-gauge latex or silicone catheter through the
abdominal wall and directly into the stomach.
11. Which feeding route is preferred when a patient is at risk for aspiration?
If a patient is at risk for aspiration, the feeding tube should be placed in the small intestine either
surgically via a jejunostomy or nonsurgically via a percutaneous jejunostomy tube.
12. Where does a nasogastric tube (NGT) extend, and what are some advantages
to its use?
The NGT extends from the nose into the stomach. NGTs are advantageous because:
• The NGT tolerates high osmotic loads without cramping, distention, vomiting, diarrhea, or fluid and
electrolyte shifts.
• It allows intermittent or bolus feedings because the stomach has a large reservoir capacity.
• It is easier to position a tube into the stomach than into the jejunum.
• The presence of hydrochloric acid in the stomach may help prevent infection.
13. Where does a nasoduodenal tube (NDT) extend, and when is it indicated?
The NDT extends from the nose through the pylorus and into the duodenum. NDT feedings are indi-
cated in:
• Patients at risk for aspiration.
• Patients who are debilitated, demented, stuporous, or unconscious.
• Patients with gastroparesis or delayed gastric emptying.
14. What is meant by continuous feeding, and what are its advantages and
disadvantages?
Continuous feeding allows a patient to receive a constant infusion of enteral feedings. The advantages
of continuous feeding are decreased risk of aspiration, bloating, distention, and osmotic diarrhea with
improved patient tolerance. The disadvantages of continuous feeding are that it requires the patient
to be physically connected to the apparatus during infusion and the expense associated with the
purchase of volumetric infusion pumps.
15. What three macronutrients are required when infusing total parenteral nutrition
(TPN)?
1. Glucose
2. Protein
3. Lipids
16. What parameters should be monitored in patients receiving TPN?
• Metabolic parameters: sodium, potassium, chloride, CO2, blood urea nitrogen (BUN), creatinine,
glucose, hematocrit, hemoglobin, white blood cell (WBC) count, calcium, magnesium, phosphorus,
and platelets
• Nutrition: daily weight evaluations, albumin, and prealbumin
• Fluid status
• Infection: If WBC count is increasing or the patient is febrile, a blood culture should be obtained and
consideration given to changing the central line.
17. What are some of the physical findings clinically seen in malnutrition?
• Temporal wasting, decreased skinfold (pinch test)
• Glossitis, cheilosis, decreased taste
• Hair loss, dry skin, edema
• Confusion, gait abnormalities, loss of tactile sense, peripheral neuropathies
18. What are the lab values typically assessed when evaluating a patient for
malnutrition?
• Albumin (20 days half-life, 3.5 to 5.0 g/dL)
• Transferrin (7 to 10 days half-life, 200 to 400 mg/dL)
• Prealbumin (2 days half-life, 16.0 to 35.0 mg/dL)
• Vitamin and mineral levels
CHAPTER 11 NUTRITIONAL SUPPORT 121
https://t.me/medicina_free
19. What is the Harris-Benedict equation?
This equation is an estimation of the daily calorie requirement at rest (expenditure) in relation to a
patient’s weight, height, and age. It usually overestimates by 20% to 60%.
Males: 66.5 + 13.8 × weight (kg) + 5 × height (cm) − 6.8 × age.
Females: 655.1 + 9.5 × weight (kg) + 1.8 × height (cm) − 4.7 × age.
This estimation can be adjusted to various levels of stress. For instance, in a patient who sustained
severe trauma, this equation can be multiplied by 1.6.
20. Other than the Harris-Benedict equation, what other method can be used to estimate the daily total calorie requirement?
30 cal/kg is a gross estimation of the total daily calorie requirement in a nonstressed patient.
21. How many calories are provided by different organic fuels (glucose, protein, fat)?
Glucose 3.7 cal/g
Protein 4.0 cal/g
Fat 9.1 cal/g
22. How much carbohydrates, fat, and protein are required in the diet of the surgical
patient?
The bulk of the energy requirement should be provided by carbohydrates (70%) and lipids (30%).
Proteins are calculated in relation to a patient’s catabolic state. Normally, 0.8 to 1.0 g/kg of proteins
are necessary, whereas 1.2 to 1.6 g/kg are required in the stressed patient.
23. Which amino acid is critical for bowel mucosa function?
Glutamine.
24. What is enteral nutrition?
Enteral nutrition is a technique to provide nutrition to a patient through the gut using a tube placed
in the GI tract. An orogastric tube (OGT) or NGT can be used to deliver special liquid formulas. These
formulations are especially useful in patients who have undergone oral and maxillofacial surgical
procedures and in malnourished patients. Long-term enteral feedings are best achieved through a
percutaneous gastrostomy tube inserted endoscopically (PEG).
25. What are the contraindications for enteral nutrition?
Enteral nutrition is possible only if the gut is functioning. In patients with intestinal ischemia, ileus, or
bowel obstruction, enteral nutrition is contraindicated. It is also contraindicated in patients in shock
and those with severe pancreatitis.
26. What are some of the problems associated with enteral nutrition?
Insertion of the tube into the trachea is possible and potentially fatal due to aspiration pneumonia.
Sometimes, tube occlusion can occur. Pulmonary aspiration (80% occurrence), nausea, and vomiting can
ensue if the infusion rate is too high. Diarrhea is a common side effect. When the carbohydrate intake is
too high, a hyperosmolar state or diabetes can complicate the feedings. Most of the issues associated
with enteral nutrition can be rectified by changing the rate or the osmotic content of the enteral solution.
27. What are the main components of enteral feeding formulas?
Protein
Calories Between 1 and 2 cal/mL
Osmolality Usually between 280 and 1100 mOsm/L, a value that is directly related to the
28. What is the best way to confirm nasogastric tube (NGT) placement?
Reviewing an abdominal radiograph showing the NGT tip in the stomach.
29. In patients undergoing enteral tube feedings, what is the minimal gastric residual
volume that may require the use of promotility agents?
250 cc. Promotility agents (such as metoclopramide) will increase gastrointestinal transit and may
decrease tube feed complications such as aspiration, gastric distension, bloating, nausea, and vomiting.
30. At which gastric residual volume may you elect to hold tube feedings?
500 cc. High residuals can increase risks outlined in question 29.
Usually 35 to 40 g/L
amount of carbohydrates
Соседние файлы в папке @xirurgi_2025