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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_4518_Библиотеки_им_академика_М_И_Перельмана
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P. Filip et al.
• Clinical: calcium-phosphate complex deposition, acute hypocalcemia
• Treatment:
– Acute hyperphosphatemia: dialysis, 0.9% NS, acetazolamide
– Chronic hyperphosphatemia: minimize phosphorus intake, phos-
phate binders
• Acid base disorders
– Acidemia: pH <7.37, due to processes that increase [H+] or
decrease [HCO3−]
– Alkalemia pH >7.43, due to processes that decrease [H+] or increase [HCO3−]
– Approach to blood gas
Look at change in [HCO3−] and/or pCO2 to see if it can account for
change in pH.
If pH is normal or if compensation is less or more than predicted, then a
mixed disorder is likely present.
If metabolic acidosis, calculate anion gap (AG):
• AG = [Na] − ([Cl] + [HCO3])
• AG >10, positive AG gap
– Metabolic acidosis
Anion gap metabolic acidosis
Etiologies: “MUDPILES”
• M—methanol
• U—uremia
• D—DKA
• P—paraldehyde
• I—Isoniazid, inborn errors of metabolism
• L—Lactic acidosis
• E—Ethylene glycol
• S—Salicylates, acetaminophen
Non-anion gap metabolic acidosis
Etiologies:
• GI loss of [HCO3−]—diarrhea, pancreatic stula, or drainage
• Renal causes—RTA, renal failure
• Ingestions—acetazolamide, sevelamer
• Dilutional—bicarbonate uid infusion
• Post-hypocapnia
• Ureteral diversion
• Treatment: directed at cause, no benet of sodium bicarbonate therapy
with ketoacidosis and lactic acidosis
– Metabolic alkalosis
10 Fluids, Hemostasis, Nutrition, andPulmonary Physiology
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Etiologies:
• Loss of acid from the GI tract or kidney—vomiting, NGT drainage,
thiazides, loop diuretics, Bartter/Gitelman syndrome,
hyperaldosteronism
• Excess alkali
• Post-hypercapnia
• Treatment: directed at cause, replete hypokalemia
– Respiratory acidosis
Etiologies:
• CNS depression—drugs, brainstem lesions
• Upper airway abnormalities—OSA, laryngospasm
• Lower airway abnormalities—obstructive lung disease, pneumonia,
pulmonary edema
• Thoracic cage abnormalities—pneumothorax, ail chest
• Neuromuscular failure—Guillain-Barre, ALS
• Treatment: directed at cause, improve ventilation, no role of sodium
bicarbonate
– Respiratory alkalosis
Etiologies:
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• Primary hyperventilation—CNS disorders, pain, anxiety, drugs, pregnancy, sepsis, hepatic encephalopathy, asthma exacerbation, mechanical ventilation
• Treatment: directed at cause, change ventilator settings
Hemostasis
Components ofPrimary Hemostasis
• Blood vessels
– Vascular injury triggers vasoconstriction.
– Disorders of the vasculature clinically are exceedingly rare but can be sepa-
rated into acquired and heredity disorders:
Hereditary: Ehlers-Danlos syndrome, William-Beuren syndrome,
hereditary- hemorrhagic telengectasias (HHT aka Osler-Weber-Rendu syndrome), osteogenesis imperfecta
Acquired: scurvy, amyloidosis
• Platelets
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– Adhesion
High sheer state of owing blood requires effective contact between platelets and the vascular endothelium (exposed collagen brils and a release of
an accessory molecule known as von Willebrand factor (vWF).
Enabled by binding of GP1b surface receptor on platelets to vWF.
– Aggregation
Formation of a platelet plug is also enhanced by the production of specic
cell-surface receptor proteins called GPIIb/IIIa, which allows platelet
aggregation to occur via a brinogen crosslink.
– Release
Occurs simultaneously with platelet aggregation with vWF; platelets
release cytoplasmic-stored granules containing ADP and thromboxane
A2 (TxA2).
Components ofSecondary Hemostasis
• Coagulation system
P. Filip et al.
– Following primary (platelet plug) hemostasis, secondary factor-driven hemo-
stasis occurs.
Clinical Assessment
• History
– A positive history suggestive of bleeding disorder is informative and can lead
to appropriate additional testing.
• Physical examination
– Several specic ndings on physical examination can suggest an underlying
hematologic condition.
Petechiae or ecchymosis → thrombocytopenia or functionally decient
platelets
Telangiectasias → underlying liver disease, but if around the mouth and
lips could suggest HHT
Presence of joint deformity suggestive of prior hemarthroses → severe fac-
tor deciencies
Hematomas → factor deciencies or inhibitors against a clotting factor
Hyperelasticity of skin, hyperextendible joints → Ehler-Danlos syndrome
or other collagen vascular disorder
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• Laboratory testing
– PT/PTT/INR: to be perfomed as a part of routine preoperative testing
– Complete blood counts: to be perfomed as a part of routine preoperative testing
– Bleeding time
• Differential diagnosis for abnormal coagulation studies
– Increased PTT
Inherited deciency of clotting factors (VIII, IX, XI, XII, PK, HK, and
vWF, which binds and prevents degradation of factor VIII).
XII, PK, and HK deciencies are not associated with increased risk for
clinical bleeding.
Acquired deciencies of multiple clotting factors:
• Inhibitors—Lupus anticoagulant (associated with thrombosis rather
than bleeding)
• Inhibitors—directed against specic factors such as factor VIII
• Heparin
• Liver disease
• Disseminated intravascular coagulation (DIC)
– Increased PT
Inherited deciencies of one or more clotting factors
Acquired deciencies of multiple clotting factors
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• Coumadin (inhibition of Vitamin K-dependent factors II, VII, IX, X)
• Vitamin K deciency
• Liver disease
• DIC
• Inhibitors (rare)
Anticoagulants
• Unfractionated heparin (UFH)
– Binds to antithrombin III (ATIII) in plasma to form AT-heparin complex,
which then selectively inhibits FIIa, Xa, IXa, XIa, and XIIa.
– Monitored with aPTT.
– Reversal with protamine sulfate.
– Heparin-induced thrombocytopenia (HIT) has an incidence of 3–5%. Results
from widespread platelet activation and aggregation following development
of an antibody to heparin platelet factor 4. Dened by platelet count less than
150,000 or a 50% reduction in baseline value 5–14 days after initiation.
Treatment involves immediate cessation of heparin and use of direct thrombin
inhibitors.
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P. Filip et al.
• Low-molecular-weight heparin (LMWH)
– Comprised of much smaller molecules of heparin.
– Binds ATIII and inhibits FXa and IIa.
– Routine measurement of aPTT is not necessary.
– HIT is a known complication of LMWH; the incidence is roughly 1%, lower
than that for UFH.
– Has no proven complete reversal treatment.
• Warfarin
– Inhibits vitamin K epoxide reductase and thereby depletes vitamin
K- dependent factors 2, 7, 9, and 10 and protein C and S.
– In the case of overdose and no bleeding, administer vitamin K based on
INR value.
– In the case of severe bleeding, give Vit K 10mg IV and FFP at 2–4 units
IV q6–8 h.
• Selective Xa inhibitors
– Includes rivaroxaban administered orally and fondaparinux administered
parenterally.
– Effect exerted through direct inhibition of factor Xa.
– These are mainly used in orthopedic patients as randomized controlled trials
(RCTs) have shown both to be superior to enoxaparin in the prevention of
venous thromboembolism.
– Rivaroxaban increases aPTT, PT, and heparin clotting time, while fondaparinux
exerts no effect on the coagulation proles.
– No known reversal.
• Direct thrombin inhibitors
– Includes dabigatran, argatroban, lepirudin, and bivalirudin
Perioperative antithrombotic therapy:
• Thromboembolic risk, procedural risk of hemorrhage, and the timing of interruption of thromboembolic therapy must be considered; this can be weighed, and
the clinician can formulate a decision on whether to interrupt antithrombotic
therapy. Patients with conditions at high risk requiring anticoagulation include
patients with recent DVTs and cardiac stents and those with atrial brillation.
Common antithrombotics and respective time frames of cessation and resump-
tion are listed below:
• Aspirin: cessation not indicated; resumption 24 h postoperatively
• Warfarin: cessation 5 days preoperatively; resumption 12–24 h postoperatively
• Dabigatran: cessation 2 days preoperatively; resumption 2–3 days
postoperatively
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• Rivaroxaban: cessation 2 days preoperatively; resumption 2–3 days
postoperatively
• Apixiban: cessation 2 days preoperatively; resumption 2–3 days
postoperatively
• Low-molecular-weight heparin: cessation 24 h preoperatively; resumption 48 h
postoperatively; if patient is not ambulatory and not on anticoagulation
Perioperative nonsteroidal anti-inamatory drugs (NSAIDs):
• Oral NSAIDs may be used for post-tonsillecotmy pain.
• Ketorolac can be used safely in children but is associated with a vefold increased
bleeding risk in adults.
• Use of NSAIDs in other areas of otolaryngology is likely safe based on lowquality evidence and therefore a subject of debate.
Nutrition
Nutritional Evaluation
• History
– Current nutritional intake
– Aspiration risk
– Recent weight loss
Unintentional loss >10% is signicant
– Concomitant chronic conditions predisposing to protein-calorie malnutrition
– Prior chemoradiation therapy → brosis of constrictor muscles, stricture
formation
– Previous operations/procedures, including gastrointestinal tract
Gastrectomy → vitamin B12 deciency
Ileal resection → vitamin B12 and fat-soluble vitamin (ADEK) deciencies
• Anthropometrics
– Scientic study of body size, weight, and proportions
– Body mass index (BMI)
Used to measure protein-calorie malnutrition, but also overnutrition
Does not incorporate percentage body fat
Mass (kg)/(height (m))
2
Underweight <18.5
Normal weight = 18.5–24.9
Overweight = 25–29.9
Obesity >30
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P. Filip et al.
– Ideal body weight (IBW)
Men: 50kg + 2.3kg for each inch over 5 ft
Women: 45.5kg + 2.3kg for each inch over 5 ft
• Laboratory evaluation:
– Serum proteins: used to assess nutritional status but can be inuenced by
many other factors including rate of synthesis, loss (gastrointestinal, renal,
cutaneous), and hydration status (dehydration may result in false elevation of
serum proteins)
Albumin
• Half-life = 20 days.
• Large volume of distribution in tandem with long half-life causes serum
values to fall and recover slowly with changes in nutrition.
• Serum levels plummet in critical illness due to transcapillary escape
secondary to endothelial membrane dysfunction. Considered an acutephase reactant.
• Albumin less than 3.5 mg/dL predictive of increased perioperative morbidity and mortality and associated with increased length of hospital stay.
Transferrin
• Shorter half-life of 8–10 days and smaller volume of distribution.
• More sensitive indicator of adequate nutrition repletion than albumin.
• Dependent on variations in iron status; iron-deciency anemia leads to
increased levels.
Prealbumin
• Half-life = 2 days
• More sensitive than transferrin
• Decrease early with malnutrition; increases quickly with repletion
Retinol-binding protein
• Half-life = 12 h
• Highly sensitive measure of protein synthesis
• Nutritional indices
– Allows risk stratication among patients in an objective manner and can be
used as a prognostic indicator.
– Subjective global assessment (SGA) is considered the gold standard as it is
clinically validated and reproducible. SGA takes into consideration many
components including:
Medical history
Changes in weight
Dietary intake
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Functional capacity
Metabolic demands
Gastroinstestinal symptoms
Physical examination
• Determination of energy requirements:
– Caloric need—about 20–25 kcal/kg/day
– For overweight patients, use an adjusted weight value to calculate caloric
need: weight = [(actual weight − ideal body weight) × 0.25] + ideal
body weight
– Factors that increase caloric need:
Trauma/surgery/sepsis (+20 to 40% kcal requirement)
Pregnancy (+300 kcal/day requirement)
Burns (+30 kcal/day × % burn kcal requirement)
– Harris-Benedict equation
Derived from healthy human subjects and calculates basal energy requirements (BEE) based on height, weight, gender, and age.
Total energy expenditure (TEE) accounts for the caloric demands of the
body under physiologic stress conditions.
Specic stress factors for various diseases are multiplied by BEE to calculate the TEE.
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– Respiratory quotient
Ratio of CO2 produced to O2 consumed (measurement of energy
expenditure)
Ranges from 0.7 to 1.0 under typical metabolic conditions
RQ > 1 (overfeeding) → lipogenesis
• Leads to ↑ respiratory rate → risk of respiratory distress in patients with
pulmonary compromise
• Treatment: ↑ fats and ↓ carbohydrates and caloric intake
RQ < 0.7 (underfeeding) → ketosis and starvation
• Treatment: ↓ fats and ↑ carbohydrates and caloric intake
• RQ is highest for carbohydrate (1.0), followed by protein (0.8), and
fat (0.7)
• Impact of nutritional deciency
– Albumin < 3.0 is associated with poor wound healing.
– Vitamin A supplementation can counteract the negative impact of steroids on
wound healing.
– Vitamin C is a necessary cofactor in collagen cross-linking and thus improve-
ment of wound tensile strength.
– In head and neck cancer patients, in particular, malnutrition and poor wound
healing increase risk for pharyngocutaneous stula/postoperative leak.
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P. Filip et al.
Nutritional Therapy
• Enteral
– Safer and less expensive than parenteral nutrition with added benet of pre-
serving gut functionality.
– “Feeding the gut” prevents opportunistic bacterial overgrowth by stimulation
of immunoglobulin A and maintenance of normal gut pH and ora.
– Contraindications:
Patients who require period of bowel rest—protracted emesis, gastrointestinal bleeding, active gastrointestinal ischemia
Patients under physiologic stress—hemodynamically unstable patients,
those with vasopressor requirements
– Access:
Gastrostomy
• Percutaneous endoscopic versus open.
• Consider if long-term enteral feeding is expected.
• Prophylactic insertion of gastrostomy tubes in HNSCC patients prior to
denitive chemoradiation is a controversial topic within the literature.
While pretreatment gastrostomy tube insertion may off-set the weight
loss attendant to chemoradiation and reduce hospitalization rates for
dehydration, there is also evidence that insertion is associated with a
higher incidence of esophageal stricture formation.
• Risk of tumor seeding the gastric wall and subcutaneous tissues has
been reported when using the standard “pull technique.”
Jejunostomy
• Consider for long-term enteral feeding in patients with contraindications to delivery of feeds in the stomach.
– Types of enteral formulas:
Polymeric
• Composed of complex sources of protein, carbohydrates, and fat.
Requires digestion and absorption by functional GI tract
Elemental
• Nutrients are provided in predigested, readily absorbable form.
Modular
• Special formulas that address nutritional needs of specic clinical condition, i.e., renal insufciency, pulmonary failure, hepatic dysfunction
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– Complications:
Nasogastric tube insertion may be associated with tracheobronchial intubation, visceral perforation, esophagitis, alar necrosis, and sinusitis.
Enteral feeds, in general, carry a risk of aspiration pneumonia, particularly
in those patients with poor gag reex and depressed mental status.
Metabolic complications—such as electrolyte imbalances (Na, K, Mg,
Phos, Ca) and hyperglycemia—can also occur and require viligant monitoring and appropriate correction.
• Parenteral
– General composition
Water
Electrolytes (Na, Cl, K, Ca, Mg, PO4, acetate)
50% dextrose solution
10% amino acid solution
Essential fatty acids, vitamins, minerals
– Indications
Only utilized when the gastrointestinal tract cannot be utilized
– Peripheral parenteral nutrition (PPN)
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Avoids complications associated with central venous access; therefore,
safer to administer than TPN.
Considered in patients who require supplemental nutrition for less than
14 days.
Requires large volumes of solution to fulll the typical patients total nutritional requirements as the low-osmolar solutions (<1000 mOsm) are
required to avoid phlebitis of the infused vein.
Prolonged therapy is rarely possible as the catheter must be moved frequently to prevent the development of phlebitis.
– Total parenteral nutrition (TPN)
High osmolarity of TPN requires administration via a central vein.
Can be concentrated in patients who require uid restriction (heart failure,
renal failure).
Complications occur in 5% of patients, and mortality rate attributable to
TPN is 0.2%. Complications can be:
• Technical: arterial puncture, pneumothorax, air embolism
• Infectious: central line-associated sepsis
• Metabolic: refeeding syndrome in severely malnourished patients,
hepatic cholestasis/acalculous cholecystitis, steatosis, hypoglycemia if
TPN abruptly withdrawn
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