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تعداد آیتم قابل مشاهده باقیمانده : 3 مورد
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Pathophysiologic changes due to ethanol intoxication in the surgical patient

Pathophysiologic changes due to ethanol intoxication in the surgical patient
Organ system Pathophysiology Intervention(s)
Gastrointestinal Decreased gastric emptying and inability to protect the airway increases risk for aspiration pneumonitis. Rapid sequence induction and intubation.
Cardiovascular

Cardiomyopathy (cardiomegaly, decreased cardiac function due to oxidative damage, accumulation of acetaldehyde and other metabolic products).

Thiamine deficiency can lead to high output heart failure with systemic vasodilation.

Perioperative monitoring with transthoracic or transesophageal echocardiography.

Thiamine (vitamin B1) replacement 500 mg over 30 minutes.

Pulmonary "Alcoholic lung" (due to decreased concentration of glutathione, abnormal surfactant synthesis and secretions, changes in alveolar-capillary barrier function and permeability) predisposes to ARDS and pneumonia.

Lung protective ventilation (tidal volume of 6 to 8 mL/kg predicted body weight, titration of PEEP as required to maintain PaO2).

Postoperative head of bed elevation.
Immune Increased risk for postoperative infections from inhibition of CD3+ T cells and decreased proliferation of CD4+ and CD8+ T cells; increased inflammatory cytokines (ie, IL-12, IFN-alpha).

Strict adherence to standard precautions.

Timely prophylactic antibiotic administration before incision (and early re-dosing if more than one blood volume lost during surgery).

Replacement of all non-sterile catheters (eg, those placed emergently without a sterile field) as soon as possible (<24 hours after insertion).
Hematologic Megaloblastic anemia due to folate deficiency; impaired platelet activation and inhibition by ethanol; increased fibrinolysis secondary to increased tissue plasminogen activator activity. Utilize viscoelastic monitoring (eg, TEG or ROTEM) to identify elements of the coagulation cascade that require correction.
Renal/metabolic

Acidosis in over 25 percent of patients caused by: 1) increased NADH:NAD ratio related to ethanol metabolism and volume depletion which may precipitate ketogenesis; 2) impairment of pyruvate dehydrogenase due to thiamine deficiency; and 3) lactic acidosis due to volume depletion.

Electrolyte disorders including hypomagnesemia, hypokalemia (resistant to treatment until magnesium deficiency is corrected), hypophosphatemia due to increased renal excretion.

Rhabdomyolysis.

Dextrose 5% in water, administered as a background infusion at 125 mL/hr to prevent ketogenesis, stimulate insulin production, and replenish glycogen stores.

Hydration with balanced electrolyte solutions (eg, lactated Ringer's, Plasmalyte, Normosol) according to dynamic and static indices to correct hypovolemia.

Electrolyte repletion as indicated (especially magnesium).

Neurologic B1 (thiamine) deficiency leading to pathological carbohydrate metabolism, which may result in Wernicke's encephalopathy/Korsakoff's psychosis. Thiamine (vitamin B1) replacement 500 mg IV over 30 minutes.
ARDS: acute respiratory distress syndrome; PEEP: positive end expiratory pressure; PaO2: partial pressure of oxygen in arterial blood; CD3+: cluster of differentiation - 3 glycoprotein; T cells: T lymphocyte cell; CD4+: cluster of differentiation - 4 glycoprotein; CD8+: cluster of differentiation - 8 glycoprotein; IL-12: interleukin-12; IFN-alpha: interferon-alpha; TEG: thromboelastogram; ROTEM: rotational thromboelastometry; NADH-NAD: nicotinamide adenine dinucleotide ("H" indicates reduced form); IV: intravenous.
Graphic 112946 Version 2.0

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