Showing posts with label Surgery. Show all posts
Showing posts with label Surgery. Show all posts

Preoperative preparation is classified into 3 categories according to an urgent degree.

Emergent operation necessary preparations should be done with the shortest time operate immediately.

e.g. rupture of the liver, large vessel in the abdomen.

Date-limited operation:  the date of operation can be selected, but cannot be over prolonged. Preparation is limited with a certain time, so sufficient preparation should be done within this limit.

Elective operation: the date of the operation does not affect the outcome of treatment.

Patients with compromised pulmonary function preoperatively are susceptible to postoperative complications, including hypoxia, atelectasis, and pneumonia.

Risk factors: COPD, smoking, advanced age, obesity, acute respiratory system infection.

Physical examination: wheezing and prolonged expiration.

The most helpful screening pulmonary function tests are forced vital capacity (FVC) and forced expiratory volume in 1 second (FEV1). Values less than 50% of predicted outcomes based on age and body size indicate significant airway disease with a high risk for complications.

The blood sugar level should be controlled before the operation, water-electrolyte imbalance and acidosis should be corrected, the nutritional state should be improved.

For a suspected infection, antibiotics should be given preoperatively

Before the operation, blood sugar should be at a steady mild elevated state (5.611.3 mmol/L) urine sugar + ~ ++.

The operation should be performed as early as possible to avoid long fasting time and ketogenesis

If the operation lasts long, glucose and insulin are given in infusion fluid with a ratio of 5:1.

Dosage of insulin after operation is determined by the urine sugar value within 4-6 h, ++++: 16 U; +++: 12 U; ++: 6 U: +: 0 U. Urine ketone positive: 6U.

Monitoring

  • Vital signs
  • Central venous pressure
  • Other special monitoring items
  • Body fluid balance

Incision classification

  • Clean Category I
  • Possibly contaminated Category II
  • Contaminated Category III

Postoperative fever classified into the infectious & noninfectious origin, with the latter occurring more earlier (1.4 d versus 2.7 d) and temperature lower than the former

Wound infection

  • Incident 3-4%, 3-4 days after operation.
  • Redness, swelling, hotness, pain & tenderness of incision.
  • With or without fever and increment of WBC
  • Discharge should be cultured for choosing antibiotics
  • Remove suture at the most obvious tender point and open the incision to release pus, etc. 


 

Caloric sources

Three major sources: protein, carbohydrate, and fat

Amount of glycogen is limited, only can supply 3765.6 KJ900 kcal),comprise ½ of daily requirement

Protein cannot be considered as an energy source.

Body fat is the main energy storage about l5Kg. In starvation fat provides the bulk of calories with little effect on organ function, but certain amount of protein also be oxidized

Anthropometry

Malnutrition: body weight loss > 15%t

Viscera protein: albumin, etc.

Incapable of oral ingestion > 5-7 days

Preoperative preparation of malnutrition patient, digestive tract fistula, acute severe pancreatitis, short bowel syndrome, severe infection, large area burning, and hepatic, renal failure, etc.

PN after major operation is beneficial to patient's recovery, especially abdominal surgery

Intestinal inflammatory diseases: ulcerative colitis, Crohn disease

Nutrition support may promote tumor proliferation and development, so it should be used in combination with chemotherapy.

Glucose

Main energy source of PN, only 100 g/24 h can save protein

Advantages: sufficient origin, low price, convenient to know its utilization status through monitoring blood & urine glucose 

Disadvantages:

  • High concentration: 25% & 50%irritable to vein 
  • Limit of body utilization: 5 mg/(kg·min)
  • Surgical patients combined with DM are more susceptible to   
  • Glucose metabolism disturbance
  • Under stress, body utilization rate decrease, extra glucose turn into fat, dispose in organs

Electrolytes

Potassium, sodium, chloride, calcium, magnesium and phosphorus 

Vitamins

Water soluble: thiamine, riboflavin, niacin, pantothenic acid, pyridoxine, folic acid, B12

Fat soluble: A, D, E, K

Trace metals

Zinc, Copper, Chronium, Selenium, Manganese, Iron

Technical complications: 

  • Related to central venous catheter: pneumothorax, injury of blood vessel, nerve or thoracic duct due to puncture.
  • Air embolism
  • Insufficient replenishment
  • Serum electrolyte disturbance
  • Trace metal deficit
  • Essential fat acid deficit

Hypo/hyperglycemia

  •        Hypoglycemia: over-dosage of extraneous insulin
  •        Glucose infusion rate too rapid
  •        Decreased utilization of glucose

Liver function damage

  •        Liver steatosis due to overfeed of glucose
  •        Use fat emulsion as part of energy source

Stone formation in the gall bladder: long-term PN without food stimulation to the gut

Mild abnormalities of serum transaminase, alkaline phosphatase and bilirubin levels may occur in many parenterally nourished patients. Intestine barrier function impaired due to lack of food stimulus to the intestine and glutamine insufficiency

Infectious complications

Sepsis secondary to contamination of the central venous catheter

Causes:
Systemic sepsis
  • Hematogenous seeding of the catheter with bacteria
  • Failure to observe strict aseptic precautions during preparation & administration of the solutions
  • Clinical manifestations:
  • Sudden development of glucose intolerance
  • Fever
  • Infectious complications
  • Sepsis secondary to contamination of the central venous catheter

Management
  • Other causes of fever also should be investigated
  • If fever persists, the infusion catheter should be removed and cultured
  • Should evidence of infection persists over 24-48 h without a definable source, the catheter should be replaced in the opposite subclavian vein, and antibiotics also should be administrated

Shock is defined as peripheral circulatory failure causing tissue perfusion to be inadequate to meet the nutritional requirements of the cells and remove the waste products of metabolism

Effective circulating blood volume:
Blood circulating through the cardiovascular system per unit time depends on adequate blood volume, effective cardiac output, and peripheral vascular resistance

Classification of shock
  • Hypovolemic
  • Septic
  • Cardiogenic
  • Neurogenic
  • Anaphylactic shock
  • Shock Monitoring

Consciousness
Reflection of cerebral perfusion & systemic circulation status

Colour and temperature of the skin
Body surface perfusion

Blood pressure
Not the most sensitive sign reflecting shock

Evidence of shock:
  • systolic pressure 90 mmHg,
  • systolic & diastolic pressure difference 20 mmHg

Pulse
  • A rapid feeble pulse appears before blood pressure drop
  • Shock index = pulse rate/systolic pressure
  • 0.5: no shock; 1.0-1.5: evidence of shock;
  • 2.0: severe shock

Urine output
  • Most sensitive index of the adequacy of vital organ perfusion
  • 25 ml/h: possibility of shock
  • Normal blood pressurebut oliguria & low specific gravity suggesting renal failure
  • 0.5 ml/kg/h: shock has been corrected

Special Monitoring of Shock
Central venous pressure (CVP)
  • Reflecting systemic blood volume & cardiac function
  • Normal value: 5-10 cmH2O
  • < 5 cmH2O: blood volume insufficient
  • >15 cmH2O: heart failure, venous excessive constriction,
  •    pulmonary circulation resistance increase
  • >20 cmH2O: congestive heart failure

Treatment and Management of Shock
General Emergent Management
  • Keep the patient recumbent, control massive  bleeding, ensure adequacy of the airway          
  • Positionhead & trunk elevated 20 30 degreelower limbs elevated 1520 degreeblood return to the heart increase
  • Large bore intravenous catheter placed
  • Oxygen administered by nasal tube or mask
  • Keep patient warm, without heating

Restore blood volume
  • Principal means of treating shock
  • Crystalloid first
  • Colloids: plasma expander, RBC, whole blood

Vigorous treatment of primary diseases
Management principle: after the rapid restoration of effective circulating blood volume, treating primary disease promptly with surgery

Correct acid-base disturbance
Principle: acid rather than basic

Adrenocorticosteroid
Main functions to shock
  • block alpha receptor, dilate vessel decrease peripheral resistanceimprove microcirculation
  • protect intracellular lysosome
  • increase myocardial contractility & cardiac output
  • improve mitochondria function and prevent aggregation of WBC
  • promote gluconeogenesis change lactate into glucose lessen acidosis

Indications: septic or severe shock


The principle of application: high dose (1-3 mg/kg of dexamethasone), intravenous drip infusion use only 1-2 times to prevent the side-effects

Definition

A controllable and reversible loss of consciousness induced by the intoxication of the central nervous system. Lowered sensitivity to external stimuli (hyporeflexia), analgesia, unconsciousness, muscle relaxation, and amnesia are significant features of general anesthesia.

Tree stages of general anesthesia

  • Induction of anesthesia
  • Maintenance of anesthesia
  • Recovery of anesthesia

Inhalational anesthesia

Inhalation anesthetics are substances that are brought into the body via the lungs and are distributed with the blood into the different tissues. The main target of inhalation anesthetics (or so-called volatile anesthetics) is the brain.

MAC

 Definition: MAC is the “minimum alveolar concentration” of an inhaled anesthetic at atmospheric pressure with 100%O2required to prevent movement in response to a noxious stimulus in 50% of subjects.

§  MAC is analogous to the plasma EC50 (concentration for 50% effect) for intravenous anesthetics.

the alveolar concentration of an anesthetic (Fa)

§   ventilation the first of five factors that govern the pulmonary inhaled anesthetic concentration

§   blood passing through the lung opposes the effect of ventilation by drawing anesthetic from the lung.

§   An increased inspired concentration of anesthetic decreases the effect of uptake (the concentration effect), and at 100% inspired concentration, uptake no longer opposes the effect of ventilation.

the alveolar concentration of an anesthetic (Fa)

§  Metabolism of anesthetics can increase uptake.

§  Anesthetic uptake may be enhanced by movement of anesthetic between tissues (intertissue diffusion)

§  Three factors determine uptake by blood: solubility (the blood-gas partition coefficient),

§  pulmonary blood flow (cardiac output),

§   the difference in anesthetic partial pressure between the lungs and venous blood returning to the lungs

The toxicity of inhaled anesthetics

§   Halothane, enflurane, isoflurane, and desflurane have been reported to induce liver injury in susceptible patients. halothane (20%) enflurane (2.5%) isoflurane (0.2%) > desflurane (0.02%). Sevoflurane does not produce acylated protein adducts.

§   inorganic fluoride levels50umol/L, fluoride-associated renal injury has not been reported.

Common inhaled anesthetics

§   Nitrous oxide: weak inhaled anesthetic potency, have no significant effect on cardiac output, heart rate, and blood pressure. Clinical concentration 50%-70%, oxygen concentration must be higher than 0.3, so as to prevent hypoxemia. To prevent diffused hypoxemia,100% oxygen should be inhaled for 5-10 min after stopping nitrous oxide. increase the pressure of the sealed cavity.

§  Enflurane: higher inhaled anesthetic potency, have an effect on EEG, depress the cardiovascular system, depress the respiratory system, but have no irritation to the airway. To maintain anesthesia with a concentration 0.5%-2%, be careful to use on the patient with epilepsy.

§  Isoflurane: high inhaled anesthetic potency, mildly depress the cardiovascular system and the respiratory system,  have no irritation to the airway. To maintain anesthesia with concentration 0.5%-2% can be used for controlled hypotension.

§  sevoflurane: higher inhaled anesthetic potency, mildly depress the cardiovascular system,  severely depress the respiratory system,  have no irritation to the airway. To maintain anesthesia with a concentration of 1.5%-2.5%.

Intravenous Anesthesia

Intravenous anesthetics are administered via the intravenous route - that is, directly into the patient's bloodstream. This allows them to reach a therapeutic level quickly and affect the brain quickly.

Common intravenous anesthetics

§   Thiopental:  rapid onset of action and short duration, water-soluble barbiturate salts in alkaline solutions PH10-11, usual concentration 2.5%. action on the GABA receptor, decrease cerebral metabolism, depress the cardiovascular system,  the respiratory system, and the sympathetic system.

§   Side effect: larygospasm bronchospasm

§   Induction:4-6mg/kg

§   Treat convulsions:1-2mg/kg

§   Ketamine: significant analgesic effect; It usually does not depress the cardiovascular and respiratory systems, but it does possess some of the adverse psychological effects ;

§   dissociative anesthesia; increase ICP; increase in intraocular pressure; increase salivation; a bronchial smooth muscle relaxant

§   Induction:1-2mg/kg iv,duration 15-20min

§   Basel anesthesia:5-10mg/kg im for children ,duration 30min

§   Etomidate: Etomidate is used primarily for the induction of anesthesia, especially in elderly patients and patients who have a cardiovascular compromise. It has a rapid onset of effect and a rapid offset even after a continuous infusion. Prolonged infusion results in inhibition of adrenocortical synthesis. The major advantage of etomidate is its minimal effect on the cardiovascular and respiratory systems. It is associated with a high incidence of burning on injection, thrombophlebitis, and postoperative nausea and vomiting (PONV). The induction dose is 0.2 to 0.3 mg/kg.

§ propofol: propofol provides rapid onset and offset with context-sensitive decrement times of approximately 10 minutes when infused for less than 3 hours and less than 40 minutes when infused for up to 8 hours. Its mechanism of action of γ-aminobutyric acid (GABA). At therapeutic doses, propofol produces a moderate depressant effect on ventilation. It causes a dose-dependent decrease in blood pressure primarily through a decrease in cardiac output and systemic vascular resistance. A unique action of propofol is its antiemetic effect.

§    induction : 1 to 2 mg/kg

§    maintenance: infusion of 100 to 200 µg/kg/min.

Muscle relaxants

§   This class of drugs has its effect at the neuromuscular junction by preventing the effects of acetylcholine. Normally, when a nerve stimulus acts to contract a muscle, it releases acetylcholine. The binding of this acetylcholine to receptors causes the muscle to contract

Different Mechanism between nondepolarizing and depolarizing relaxants

§   Nondepolarizing muscle relaxants produce neuromuscular blockade by competing with acetylcholine for postsynaptic receptors.  Depolarizing ones produces prolonged depolarization that results in decreased sensitivity of the postsynaptic nicotinic acetylcholine receptor and inactivation of sodium channels so that the propagation of the action potential across the muscle membrane is inhibited.

Depolarizing muscle relaxants

§   Succinylcholine is the only available neuromuscular blocker with a rapid onset of effect and an ultrashort duration of action.

§   Induction:1-2mg/kg peak time:60sec

§   Side effect:sinus bradycardia; increase plasma potassium;increase intragastric pressure, increase ICP; increase in intraocular pressure

Nondepolarizing muscle relaxants

§   Pancuronium: onset time:3-6min;duration :100-120min; Induction:0.1-0.15mg/kg

§   Vecuronium: onset time:2-3min;duration :25-30min; Induction:0.07-0.15mg/kg

§   Rocuronium: onset time:1-1.5min;duration :25-30min; Induction:0.6-1.2mg/kg

§   Cisatracurium: onset time:2-3min;duration :50-60min; Induction:0.15-0.2mg/kg,hofmann elimination