PUZZLES IN GENERAL SURGERY: A STUDY GUIDE (2nd Edition)

support.

PUZZLE 1

PRINCIPLES OF GENERAL SURGERY

FLUID AND ELECTROLYTE THERAPY

•Anatomy of Body Fluids

◦Total body water (TBW) constitutes 60% of lean body weight

◦Muscles have more water than fat. Male, young, and thinner people have higher TBW than female, elderly, and obese patients

◦TBW = 40% intracellular (IC) and 20% extracellular (EC)

◦IC: K and Mg are major cations; PO4 and protein are major anions

◦EC: Na and Ca are major cations; Cl and HCO 3 are major anions

•Physiology of Acid-base (AB) Balance

◦H Ion is expressed in pH Unit

▪H = 24 x (PaCO 2 ÷ HCO 3 ). The body changes PaCO 2 and HCO 3 levels to keep the equation constant

◦Why Acid-base Imbalance is Harmful?

▪Acidosis: causes cardiac depression and enzyme-activities inhibition

▪Alkalosis: reduces cardiac output, results in vasoconstriction (reduces Ca availability), shifts Hb-O 2 dissociation curve to left (Hb will not let go of O 2 ), and increases O 2 consumption by increasing glycolysis

▪Alkalosis is more detrimental than acidosis

◦Changes in pH could be from

▪PaCO 2 increase or decrease: called respiratory acidosis (RAC) and alkalosis (RAL), respectively

▪HCO 3 increase or decrease: called metabolic alkalosis (MAL) and acidosis (MAC), respectively

▪Mixed vs. compensated

•Mixed: normal pH, but both PaCO 2 and HCO 3 are abnormal

•Compensated: abnormal pH, and both PaCO 2 and HCO 3 are abnormal (compensating change is not enough to normalize pH)

◦How to read an ABG from acid-base balance standpoint

▪Check pH

•When normal (pH 7.35 – 7.45): might indicate normal ABG or mixed derangement

•When increased (pH > 7.45): indicates alkalosis, which could have three possibilities:

1. Decreased PaCO 2 → RAL

2. Increased HCO 3 → MAL

3. Compensation (when both are abnormal)

•When decreased (pH < 7.35): indicates acidosis, which could have three possibilities:

1. Increased PaCO 2 → RAC

2. Decreased HCO 3 → MAC

3. Compensation (when both are abnormal)

◦General principles in the management of A-B imbalance

▪Acidosis: treat underlying cause; if pH < 7.1, give HCO 3 (be careful, as this may increase PCO 2 and lactate)

▪Alkalosis: treat underlying cause

•When Cl is depleted → administer NS IV fluid

•If did not correct → administer Acetazolamide (Diamox ® ), which inhibits HCO 3 reabsorption → cause Na loss → leads to diuresis (be careful, as this may lead to hypokalemia and hypovolemia)

◦Anion Gap (AG) = Na – (CL + HCO 3 )

▪Normal range = 8–16 mEq/L

▪AG determines whether metabolic acidosis is due to accumulation of acid or just a loss of HCO 3

▪Causes of high AG metabolic acidosis (summarized in LEAK)

•L actic acid, E thylene glycol, A SA and K etoacidosis

◦Lactic Acidosis

▪What does high lactate indicate?

•When the body cannot produce energy from glucose (low supply of glucose or O 2 , or poor utilization), it switches to anaerobic metabolism, which leads to lactate production used to produce energy

▪Why don’t we like high lactate?

•Lactic acidosis per se is not harmful but the underlying cause is the problem

•The faster you normalize lactate level (< 2 mg/dl) within 24 hrs the better the outcome. The level is not as important as how fast you normalize the level

▪When the patient has high lactate, think of two potential problems:

1. Impaired tissue perfusion (shock, ischemia)

2. Sepsis: could be from shock or impaired O 2 utilization at the cellular level (toxins from the invading organism)

•Fluid Therapy

◦IV Fluid is a Drug

▪Ringer’s lactate: first choice in critically ill patients to avoid hyperchloremia, which is associated with worse outcome

◦Indication of IV Fluid:

1. Replace Deficit (Resuscitation)

•Fluids of choice: Ringer’s Lactate (first choice in trauma and septic patient) and Normal Saline (should be avoided to prevent hyperchloremia)

•Composition of RL and NS in mmol/L:

◦Ringer’s Lactate (RL): Na (130), K (4), Ca (5), Cl (109), lactate (28), and a pH of 6.5

◦Normal saline (NS): Na (154), K (0), Ca (0), Cl (154), and pH of 4.5

2. Replace Sensible and Insensible Losses (Maintenance)

•Fluid and electrolyte requirements:

◦4:2:1 rule

◦4cc for first 10kg of patient’s weight, 2 cc for second 10 kg, and 1cc for each kg > 20; or 35–40 cc/kg/day plus 8–12 ml/kg/day (insensible loss)

•Sodium requirement is 1–2 mEq/kg/day, potassium requirement is 0.5–1 mEq/kg/day and glucose requirement is 100–150g/day dextrose

•D5 in ½ NS is the most widely used maintenance fluid

◦Urine output should be at least 0.5 ml/kg/hr

•Electrolyte Therapy

◦Sodium (Na)

▪Hyponatremia

•Defined as Na < 135 mEq/L. It can be mild (130-135), moderate (120-130) or severe (<120 mEq/L)

•It may be hypertonic, isotonic, or hypotonic (the latter is the most common) and it may occur in the setting of hypervolemia, euvolemia, or hypovolemia)

•Hyponatremia is usually due to excessive fluid administration or diuresis

•Treatment: calculate Na deficit = (140 – Na) x (0.6 x body wt in kg) then

◦In asymptomatic patient with very low Na: restrict fluid

◦If chronic and symptomatic: correct it, but to avoid cerebral demyelination, do not correct Na level faster than 8–10 mEq/day

◦If acute and symptomatic: acceptable to correct the problem faster

▪Hypernatremia

•Defined as Na > 145 mEq/L, it is almost always associated with a hypertonic state. It could be mild, moderate or severe (>160 mEq/L)

•Treatment

◦First calculate water deficit

▪Water deficit = 0.6 x wt x {serum Na ÷ (140 – 1)}

◦Water deficit is replaced with intravenous free water according to the following step:

▪Administer ½ of the calculated deficit over a 24-hr period, and then administer the rest over a 24–48-hr period. Correction rate of 0.5 mEq/hr prevents cerebral edema (8–10 mEq/day)

▪Correction with enteral free water is preferred in asymptomatic patients to avoid fluid overload

▪Special considerations

•Pseudohyponatremia

◦Na level is falsely reduced

◦Etiology: hyperglycemia (each 100 mg/dl increase in glucose level reduces Na level by 1.5–2 mEq/L) and a marked elevation in plasma lipid or protein (dilutional effect)

◦Treatment: Correct the underlying cause

•Diabetes insipidus (DI)

◦Clinical features: polyuria with diluted urine, hypernatremia and the presence of risk factor

◦Types: It could be central (early, severe) or nephrogenic (milder form)

◦Treatment: water replacement (slow correction of hypernatremia) and vasopressin (for central DI)

◦Potassium (K)

▪Hypokalemia

•Defined as K < 3.5 mEq/L (mild). When level is < 2.5 mEq, it is called severe

•Etiology: most often the result of K loss (via gastrointestinal [GI] tract, fistula, urine, and/or a transcellular shift) than reduced intake

•Watch for electrocardiogram (ECG) changes: flat P and T (or inverted) waves, Delta wave, and depression of ST segment

•Treatment

◦Note: Hypokalemia is often accompanied by hypomagnesemia (increase in K urinary loss), which should be corrected first

◦Oral replacement: indicated when K level is above 3 mEq

◦IV replacement: at a rate of 10-20 mEq/hr, indicated when patient cannot tolerate oral intake or K < 3 mEq (don’t administer > 40 mEq/L in peripheral line)

▪Hyperkalemia

•Defined as K > 5 mEq/L

•Etiology: renal failure, acidosis, insulin deficiency, rhabdomyolysis, cell lysis (pseudo-hyperkalemia), drugs (succinylcholine, aldactone) ischemic-reperfusion syndrome, and massive transfusion (K level increases by 0.2 per unit, more with blood older than 3 weeks [in which one unit may contain 80 mmol/L])

•Treatment

◦Note: Always re-check K level in healthy, young, asymptomatic patient (pseudohyperkalemia) before making any corrections

◦Stop all K supplementation

▪Obtain ECG; and if there are changes or the level is >6.5 mEq, give 10 cc of 10% Ca gluconate

•The first sign of hyperkalemia is a peaked T-wave; then QRS becomes wider, with ± ventricular ectopy

◦The most rapid (but temporary) therapy is Insulin (10U) with 1 ampule of D50% (this decreases K level by 1 mEq/hr approximately)

◦Definitive therapy is excretion of K by:

▪Kayexalate resin (15–30g) to facilitate stool excretion; each gram removes 0.1 mEq of K from GI (takes hours–days)

▪Loop diuretics: to excrete K in urine

▪In the case of renal failure, begin hemodialysis

◦Calcium (Ca)

▪Daily requirement is 1000–1500 mg

▪Hypocalcemia

•Defined as ionized Ca (iCa) < 2.1 mmol/L or < 4.5 mg/dL. Ca level changes by 0.8 mg/dL for every 1.0 g/dl changes in albumin level

•Etiology: Hypoparathyroidism (most common cause), fluid resuscitation, hypomagnesemia, tumor lysis syndrome and pancreatitis are common

•Treatment

◦Treat the underlying cause then replace Ca and correct low Mg

◦Give oral Ca replacement for asymptomatic patients

◦When Ca level < 7 mg/dL or iCa < 1.9 mmol/L: give 10 ml of 10% of IV Ca gluconate over 10–15 min

▪Avoid Ca chloride because in case of extravasation, it will cause tissue necrosis

◦When Ca is given in IV form, connect patient to cardiac monitor because bradycardia and hypotension are possible risks

▪Hypercalcemia

•Defined as ionized Ca (iCa) > 2.5 mmol/L or >10.5 mg/dL

•Etiology: hyperparathyroidism (most common) and malignancy (in-patient)

•Treatment (correct the underlying cause)

◦IV fluid infusion (mainstay)

◦Furosemide IV (40–80 mg every 2–4 hrs.)

◦Steroid: in case of lymphoma, multiple myeloma, and granulomatous disease)

◦Bisphosphonate (pamidronate): Indicated for severe cause when iCa level > 14 mg/dL at a dose of 90 mg over 24 hrs. The effect will peak after 48–72 hrs

◦Magnesium (Mg)

▪Hypomagnesemia

•Defined as Mg < 50 mmol/L or < 1.5 mEq/L

•Etiology: excessive IV fluid administration (common), poor intake, diuretics, and GI losses (biliary or small bowel fistulae and massive diarrhea). Common among alcoholics

•Treatment

◦Note: Usually, hypomagnesemia is associated with hypokalemia (40%), hypophosphatemia (30%), and hypocalcemia (20%, due to reduced PTH release). Therefore, replacing Mg also helps to correct K or Ca levels

◦If the level is > 1 mEq/L, administer oral Mg

◦If the level is < 1 mEq/L, administer 2g of IV MgSO4 over 2 hrs, or 4g over 4 hrs. (administer slowly to avoid hypotension)

▪The dose should be reduced in patients with renal impairment

◦Phosphate (PO 4 )

▪Hypophosphatemia

•Defined as PO4 < 60 mmol/L

•Etiology: urine loss (diuretic, alkalosis) and GI loss

•Treatment: IV of 15 mmol NaPO4 over 3 hrs., or 30 mmol over 6 hrs. May be replaced orally (by oral fleet), if the patient tolerates oral intake

NUTRITION THERAPY

•General

◦Body tissue is divided into: 30% fat, 30% protein, and 30% extracellular water

◦In catabolic status, extracellular fluid increases to 60% (salt retention), whereas fat and protein decrease to 20%

◦100g/day of dextrose spares protein from breakdown

◦Malnutrition increases postoperative complications (mainly infection) and mortality

◦Preoperative nutrition is only beneficial for patients with severe malnutrition

◦Malnutrition is usually due to starvation or metabolic dysfunction (acute or chronic disease-related)

◦Daily Calorie Requirement: 20–25 kcal/kg/day

▪Usually start with lower kcal/day (e.g., 18 kcal/kg/day) for 24–48 hrs; then increase it (e.g., to 20–25 kcal/kg/day)

▪Patients with major stress (major trauma, burn, sepsis) need high kcal; up to 30 kcal/kg/day

•Etiology : Mechanism of Catabolism in Stress, Trauma and Sepsis

◦Increased proteolysis, which is suppressed during starvation

▪Caused by IL-1, IL-6, TNF, IFN-gamma, and nitric oxide

▪These cytokines with anorexia are responsible for severe weight loss and cachexia

◦Sepsis reduces synthesis of certain proteins (like albumin and prealbumin) and increases production of others (like C-reactive protein and glutamine)

◦Peripheral insulin resistance: hyperglycemia

◦Gluconeogenesis continues despite fat and glucose administration

•Diagnosis: How to Assess the Nutritional Status

◦Clinical history is the most important indicator

◦Body composition analysis: lean body mass assessment

◦Indirect calorimetry: O 2 consumption and CO 2 production (respiratory quotient RQ)

◦Body measurement: body weight and skin folds

▪Lean body mass (LBM): reflects the nonfat mass (muscle mass). Drop in LBM increases mortality. It can be measured by dual-energy x-ray absorptiometry, ultrasound and computed tomography (CT) scan.

◦Biochemical measurement: albumin (preoperative value of less than 30 mg/dL increases postoperative complications), prealbumin, and transferrin

◦Nitrogen balance and immunological function measurement

•Treatment and Prevention of Malnutrition

◦Indications for Nutritional Support, In General

▪Weight loss > 15% over 6 months and reduced oral intake (< 50% of daily requirement) are good indicators for malnutrition, and this group of patients has increased perioperative complications

▪Starvation for > 7 days (enteral method is preferred)

▪Severe insult (surgical, burn, inflammatory, or sepsis): nutritional support should be started within the first 48 hrs of injury or insult.

▪Serum albumin < 30 mg/dl or transferrin < 200 mg/dl (in the absence of inflammatory status)

•What to Administer: TPN or EF ?

◦Indications of Total Parental Nutrition (TPN)

▪Therapeutic effect

•Increases rate of closure and may reduce mortality in patients with an enterocutaneous fistula

•Reduces mortality in patients with acute renal failure, liver failure, severe burn, and/or short gut syndrome

▪Supportive effect

•Inflammatory bowel disease, acute radiation enteritis, and prolonged ileus

▪Unclear effect

•Perioperative TPN: reduces perioperative septic complications in severely malnourished patients (weight loss > 15%), if started 7–10 days preoperatively; however, TPN increases the risk of infection-related complications in patients with mild-to-moderate malnutrition

▪No proven effect

•Does not affect mortality in patients: with cancer (except GI cancer with severe malnutrition), before cardiac surgery, or with respiratory failure, and does not help in the healing of large wounds

•Not proven to alter the course of inflammatory bowel disease

◦Advantages of EF over TPN

▪Less expensive

▪Improves liver function and gut motility

▪Maintains gut mucosa integrity and reduces bacterial translocation in burn, trauma, pancreatitis (start within 24 hrs of admission to reduce complications and mortality) and shock patients

▪Attenuates the inflammatory response and decreases morbidity from sepsis

•Nutrition Therapy—When and for Whom?

◦Preoperative Nutrition

▪Studies show that preoperative TPN decreases major complications such as anastomotic leak and wound dehiscence in severely malnourished patients

▪However, infection is increased with no benefit in those who received preoperative TPN for mild to moderate malnutrition

▪7–15 days of preoperative nutritional support is the standard. Calculation is based on the Harris-Benedict equation, which calculates the basal energy expenditure (based on sex, age, weight, and height)

•For male: 66.5 + (13.75 x weight in kg) + (5.003 x height in cm) - (6.775 x age in years)

•For female: 655.1 + (9.563 x weight in kg) + (1.850 x height in cm) - (4.676 x age in years)

▪Methods of Preoperative Nutritional Support

•TPN

◦Should only be given to severely malnourished patients with non-functioning GIs (e.g., Crohn’s disease)

◦Composition of the fluid:

▪Caloric requirement: 150% of Basel Energy Expenditure (BEE)

▪Dextrose: 4–6 mg/kg/min and lipid should not exceed 30% of total caloric intake (70:30 ratio)

▪Free amino acid: 1.5g/kg. Maintain a calorie-to-nitrogen ratio of 150:1 to support protein synthesis

▪Monitor blood sugar and electrolytes (drop in levels of K, Mg, and PO4 in re-feeding syndrome)

•Enteral feeding (EF)

◦Use for all patients, unless they have non-functioning Gastrointestinal tract (GIT) or in high-dose inotropic support

◦If the gut is not functioning well, administer at least 20% of the daily requirement enterally and administer the rest parentally, until the GIT starts to function well

◦If the patient cannot tolerate oral intake, post-pyloric feeding is the preferred method:

▪NG route is for short-term (< 4 weeks) use

▪Gastrostomy is placed for long-term (> 4 weeks) use

▪Percutaneous endoscopic gastrostomy (PEG) is becoming the method of choice in placing gastrostomy tubes; G-J tube (inserting jejunostomy tube through existing gastrostomy tube) or jejunostomy are good alternatives

◦Different formulas are available

◦Postoperative/ICU Nutrition

▪TPN

•Indicated in patients unable to have good PO intake for more than 5–7 days postoperatively, and patients with GI complications (e.g., fistula)

•Most patients are fine with 25–30 kcal/kg/day along with 0.8–1.5g/kg/day of amino acid with 20% lipid

•How to prepare TPN for a 70kg patient

◦Total calories: 70 x 30 = 2100 kcal

◦Calories from protein: (1.5 x 70 = 105-g protein) x 4 kcal/g = 420 kcal

◦Calories from lipid (20% of total calories)

▪(2100 x 20) ÷ 100 = 420 kcal

▪420 ÷ 9 kcal/g = 47 g of lipid

◦Remaining kcal

▪2100 – 420 (lipid) – 420 (protein) = 1260 kcal should be provided as dextrose

▪1260 x 3.4 kcal/g = 370 g of dextrose

◦Determine the volume

▪25% dextrose solution = 250 g/L

▪Need 1.5 L per day = 62 ml/hr

•Visceral protein markers

◦Albumin: not a good indicator (half-life is 21 days)

◦Transferrin: it is a positive acute phase marker (half-life is 9 days)

◦Pre-albumin: negative acute phase marker (half-life is 24–38 hrs); most commonly used marker

•Administer insulin as an IV infusion or subcutaneously

•If you need to stop TPN abruptly, follow these steps

1. Stop TPN

2. Run 50% dextrose (D50%) at the same rate for 6 hours then stop

3. Check blood sugar every 2 hours while running D50%

▪Postoperative EF

•In general, early enteral feeding in critically ill patients is recommended (as opposed to TPN, which is preferred to delay)

•Start EF as soon as the patient is hemodynamically stable (within first 12–72 hrs from admission). Exceptions: start head injury and burn patients within the first 24 hrs

•Start at 10–20cc/hr and increase by the same amount every 8–24hrs if there is NO

◦High residual volume (< 200cc, checked every 4–6 hours)

◦Persistent abdominal distention (if present, decrease the administration rate)

•Gastric vs. duodenal tube placement

◦No difference in terms of risk of aspiration or tolerance. However, post-pyloric feeding is preferred in patients at high risk of aspiration

◦Most surgeons prefer post-pyloric feeding

▪Adjust the head of the bed to around 30–40°

▪Pro-kinetic agents are recommended

◦Duodenal placement is associated with increased risk of losing the tube and the need of reposition

•Formulas

◦Regular formula provides 1–2 kcal/mL

◦Daily requirement is 20–25 kcal/kg/day

◦Special formulas:

▪Renal: 2 kcal/mL and less protein

▪Pulmonary formula: high lipid concentration (less dextrose → less CO 2 production)

▪Bowel formula: protein in small peptide forms, instead of intact protein (easy to absorb)

▪Hepatic formula: contain branched amino acids that reduce production of false neurotransmitters, which reduces risk of encephalopathy

▪Diabetic formula

•Supplemental nutrients

◦Glutamine (recommended): fuel for enterocytes (also effective when it is given in TPN) and it may reduce infection complication and ICU mortality

◦Fibers: help with digestion and improving diarrhea

•Contraindication

◦Shock status (may increases risk of bowel ischemia in patient with high inotropic support), bowel obstruction, and bowel ischemia

•Potential Complications with Nutrition Therapy

◦Parental Nutrition

▪Liver Dysfunction

•Ranges from liver function elevation to cirrhosis

•Mechanism: steatosis, cholestasis (due to lack of enteral stimulation and reduced cholecystokinin release), and chronic inflammation (elevation of TNF and C-reactive proteins from fatty acid)

▪Metabolic bone disease and re-feeding syndrome

▪Glucose (commonest) and electrolyte imbalance

▪Sepsis (central venous line sepsis)

▪Bowel atrophy and acalculous cholecystitis

◦Enteral Nutrition

▪Tube-feeding complication: displacement, aspiration and tube replacement

▪Possible bowel ischemia in very sick patients on vasopressor medication

PERIOPERATIVE PERIOD

Perioperative Assessment and Prevention of Complications

•Preoperative Assessment (PreOp)

◦Aim: to identify and control comorbidity that may affect operative and postoperative outcome. Preop assessment is determined by the risk of surgical procedure, anesthesia type, patient factors (inpatient status, sepsis, age > 80 and cardiac disease have the highest perioperative morbidity and mortality) and postoperative disposition (going home, regular ward or ICU)

•Cardiac System

◦General

▪All patients should be assessed for perioperative cardiac risk

•Electrocardiogram (ECG): usually all patient above age of 45 years

•Cardiac risk: stress test, Echocardiogram ± angiogram (percutaneous coronary intervention-PCI)

▪Monitor blood pressure (BP) and Central venous pressure (CVP)

▪Patient post PCI should NOT undergo elective surgery within

•One month after PCI balloon angioplasty or metal stenting

•12 months after drug-eluted stent

◦Perioperative MI

▪General

•Risk of Acute Coronary Syndrome (ACS) is < 5% in noncardiac surgical patients

•Reinfarction risk is 15% if surgery is done within 3 months from infarction and 3.5% if it is done within 3–6 months

◦Elective surgery should be delayed > 4–6 weeks post-MI

•Risk of infarction is the highest within the first 72 hours postoperatively

•Postop MI increase mortality up to 25%

•Tachycardia is a potent inducer of MI

•For patients at risk of postoperative MI: ECG postoperatively; then daily for 2 days, accompanied with Troponin level every 12 hrs for 24 hrs; and then ECG in the 3rd – 4th postoperative day (this is the period in which MIs commonly occur)

▪Prevention

•Major Predictors of Perioperative Cardiovascular Risk

◦Acute MI (within 7 days) and recent MI (within 7 – 30 days)

◦Decompensated CHF (S3 gallop) and unstable or severe angina

◦Significant arrhythmia (complete heart block and ventricular arrhythmia)

◦Severe valve diseases (aortic stenosis)

•Continue cardiac medication, especially B-blocker (best preventive medication), clonidine (severe rebound hypertension, if stopped abruptly), and ACE inhibitor

•Hold diuretics 24 hours before surgery

◦Postoperative Arrhythmia

▪Sinus tachycardia and atrial fibrillation/flutter (due to electrolyte imbalance, history of arrhythmias, fluid overload, and chronic obstructive pulmonary disease [COPD]) are the most common

▪Treatment

•Consult cardiology

•Monitor bed and Check hemodynamic status continuously

•Obtain ECG and cardiac enzymes

•Correct electrolyte abnormality and precipitating cause

•Treat arrhythmia as per Advanced Cardiac Life Support (ACLS ® ) protocol

•Administer Diuretics, when suspecting overload

◦Infective Endocarditis (IE)

▪General: Incidence is extremely low

▪Etiology

•Mechanism

◦Thrombus in the valve with bacteremia leads to IE

◦Bacteremia from tooth extraction or GI/GU endoscopy is similar to bacteremia that occurs during tooth brushing

•Risk factors

◦Prosthetic valve (mechanical or biosynthetic)

◦Prior IE

◦Congenital heart disease: unrepaired, partially repaired, or repaired with synthetic material

◦Valve disease in transplanted heart

•Procedures associated with IE

◦Dental procedure

◦GU/GI tract procedure (endoscopy, Endoscopic retrograde cholangiopancreatography -ERCP, biopsy)

▪Not an indication for antibiotic prophylaxis any more (risk of IE is 5%)

▪For existing infections (ERCP for biliary obstruction, EUS-FNA for pancreatic cyst), administer antibiotic

◦For PEG insertion, administer antibiotic

◦Respiratory tract procedure

•Endoscopy does not require antibiotic administration; unless biopsy is taken.

◦Any procedure that needs a prophylactic antibiotic to prevent wound infection needs antibiotic administration to prevent IE

•For example, bowel resection, which usually needs an antibiotic to prevent wound infection with gram negative

▪Prevention

•Good oral hygiene can prevent IE during dental procedures

•No prospective study has proven the benefit of prophylactic antibiotics

•Prophylactic antibiotics should cover streptococcus (dental, respiratory tract) and enterococcus (GIT)

◦Amoxicillin 2 g PO (ampicillin 2-g IV) 30–60 min. before procedure

◦For bowel, biliary, and pancreatic surgeries, add Gentamicin 1.5 mg/kg to preoperative antibiotic

◦Postoperative dose: ampicillin 1g IV 6 hours after surgery

•For patients with penicillin allergy

◦Intravenous 600 mg clindamycin or 1g vancomycin

•Pulmonary System

◦General

▪Factors increases complications: Age, smoking (COPD), ASA >II, OR time >3 hrs, surgical site, emergency operation and obesity

▪Assess high-risk patients by room air arterial blood gas (ABG) and pulmonary function tests

•Forced expiratory volume in 1 second FEV1 is the most important number

•FEV1 < 0.8L/sec (< 30% of predicted value or < 2L) indicates higher risk for pulmonary complication

▪The cornerstones of pulmonary therapy are good pain control and early mobilization ± chest physiotherapy

▪After any abdominal or thoracic incision, functional residual capacity and vital capacity are markedly reduced (up to 50%)

◦Atelectasis

▪The most common postoperative pulmonary complication, and the most common cause of fever in the first 24 hours postoperatively

◦Aspiration Pneumonitis

▪Defined as aspiration of gastric content (Mendelson’s syndrome). It causes inflammation only; therefore, antibiotic is not needed, unless pneumonia is suspected

◦Pneumonia

▪May be acquired in the hospital, ventilator-associated (VAP) or from aspiration (oropharynx flora or gastric content)

▪I could be responsible for fever in the first 48 hrs. So, DO NOT always think that atelectasis causes fever in first 24 hrs.!!!

◦Pulmonary Edema

▪Occurs due to fluid overload; may be due to intraoperative fluid administration or postoperative fluid mobilization

◦Acute Lung Injury (ALI)

▪Defined as acute bilateral lung infiltrate, PaO 2 /FiO 2 < 300 and wedge pressure < 18 mmHg

◦Acute Respiratory Distress Syndrome (ARDS)

▪The same criteria for acute lung injury but with a PaO 2 /FiO 2 ratio of < 200 (instead of 300)

◦Venous Thromboembolism (VTE)

▪General

•Includes Pulmonary Embolism (PE) and Deep Vein Thrombosis (DVT)

•50% of patients with proximal DVT develop PE, and 30% of patients with PE have positive Doppler for DVT (80% have positive venography)

▪Etiology

•Risk of DVT in patients with inflammatory bowel disease is 5%, malignancy is 10%, and trauma is 50%

▪Diagnosis: When PE is suspected, obtain the following:

•CXR, ECG, ABG, and D-dimer (negative result is useful)

•Lower extremity Ultrasound (U/S)

◦If positive → treat for PE

◦If negative → spiral CT chest or V/Q scan

•If the CT is equivocal or negative in high-risk patients, you may consider treatment ± angiogram

▪Prevention (always encourage ambulation as early as possible)

•Low risk: ambulation

•Intermediate risk: Un-fractionated heparin: given 5000 units every 8hrs or low molecular-weight heparin

•High risk: low molecular-weight heparin with compression devices

•IVC filter to protect against PE: it is indicated in patients with contraindication for DVT prophylaxis (bleeding and HIT) or who developed DVT/PE when fully heparinized

▪Treatment

•Heparin infusion followed by warfarin or only low molecular-weight heparin

•In unstable patient from massive PE: perform thrombolysis/thrombectomy, then start anticoagulation (if there is no contraindication)

▪Special consideration

•If patient developed DVT/PE preoperatively, consider the following:

◦Elective surgery: delay surgery for a few months

◦Emergency surgery: stop heparin (follow protocol) or operate on low-dose heparin infusion in very high-risk patient; or consider IVC

•Neurological Assessment, Monitoring and Care

◦General

▪Preop assessment of cognitive impairment (Mini Cog © ), depression and postoperative delirium risk is very important to improve outcome

▪If the patient has a persistent decrease in the level of consciousness, even after cessation of sedation, rule out drug-related causes and get a head CT scan

▪Daily Sedation vacation is important to prevent accumulation of sedation in the intensive care

▪Polyneuropathy of ICU: 25% of patients demonstrate severe muscle weakness, especially if intubated for duration > 1 week

•Steroid and paralytic agents are risk factors

◦Delirium and Psychosis

▪is associated with increased morbidity and mortality

▪Always rule out sepsis as a common cause of delirium

▪Always first look for the causes; then treat, if possible:

•Old age, alcohol-ethanol (EtOH) withdrawal, and ICU psychosis

•Drugs

◦Sedation and narcotics

◦Oral hypoglycemic agent

◦Antibiotic (cephalosporin)

◦Antihistamine, steroids, and non-steroidal anti-inflammatory drugs (NSAID)

◦Anticonvulsant and anxiolytic

◦Cardiac medications (B-blocker and digoxin)

•Infection and sepsis

•Respiratory, cardiac, hepatic, and renal failures

◦Stroke

▪Ischemic type is the most common (perioperative hypotension and embolic phenomenon in patient with atrial fibrillation (A. fib) or MI

◦Seizure

▪Patients at risk: history of seizure, alcohol, or medication withdrawal, or receiving medication, like antidepressant, hypoglycemic, and lidocaine

▪Metabolic disorder (hypoglycemia, electrolyte imbalance) and sepsis are common causes

◦Malignant Hyperthermia (MH)

▪Etiology

•Autosomal dominant: abnormal efflux of calcium into the muscle, which leads to muscle rigidity and hypermetabolism

•This condition is triggered by any halogenated inhalational anesthesia (halogen, isoflurane), depolarizing muscle relaxant (succinylcholine) and stress

▪Presentation

•Patient failure to open the mouth for intubation is a pathognomonic sign

•Rhabdomyolysis and excessive heat production leads to DIC, hyperkalemia, CHF, bowel ischemia, and compartment syndrome

▪Diagnosis

•Family history is crucial

•Increased end tidal PCO 2 could be the first sign of MH

•Tachycardia and jaw spasm 30 min. after induction are early signs

•Hyperthermia, elevated lactate, and acidosis occur later

•Muscle biopsy (for definitive diagnosis)

▪Treatment

•Stop the triggering agent and postpone the operation

•Administer Dantrolene

◦Prevents Ca release → muscle relaxation

◦Dose: 2.5 mg/kg bolus, then repeat every 5 minutes (max. 10 mg/kg)

◦Side effects: muscle weakness, phlebitis, respiratory failure, hepatotoxicity, and confusion

•Supportive measures for acidosis, arrhythmia, and hyperkalemia

•Renal System

◦General

▪Always identify patients at risk of developing perioperative acute kidney injury (AKI)

▪Hypovolemia with hypotension is the most common cause of low urine output

•Good fluid resuscitation is the most important preventive measure of AKI postoperatively and after CT contrast examination

▪N-acetylcysteine given 24 hrs before and after CT may reduce the risk

◦Urine Retention

▪General: commonly seen after low anterior resection, procedure in the perineum, and hernia repair

▪Etiology: it is due to benign prostatic hypertrophy (BPH - most common), disruption of the nerve supply, excessive fluid administration, and poor pain control, which leaks to bladder muscle dysfunction

▪Prevention

•Good pain control and judicious IV fluid administration

▪Treatment: straight catheter or Foley’s catheter, better pain control, and proper fluid administration

◦Acute Kidney Injury (AKI)

▪General: defined as increased serum creatinine or acute reduction in urine output

•Increase creatinine by ≥ 0.3mg/dL within 48 hrs or increase ≥ 1.5 times the baseline value within the last seven days or decrease urine volume < 3 ml/kg over 6 hrs

•Could be oliguric (< 480cc/day), polyuric (> 2L/day) or anuric (no urine output)

▪Etiology: prerenal, renal, and postrenal

▪Treatment

•Careful fluid management and correct electrolyte balance

•Stop the nephrotoxic agent

•Adjust medication doses until kidney function recovers

▪Nephrology consultation, if in doubt

•Hematological System

◦If there was intraoperative bleeding, obtain a postoperative complete blood count (CBC) and coagulation profile

◦Keep hematocrit (Hct) above 30% in patients with significant cardiac disease

◦Deep venous thrombosis (DVT) prophylaxis is mandatory (Heparin and Low molecular-weight heparin-LMWH)

▪Stop warfarin 4–5 days prior to surgery; if the patient has been treated for DVT, pulmonary embolism (PE) or arterial embolism, start heparin

•Check INR: should be < 1.5

•Stop INR 6 hours prior to surgery, then resume it 6 hrs. after surgery without bolus

•Elective surgery should not be done within 1 month from the diagnosis of DVT/PE

▪Okay to stop warfarin for patients with atrial fibrillation (A. fibrillation or A. fib.) without starting heparin. Postoperatively, administer heparin SC until patient can eat; then resume warfarin

•Endocrine System

◦General

▪Good glucose control (110–180 mg/dL) is associated with reduction in mortality as well as a decrease in ARF, infection, and polyneuropathy

•Note: Avoid tight glucose control (< 100 mg/dL), as such over-control may result in hypoglycemia and its complications

◦Adrenal Crisis

▪General: normally, the body secrets 30 mg of cortisol, which goes up to 100 mg after major surgery

▪Etiology: abrupt cessation of steroid and very critically ill patients (sepsis and trauma)

▪Presentation

•Hypotension not responding to fluid (cortisol increases vascular tone and its sensitivity to catecholamine)

•Fever, hyponatremia, hypoglycemia, and azotemia

▪Prevention: which patients need a perioperative steroid?

•Some surgeons give stress dose routinely for any patient on steroids preoperatively, regardless of the dose

•Which patients are at risk?

◦Patients on long-term dosage of ≥ 10 mg of prednisolone

◦Patients who received 10 mg of prednisone within the past 3 months

◦High dose inhalation steroid (≥ 1.5 mg beclomethasone a day)

◦6–10 mg prednisone (may need stress dose)

◦In summary: any patient taking ≥ 5 mg of prednisone for > 2wks within the past year is at risk of adrenal insufficiency

◦Patients with Cushing’s syndrome, Severe sepsis, and bad burn/trauma are at high risk

•How much stress dose should be given?

◦5 mg prednisone is equivalent to 20 mg hydrocortisone

◦Patients may self-administer steroids preoperatively, or you may, instead, administer 100 mg hydrocortisone on induction and then every 8 hours for 24 hours after that; then the dosage may be tapered down by 50% every day (usually over 3 days). The patient’s preoperative dosage may be resumed once the patient is on oral diet

▪Treatment

•Random serum cortisol level

◦Level should be at least above 20μg/dl under major stress (sepsis, trauma, and burn)

•IV dexamethasone (does not affect synacthen test, whereas hydrocortisone does); then perform short synacthen test

◦Administer ACTH then measure cortisol level. Failure of the cortisol to rise is suggestive of adrenal insufficiency

◦Hyperthyroid Crisis

▪General: occur in patients with Graves’ disease experiencing stressful events like surgery or sepsis

▪Presentation

•Tachycardia, hypotension, arrhythmia, CHF, fever, CNS (delirium to coma), GI complications (diarrhea), and organ dysfunction

▪Treatment

•Stop precipitating factors

•Supportive: O 2 , IV fluid, and sedation

•Steroid, B-blocker (PO or IV for sick patient), Propylthiouracil

•Lugol’s solution after administering propylthiouracil

•Plasmapheresis for refractory cases

◦Syndrome of Inappropriate ADH Secretion (SIADH)

▪Etiology: head (trauma, cancer, bleeding) and lung disease (cancer, TB) leads to excessive secretion of ADH, which leads to normovolemic hyponatremia

▪Diagnosis

•Hyponatremia (Na < 135); normal renal function; low plasma osmolarity and high urine osmolarity, with high Na excretion in urine

▪Treatment

•Fluid restriction, 3% saline may be used in symptomatic patients after calculation of Na deficit

◦3% saline contains 513 mmol Na in 1L

◦Na deficit = pt. wt x 0.6 x (target Na level – pt. Na level)

◦Correction should not be faster than 0.5 mmol/L/hr = 8–10 mmol/L in first 24 hrs

•Gastrointestinal System

◦General

▪Stress ulcer prophylaxis and early enteral feeding are essentials

▪Take the patient off the ventilator faster and correct coagulopathy, thereby avoiding stress ulcers

◦Postoperative Bowel Obstruction

▪General

•Ileus occurs immediately after surgery and resolves within 2–4 days in the absence of precipitating factors

•Consider mechanical bowel obstruction if ileus continued in the absence of precipitating factors

▪Etiology: Why does ileus happen?

•After laparotomy, the small bowel recovers within hours (first to be lost but first to recover), the stomach recovers within 24–48 hours, and the colon recovers within 48–72 hours

•Anesthesia and opiates suppress neuronal excitability

•Surgery and manipulation of bowel causes release of hormones and inflammatory mediators, which suppress the neuromuscular system

•Resection and anastomosis: distal bowel is disconnected from the pacemaker in the duodenum, causing failure of peristalsis waves to propagate

▪Prevention: good tissue handling, minimal dissection, covering bowel with moist towel, maintaining hemostasis, and avoiding fluid collection

▪Treatment

•Nil Per Os (NPO) and nasogastric (NG) suction

•Rehydrate and correct electrolyte imbalance

•Identify and stop the precipitating factor (e.g., use NSAIDs instead of opiates)

•Surgical intervention is indicated for mechanical bowel obstruction that fail conservative therapy; high grade, closed-loop obstruction cases and patients with peritonitis

◦Postoperative GI Bleeding

▪Etiology

•Bowel anastomosis is the most common source

◦Stress ulcers and Mallory-Weiss tears are common causes

•Similar to causes of GI bleeding in the community (when there is no bowel anastomosis)

▪Treatment: usually self-limited

•Resuscitation and blood transfusion

•Correction of coagulopathy

•Identify and treat the cause: Endoscopy ± surgery

◦Stoma Complications

▪Stenosis/stricture

•Etiology: could be benign (post ischemia, radiation, or IBD) or malignant cause

•Treatment

◦Dilatation → if fails → local resection of involved part and mature a new one through the same defect. May need laparotomy, especially end colostomy because it is less mobile

▪Obstruction

•Etiology: stool (constipation), stricture (benign or malignant), hernia or inflammation (Inflammatory bowel disease-IBD)

•Treatment depends on the etiology

▪Retraction

•Etiology: occurs due to ischemia or tension on the mesentery (early) or increased skin thickness from gaining weight (late)

•Treatment: needs revision / relocation of the stoma

▪Dehiscence

•Etiology: due to poor fixation with tension; infection plays a role

•Treatment: immediate re-operation is warranted

▪Prolapse

•Etiology: Poor technique and higher with colostomy (the cause is unknown)

•Treatment

◦Usually does not require treatment, unless it becomes symptomatic (difficult to apply appliance), ulcerating and bleeding, or obstructed

◦Stoma is not needed any more → close it

◦End stoma: Altemeier-like procedure, locally

◦Loop stoma: convert to double-barrel or end stoma

▪Necrosis

•General: could be partial or full-thickness, superficial or deep necrosis

•Diagnosis: clinically (with test tube and light source) and endoscopically

•Treatment

◦Superficial/partial (few mm and above fascia) thickness: conservative therapy; it may stricture down

◦Deep (deep to fascia) and full thickness: surgery

▪Bleeding

•Etiology: it is usually from mucosal edge or skin vessels

•Diagnosis: take the pouch off and examine the stoma

•Treatment: cauterize or oversaw it

▪Parastomal hernia (PSH)

•General: risk is > 50%

◦Almost all types of stomas develop a hernia (slightly higher risk with loop colostomy), usually lateral to stoma

•Etiology: risk factors

◦Procedure-related and patient-related (DM, obesity, malnutrition, COPD, steroid, and/or wound infection)

•Diagnosis

◦Can be diagnosed clinically and with imaging (CT)

•Treatment

◦Does not typically need repair, unless it is large and symptomatic (difficult to apply appliance), obstructed, or strangulated

◦Asymptomatic: stoma nurse follow-up, education and stoma hernia belt

◦Repair of the defect with mesh

▪Preferred option because it has lower recurrence rate (< 10%) compared to re-location, but there are no strong evidences to support that

▪Types: onlay (absorbable) vs. underlay (open vs. laparoscopic)

•Sugarbacker: circle-shaped mesh to cover the hole and the stoma laparoscopically

•Key-hole: fashion a hole to accommodate the stoma, then place it laparoscopically

◦Relocation has higher recurrence rate (at least as high as after the primary stoma plus risk of incisional hernia at the previous stoma site)

◦Prophylactic mesh

▪May reduce risk of PSH but claim lacks strong evidence

▪Peristomal fistula

•General: it is a fistula that discharges bowel content around the stoma

•Etiology: ischemia, perforation, IBD, or malignancy

•Diagnosis

◦Clinically and with CT (to rule out intra-abdominal abscess and fistula)

◦Contrast study and endoscopy may be needed to reach the diagnosis and to take biopsy

•Treatment

◦Control sepsis: drainage of abscess and antibiotics

◦Ileostomy: NPO, TPN ± resection and re-site

◦Colostomy: low residual diet. Usually, it closes with conservative management, but if did not → diversion is needed

◦Closure of stoma: may be done when local sepsis is controlled and stoma is not needed anymore

▪Skin excoriation, dermatitis, and pyoderma gangrenosa

•Prevention: good and well-fit appliance, skin barrier, antihistamine, and topical or oral steroid

•Treatment

◦Topical immunosuppressant may be needed (Pyoderma gangrenosa)

◦NPO, TPN, and even stoma re-site may need treatment in refractory and severe conditions

▪Peristomal varices: in patients with portal hypertension (portal HTN)

▪Systemic complications

•General

◦Electrolyte imbalance and dehydration from excessive stoma output

•Etiology

◦Usually with ileostomy (normal is up to 1L/day)

◦Others: proximal stoma, IBD, or infection (clostridium difficile in patients with colostomy)

▪Prevention is the key

•Do your part by perfecting your surgical techniques

•Incision: 2-cm circular skin incision, 4 fingerbreadths lateral and inferior/superior to umbilicus, fat-preserving, transrectus hole (reduce risk of hernia) that admits 2–3 fingers, based on the type of stoma

•Stoma: healthy, tension-free (when bring it out, it should remain out about 3–4 cm above skin) stoma with good blood supply

•Maturation: full-thickness to subcuticular maturation, and brook the end ileostomy

◦Clostridium difficile colitis (CDC)

▪Etiology

•Antibiotic administration is almost always the cause of CDC (single dose could cause CDC)

•Hospital-acquired infection

▪Presentation

•Ranges from mild diarrhea to fulminant toxic colitis with pseudomembranous formation (present in 40%)

▪Diagnosis: history and by testing the stool for toxin A or B (Cytotoxic test is the gold standard)

▪Treatment

•Rehydrate and correct electrolyte imbalance

•Stop the precipitating antibiotic

•Oral or IV metronidazole and/or oral or enema vancomycin for 2 weeks

•Avoid antimotility agents and narcotics

•30% risk of recurrence (reinfection or reactivation)

•Surgical therapy

◦Indications

▪Failure of medical therapy

▪Perforation, toxic megacolon, septic shock with progressive colitis, and worsening dilatation on X-ray/CT

◦Subtotal colectomy and ileostomy are the treatment of choice, leaving a rectal stump (rectal tube) or bring the rectal stump as mucus fistula (when possible)

◦Anastomotic leak

▪Etiology: summarized in acronym LEAKING:

•L ocation: low rectal and esophageal anastomosis are at higher risk due to the absence of serosa

•E mergency surgery, A rterial supply

•K inking (tension), I nflammation and Irradiation

•N eoplasm and G lucocorticoid therapy

▪Presentation

•Ruling out a leak is a must for patients with the following during the 4th–5th postoperative days

◦Malaise, fever, abdominal pain, prolonged ileus, elevation of WBC, draining bowel content through the wound, or peritonitis

•Contained leak leads to abscess or fistula formation

•Free leak presents with peritonitis and sepsis

▪Treatment

•Prevention is the key: good surgical techniques and proper patient preparation

•Resuscitation: NPO, NGT, and TPN

•Localized leak

◦Intrabdominal abscess: percutaneous drainage

◦Wound abscess: open the wound—it will become a controlled fistula—then treat it accordingly

•Free leak: resection and stoma

◦Intra-abdominal infections

▪Definition of peritonitis

•Primary: peritonitis without perforation (e.g. spontaneous bacterial peritonitis)

•Secondary: peritonitis with perforation

•Tertiary: peritonitis from failure to control or cure secondary peritonitis

▪Etiology

•Community-acquired: E. coli, Klebsiella, streptococcus, staphylococcus, and anaerobes (no enterococcus)

•Hospital-acquired: add enterococcus, pseudomonas, citrobacter, and fungus

▪Diagnosis: clinically observe abdomen and obtain a CT of the abdomen

▪Treatment

•Resuscitate and administer antibiotics

◦Initiate empiric therapy once the diagnosis of peritonitis is made

◦Start with board-spectrum antibiotic, because starting with the wrong antibiotic increases morbidity and mortality

◦There are several factors to consider in antibiotic selection (see Table 1 ), including:

▪The source and severity of peritonitis

▪Host: immunity, co-morbidities, excreting organ function and allergy

▪Intra-operative culture when the patient is not responding to empiric therapy (intra-operative culture does not reduce the risk of treatment failure)

▪Community vs. acquired infection

▪No need to cover enterococcus in patients with community-acquired infections (no improvement in outcome)

▪Oral antibiotics with good bioavailability

•Clindamycin (gram positive and anaerobe), Ciprofloxacin/Levofloxacin (gram positive and negative), Amoxicillin/Clavulanic (gram positive and negative and anaerobe), and metronidazole (for anaerobe)

•Remove the cause (e.g., appendectomy for appendicitis)

•Drain the abscess: percutaneous or open procedure

Table 1: Types of antibiotics

▪Outcome

•Mortality ranges from 1% to > 30% in diffuse suppurative peritonitis

•Intra-operative Shock

◦Etiology: always think of bleeding as the cause

▪Hypovolemia: dehydration vs. bleeding

▪Septic shock

•Worsens during manipulation of infection due to showering of bacteria into the blood stream

▪Anaphylaxis

•Etiology: muscle relaxant and latex are the most common causes (Lymphazurin, in the case of SLNB)

◦Presentation

▪Hemodynamic instability, bronchospasm, skin rash, and death

◦Treatment

▪Cessation of offending agent and treat the underlying disease

▪Resuscitation and antibiotics

▪For anaphylaxis

•Epinephrine 0.5 mg of 1:1000 SC or IV

•Antihistamine (diphenhydramine 50-mg IV)

•Ranitidine 50-mg IV

•Steroid 100-mg IV

•Surgical Site Complication

◦General

▪Better no to shave the operative site but if needed, use clippers rather than razors to shave the operative site, as razors increase the risk of wound infection

▪Aseptically cleanse hands, use sterile barriers during invasive procedures, and use appropriate antibiotic to help prevent infection

▪Always check the wounds for signs of infection

◦Seroma

▪General: defined as serum, lymph, and liquefied fat collection in subcutaneous tissue layer

▪Etiology: large skin flap is the main risk, like in ventral hernia repair

▪Presentation: swelling or clear to yellowish discharge

▪Prevention: suction drain in large dead space ± abdominal binder

▪Treatment: observe, especially if there is a mesh beneath. If did not reabsorb, then aspirate

◦Hematoma

▪General

•Defined as abnormal collection of blood in a dead space

•Higher risk of infection than seroma

▪Etiology: poor hemostasis, coagulopathy, and medications (blood thinner) are risk factors

▪Presentation: either swelling or dark, bloody discharge

▪Prevention: control the risk factors

▪Treatment: observe small ones; drain big symptomatic ones

◦Wound dehiscence

▪General

•Defined as separation of the fascia after fascial closure

•Incidence: < 3% after abdominal surgery

•Usually occurs between day 7–10 postoperatively, but may occur from day 1 to day 20 postoperatively

▪Etiology: risk factors are poor techniques, infection, increased intra-abdominal pressure, and emergency surgery

▪Presentation: large amount of salmon-like discharge from the wound

▪Prevention: good surgical technique (interrupted suture closure is better in high-risk patients); prevent and drain wound infection; and prevent and treat ileus

▪Treatment: evisceration → OR for formal fascial closure

•Fascial dehiscence with intact skin (do not remove staple if suspecting fascial dehiscence) may be managed conservatively (deal with incisional hernia later)

◦Surgical Site Infection (SSI)

▪General

•SSI is the most common nosocomial infection in surgical patients

•UTI is the most common cause of nosocomial infection in all patients

•Hospital- or Ventilator-Associated Pneumonia (HAP or VAP). VAP is the most common nosocomial infection in the ICU for all patients

•Definition

◦Infection of the surgical site (SSI) within 30 days (most commonly 5–6 days postoperatively) after the operation (up to one year, if an implant is used)

•Could be superficial, deep, or involve an organ or space (e.g., pelvic abscess after colectomy)

▪Etiology

•Risk factors

◦Patient-related

▪Age, ASA ≥ III, obesity, DM, smoking, malnutrition, immunosuppression, duration of preoperative admission, or presence of remote body site infection

◦Perioperative-related

▪Preoperative showering and hair shaving, duration of surgical scrub, skin antiseptic, antimicrobial prophylaxis, duration of surgery

▪Operative technique: wound classification, inadequate hemostasis, tissue trauma, dead space, foreign body, or drain use

•Microbiology

◦Staphylococcus (most common)

▪Coagulase Positive S. aureus then Coagulase Negative S. epidermidis (the most common cause of nosocomial bacteremia)

▪Methicillin-resistant Staph (MRSA) is increasing

◦Enterococci

▪B-hemolytic streptococcus commonly causes hospital-acquired infections. Vancomycin resistance (VRE) is increasing in incidence

◦Gram negative rods (common with GI operations)

▪Facultative anaerobic: E. coli, Klebsiella, and Proteus

▪Aerobic: pseudomonas and acinetobacter are associated with hospital-acquired pneumonia

▪Stenotrophomonas maltophilia: emerge during the use of carbapenems (meropenem)

◦Anaerobes

▪Bacteroides: metronidazole, clindamycin, and B-lactamase inhibitor combination (e.g., amoxicillin and clavulanic acid)

▪Clostridium: Gram positive, exotoxin, and spore-forming anaerobic rod

•C. perferingins: penicillin G, clindamycin

•C. difficile: metronidazole and vancomycin

◦Fungi

▪Candida from wound or perforation of peptic ulcer does not need treatment. Candida from intra-abdominal abscess or urine in immunocompromised patients must be treated

▪Fluconazole is the first line for candida albicans. However, other candida species are resistant to fluconazole; therefore, Anidulafungin, Caspofungin or amphotericin-B are the antibiotics of choice

◦Bacteria < 10^5 will not cause infection except beta-hemolytic streptococcus that can cause infection at any count

•Wound types and risks of SSI

◦< 2.5% clean, 10% clean-contaminated, 15% contaminated, and 30% dirty

•Diagnosis: criteria for SSI diagnosis

◦Purulent discharge, local signs of inflammation, positive culture from the wound, and whenever the surgeon makes the diagnosis

◦Occurs within 30 days postoperatively (after 4th day) up to 1 year, if foreign body is used

◦Sternal instability may be early sign of infection

▪It is mandatory to check sternal stability (finger on each side of the incision while patient is coughing) every day following sternotomy

◦Non-necrotizing infection (abscess vs. cellulitis)

▪Usually an abscess has fluctuation, except in areas that have fibrous septa, like perirectal, breast abscess, carbuncle (back of neck or upper back), and infection of distal phalanx (felon)

▪Necrotizing infection

▪Skin infection with bruising and blistering, central necrosis, poorly defined borders, dishwater-like discharge, and thromboses vessels

▪May occur postoperatively within 48 hrs

▪Any organism may cause gas gangrene (usually polymicrobial):

•Staphylococcus, streptococcus, E. coli, and anaerobes

•Clostridium is the classical cause, which usually causes very extensive infection with myonecrosis: C. perfringens, novyi, and septicum; they are anaerobic, spore-forming, gram-positive rods

•Prevention

◦Aseptic and antiseptic measures

▪Treat all remote infections before surgery, remove hair just before scrubbing with electric clipper, shower patient with antiseptic solution the night before surgery (only decrease bacterial colony not the rate of SSI), require patient cessation of smoking at least 6 wks before surgery, and shorten the hospital stay

◦Antimicrobial prophylaxis

▪Single dose of 1st or 2nd generation cephalosporin (cefazoline or cefoxitin 2g IV) or fluoroquinolone with clindamycin or metronidazole

▪Clindamycin or vancomycin for patients with penicillin allergy

▪Administer 30–60 min (better to be closer to incision time) before surgery. Repeat every 1–2 half-life, and for every 3–4 units of blood loss. No need for postoperative re-dosing

▪Indicated for clean, contaminated wounds and clean wounds (if foreign body is used)

▪Administer a non-absorbable PO and IV antibiotic for colorectal surgeries to reduce SSI. Note: Mechanical bowel preparation does not reduce the risk of leakage or SSI

◦Local wound care

▪Good hemostasis, removal of dead tissue and foreign bodies, gentle tissue handling and less burning with diathermia

▪Closure of dead space with suture does not prevent SSI. In this case, use closed system suction. Note: Penrose drains increase infection risk, unless the wound is already infected

▪Keep the wound covered for 48–72 hrs postoperatively

◦Wounds that you should not close:

▪Wounds older than 6 hrs; contaminated, necrotic tissue; and traumatic wounds, including gunshot wounds. Some argue not to close stab wounds, too

◦Patient factors

▪Poor oxygenation, hypothermia, malnutrition, and low albumin increase SSI risk. Good glucose control (8–11 mmol/L) is recommended

•Treatment

◦Drainage of the abscess is the mainstay therapy (probe the wound before removing staples to localize the abscess)

◦No antibiotic is needed unless there is

▪Cellulitis or a deep-seated abscess

▪Early necrotizing wound infection occurring within the first 48 hrs. after surgery: C. perfringens or B-hemolytic streptococci pyogenes are the main organisms. Patient is very sick and toxic

•Treat with IV clindamycin (counteract the effect of cytokines) and penicillin-G with urgent debridement

▪Necrotizing infection: administer a broad-spectrum antibiotic, including initiation of a single (Piperacillin/Tazobactam, Tigecycline or Meropenem), triple, or even quadruple by adding Vancomycin (MRSA) or Linezolid (MRSA, VRE) regimen

•Outcome

◦Mortality of 2–3%, which reaches 20% when it is deep (organ or space) and up to 45% for necrotizing cases

◦Fistula

▪General: defined as a communication between 2 epithelial surfaces

▪Etiology: most commonly iatrogenic, following anastomotic leak, missed bowel injury, or after drainage of fluid collection (appendicular or diverticular abscess or pancreatic fluid)

▪Etiology for persistent fistula

•FISTOLA:

◦F (foreign body)

◦I (inflammation)

◦S (sepsis)

◦T (tumor)

◦O (obstruction)

◦L (luminal epithelialization)

◦A (abdominal radiation)

•Lateral duodenal, stomach and ileum, > 1-cm fistulas are difficult to heal in contrast to duodenal stump, jejunum, pancreaticobiliary, and colonic fistulas, which have better closure rate (less volume and harder consistency of fluid)

▪Presentation

•Bowel or pancreatic fluid discharge from the wound

•Low (< 200cc/day) or high output (> 500cc/day)

•Ileum is responsible for > 50% of high-output fistulas

▪Treatment

•40–80% close with conservative management

•Maintain good hydration and electrolyte balance

•Try to reduce output

◦Rest the gut and start TPN

◦H2 antagonist or PPI

◦Somatostatin analogue

•Treat sepsis (if present) with antibiotics and abscess drainage. Note: This may first be diagnosed by a CT scan

•Employ proper wound care and the use of vacuum closure (when it is associated with opened wound) to expedite wound healing

•Rule out the causes that prevent fistula closure (FISTOLA)

•Surgical resection of the fistula is needed in 30–60% of cases after failure of medical therapy

•Mortality

◦Risk factors for increased perioperative mortality

▪Age: independent risk factor for increased mortality, highest when > 80 years

▪Poor functional and nutrition status

•Severe malnutrition is associated with increased mortality. In this group of patients, preoperative TPN reduces morality by > 30%

▪Inpatient status is associated with increased mortality. Therefore, Admission on the day of surgery should be the standard of care

▪Preoperative sepsis and underlying cardiac disease

▪Obesity: BMI > 40 or > 35 with co-morbidities increases mortality, wound infection, and DVT dramatically

GERIATRIC PATIENTS

•General

◦2 challenges in dealing with surgical geriatric patients

▪Disease presentation is different

▪Physiological and functional reserve and response are different

◦All geriatric patients should perform specifically

▪Functional assessment

•American society of anesthesiologist (ASA)

◦ASA I: Normal

◦ASA II: mild systemic disturbance, no increase in mortality

◦ASA III: severe systemic disturbance, increased mortality with surgery

◦ASA IV: severe systemic disturbance, life-threatening with or without surgery

◦ASA V: little chance to live for > 24 hrs, surgery is the last resort

◦ASA VI: brain dead for organ donation

•Daily activity (feeding, dressing, bathing, and transferring)

•Exercise tolerance: most sensitive predictor

▪Cognitional Assessment

•Mini-Cog© and Folstein’s mini-mental status examination

▪Nutritional Assessment

•History and physical examination are an effective, objective measure of nutritional status

•Perioperative Assessment and Prevention of Complications

◦Essential work-up

▪Blood work: CBC, electrolyte, liver function, and coagulation profile

▪Urine analysis, CXR, and ECG with complementary Echo

◦Cardiovascular system

▪Cardiac disease is the most common comorbidity and the leading cause of death

▪Normal vitals provide false sense of security (drug-effect), Normal vitals means abnormal hemodynamics

▪Diastolic dysfunction is very common above age of 80 years and relaxation consume more oxygen than contraction

▪Pulmonary artery catheter does not add any benefit to the patient

▪Re-initiation of cardiac medications early in postoperative period (especially B-blocker) is associated with reduced mortality

▪Improve O 2 delivery by maintaining a higher hemoglobin level (above 9 g/dL)

◦Respiratory system

▪Chronic lower respiratory disease is the fourth leading cause of death

▪Respiratory complication is the most common postoperative complication in elderly

▪Reduced vital capacity, increased shunting, and decreased maximum inspiratory and expiratory forces (by 50%) are common

▪50% reduction in body response to hypoxia and hypercapnia

▪Obtain pulmonary function test for patients with lung disease

▪Cessation of smoking is critical (at least 6 weeks)

▪Reduce pneumonia risk by shortening the period of intubation/ventilation (thus reducing the risk of ventilation-associated pneumonia—VAP), providing good pain management, and providing aggressive chest physiotherapy

◦Central nervous system

▪Cognitive function deteriorates postoperatively

▪Duration of delirium is associated with poor outcome

▪Perioperative stroke may happen secondary to inadequate perfusion or thromboembolism

◦Renal system

▪Reduction in renal blood flow and glomerular filtration rate (GFR) is common

•40% reduction by age of 80 years

▪Serum creatinine may be misleading due to reduction in muscle mass and 24-hr urine collection for creatinine clearance is practical

•Calculating creatinine clearance (CrCl) is recommended

•Tissue inhibitor of metalloproteinases (TIMP-2) and insulin-like growth factor-binding protein 7 (IGFBP-7), Neutrophil gelatinase-associated lipocalin (NGAL, urine or plasma) N-acetyl-d-glucosaminidase (NAG) and cystatin C (Cys-C)

•TIMP-2 and IGFBP-7: predict which patient will develop moderate to severe AKI in the ICU within 24 hrs

▪Be cautious when using IV contrast because geriatrics are at high risk of developing acute renal failure from the contrast, which is associated with 50% mortality in the ICU setting

◦Musculoskeletal system

▪Early mobilization with prophylaxis against DVT is crucial

▪Rehabilitation and physiotherapy may be indicated

◦Metabolism, nutrition, and immune system

▪Geriatrics are prone to malnutrition and reduced immunity and poor response to infection/stress → poor outcome from infection

▪Perioperative nutritional supplementation may be needed

▪Abnormal glucose metabolism is present in 20% of patients older than 60 because of reduced beta cell function and/or increased insulin resistance

ANESTHESIA

•General: four components of anesthesia: produces unconsciousness, amnesia, analgesia, and muscle relaxation

•General Anesthesia

◦Inhalation Agents

▪2 main characteristics: blood/gas (B/G) solubility coefficient and minimal alveolar concentration (MAC)

▪B/G measures the uptake of an agent by blood. Less soluble agent (low B/G) like nitrous oxide has rapid induction and emergence

▪MAC is the concentration of an agent required to prevent movement following skin incision in 50% of patients. The higher the MAC the less potency

▪Isoflurane is the most commonly used inhalation (NOT for induction) agent (cheap, less effect on cardiac output, less sensitization to catecholamine-induced arrhythmia and < 2% metabolized

◦IV Agents

▪Induction agent

•Propofol (short-acting, not nauseating, good for asthmatic), Etomidate (excellent for hypotensive patient, might cause adrenal suppression), ketamine (Least depressive effect on respiratory, good for asthmatic, good for short, superficial surgery) midazolam, and thiopental

▪Opioids: Benefits include MAC reduction, control tachycardia and HTN during intubation and have strong analgesic, hypnotic and amnesic effect at higher doses

▪Neuromuscular blockers

•Succinylcholine (depolarizing) and non-depolarizing agents

◦NPO for 2 hours after clear fluid intake and at least 6 hours following solid food intake

•Regional Anesthesia

◦Drugs

▪Amide (lidocaine and bupivacaine) and ester (procaine)

▪Work by blocking Na currents in nerve fibers

▪Dose: 3-5-7 mg/kg role

•Bupivacaine 3 mg/kg

•Lidocaine 5 mg/kg

•Lidocaine with epinephrine 7 mg/kg

▪Not effective in an acidic environment (abscess)

▪Best way to avoid toxicity is to avoid intravascular injection

•Earliest signs of toxicity: CNS (lightheadedness, metallic taste, tongue/lips numbness/tingling or hearing/visual disturbance) and CVS (arrhythmia)

◦Types: peripheral nerve block, spinal (subarachnoid) and epidural (reduce mortality and pneumonia but NOT MI when compared to general anesthesia) anesthesia

•Conscious Sedation

◦Requires patient monitoring during and after finishing the procedure

◦Surgeons should be familiar with the medication (dose, side effects, and antidotes)

◦Opioid (fentanyl) and anxiolytic (midazolam) are commonly used

▪Start with very small dose and titrate it up rather than starting with large dose that may lead to over sedation and respiratory arrest

DISEASES OF THE BLOOD

Perioperative Coagulopathy

•Preoperative Assessment of Hemostasis

◦History is the most important preoperative test of hemostasis

▪Easy bruising, mucosal bleeding

▪Heavy bleeding after surgical procedure or with menses

▪Family history of bleeding disorder

▪Medication list

◦Coagulation profile (PT, PTT, and INR) and platelet count:

▪PT measures extrinsic pathway (V, VII, X)

▪PTT measures intrinsic pathway (VIII, IX, X, XI, XII)

▪Bleeding time: assess platelet function; it has no role for preoperative evaluation

•Congenital Coagulation Disorders

◦Von Willebrand’s Disease (vWD)

▪General: most common congenital bleeding disorder

▪Etiology: deficiency of vWF with factor VIII deficiency (vWF is the carrier for factor VIII)

▪Types

•Type I (autosomal dominant, partial deficiency, most common)

•Type II (autosomal dominant, dysfunctional factor)

•Type III (autosomal recessive, complete absence)

▪Diagnosis: prolonged PTT and bleeding time with normal PT

•Screening: plasma vWF antigen and activity

▪Treatment

•Preoperative level should be > 50% for few days

•Type I: desmopressin DDAVP

•Type II and Type III: cryoprecipitate and vWF-rich factor-VIII concentrate

◦Hemophilia A (factor VIII) and B (factor IX)

▪Etiology: X-linked recessive disorder in male kids of carrier mothers

▪Classification: mild (factor > 5%), moderate (1–5%), and severe (< 1%)

▪Presentation: large hematoma or hemarthrosis, and rarely mucosal bleeding

▪Diagnosis: prolonged PTT, normal PT and platelet with low specific factors

▪Treatment

•Preoperative infusion to keep level >30% for minor surgery and >80% for major surgery, 30-60 min before surgery and to keep it above 50% postoperatively until the wound is healed

•Mild and minor surgery: DDAVP

•Moderate and Severe or major surgery: factors (VIII or IX)

•Recombinant activated factor VII (rFVIIa)

◦Has been used to stop bleeding in hemophilia patients and non-hemophilia patients with antibodies to factor VII

◦Mechanism of action is unclear; may be platelet activation and thrombus formation

◦Controlled bleeding from congenital disorder may be achieved by:

▪FFP (contains all factors), Cryoprecipitate (contains VIII, XIII and vWF and fibrinogen), recombinant FVIIa (activate platelet aggregation)

▪Amicar ® (aminocaproic acid), aprotinin, and fibrin sealant

•Acquired Coagulation Disorders

◦General: more common than congenital disorders

◦Vitamin K Deficiency

▪Etiology: decrease intake, antibiotic (cephalosporin, sulfa drugs, and quinolone), obstructive jaundice and malabsorption

▪Treatment: give vitamin K IV, SQ, or IM at dosage of 5–10 mg every 12–24 hours to correct INR

◦Anticoagulant Drugs

▪Warfarin

•Mechanism: blocks vitamin-K dependent factors (X, IX, VII, and II) with half-life of about 2 days; its effect is reversed by vitamin K and FFP

•Patients on warfarin for DVT/PE

◦Risk of re-clotting is highest within first 3 months; therefore, elective surgery should be delayed for 2–3 months from onset of DVT/PE

◦If the surgery is urgent, the patient should wait for a few days before going ahead with surgery (might have to operate on lower dose of heparin or insert filter in very high-risk patients)

•Patients on warfarin for arterial clot without heart valve

◦Atrial fibrillation is the most common cause of arterial embolism: risk of embolism is 5% per year in the absence of high-risk criteria (DM, embolic events, and the elderly)

•Patients on warfarin for heart valve

◦Risk of thrombosis is 5% per year without warfarin (1% per year on warfarin and 2% per year on ASA)

•Intermediate- and low-risk patients do not need bridging therapy with heparin

▪Unfractionated heparin (UFH)

•Mechanism: blocks activation of factor X by binding and activation of Anti-thrombin III (AT-III) and thrombin (II); causes prolongation of PTT and it takes 6 hours to be cleared off the circulation

•It may be neutralized by IV protamine sulfate (100 U of heparin = 1 mg of protamine), which may cause severe hypotension as a side effect

▪Low molecular-weight heparin (LMWH)

•Mechanism: has more anti-X effect with good and stable bioavailability (does not bind to plasma protein or endothelium)

•It is associated with

◦Less bleeding (does not affect platelet function, vascular permeability, or platelet-vessel interaction)

◦More effective in preventing DVT in high-risk patients (orthopedic and trauma patients)

◦Lower risk of heparin-induced thrombocytopenia (HIT-1%), lower postoperative bleeding, and lower risk of osteoporosis

•May be given once (Dalteparin 5000U, Enoxaparin 40 mg) or twice (enoxaparin 30 mg for high-risk patients)

▪Direct thrombin inhibitors

•Like dabigatran: should be stopped >24 hrs before surgery, no antidote

▪Factor Xa inhibitors

•Like rivaroxaban and apixaban

•Stop 48-72 hrs before surgery, no test to assess effect, no antidote

◦Hepatic and Renal Dysfunction

▪Liver failure: platelet dysfunction and decreased clotting synthesis (liver synthesizes all clotting factors except VIII)

▪Uremia can cause platelet dysfunction (decreased platelet factor II is necessary for aggregation and adhesion)

•Treated by DDAVP

◦Hypothermia

▪One of the most common causes of coagulopathy, especially when body temperature falls below 34ºC

•Platelet Disorders

◦Either quantity or quality disorders

▪Common medications cause thrombocytopenia, including: quinidine sulfa, H2 blockers, antidiabetic agents, rifampin, and heparin

◦Treatment of quantitative disorder: platelet transfusion

▪Platelet count > 50,000 is sufficient for hemostasis

▪Each unit of platelet increases the count by 5000

◦Treatment of qualitative disorder

▪Platelet transfusion ± DDAVP have proven useful; rFVIIa may be used (not studied yet)

•Vascular Disorders

◦Should identify common vascular disorders (hereditary hemorrhagic telangiectasia, amyloidosis, congenital hemangioma, and scurvy)

•Intraoperative Bleeding

◦General: Assess character of bleeding: rapid, single location vs. multifocal oozing

◦Etiology: rule out surgical cause (bleeding vessel or organ)

◦Diagnosis

▪Obtain PT, PTT, Hb, platelet, fibrinogen, and heparin contamination

▪Review history and preoperative labs (LFT and renal function)