Puzzles in General Surgery: A Study Guide

ICU

Preface

Surgery is about knowledge and skills. Books and literature are the main sources of knowledge. It is not always convenient to go through a big textbook to look for a small piece of information. It is about time to change the way surgical books are written. The author went through many textbooks, handbooks, and articles during medical school and residency to come to a decision to write his own notes that are up-to-date and concise but thorough. This mini textbook is a hybrid. It is thorough like a textbook, concise like a handbook, and up-to-date like an article. This book provides medical students, surgical residents, and junior surgeons all the important pieces of information they need for each surgical topic. It is easy to read and memorize. It discusses in depth all aspects of a disease in a systematic and to-the-point fashion. It provides a quick but thorough review before any surgical examination of all levels.

Acknowledgments

There are a few extraordinary people who contributed to this book in different ways. My parents provided me with all the support, guidance, and love to be successful and to be able to write this book. Without them, after God’s will, I would have not made it this far. My siblings were there every time I needed to vent out my stress. Marring my wife Sawsan was the beginning of endless success. She is always there when I need her. She contributed to this with her love, patience, and imagination (she is the illustrator of this book and the brain behind book cover idea). I am thankful to my kids for keeping the smile on my face and for nourishing my life with love and happiness. I am very appreciative to faculty members of Umm Al-Qura University, all surgeons at the University of Manitoba and to all trauma surgeons at the University of Miami/Jackson Memorial Hospital for providing all their support and guidance. At the end, I would like to thank my editor and designer for their remarkable work and 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 HCO3 are major anions

Physiology of Acid-base (AB) Balance

H Ion is expressed in pH Unit:

H = 24 x (PaCO2 ÷ HCO3). The body changes PaCO2 and HCO3 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-O2 dissociation curve to left (Hb will not let go of O2), and increases O2 consumption by increasing glycolysis

Alkalosis is more detrimental than acidosis

Changes in pH could be from:

PaCO2 increase or decrease: called respiratory acidosis (RAC) and alkalosis (RAL), respectively

HCO3 increase or decrease: called metabolic alkalosis (MAL) and acidosis (MAC), respectively

Mixed vs. compensated

Mixed: normal pH, but both PaCO2 and HCO3 are abnormal

Compensated: abnormal pH, and both PaCO2 and HCO3 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:

Decreased PaCO2 → RAL

Increased HCO3 → MAL

Compensation (when both are abnormal)

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

Increased PaCO2 → RAC

Decreased HCO3 → MAC

Compensation (when both are abnormal)

General principles in the management of A-B imbalance

Acidosis: treat underlying cause; if pH < 7.1, give HCO3 (be careful, as this may increase PCO2 and lactate)

Alkalosis: treat underlying cause

When Cl is depleted → administer NS IV fluid

If did not correct → administer Acetazolamide (Diamox®), which inhibits HCO3 reabsorption → cause Na loss → leads to diuresis (be careful, as this may lead to hypokalemia and hypovolemia)

Anion Gap (AG) = Na – (CL + HCO3)

Normal range = 8–16 mEq/L

AG determines whether metabolic acidosis is due to accumulation of acid or just a loss of HCO3

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

Lactic acid, Ethylene glycol, ASA and Ketoacidosis

Lactic Acidosis

What does high lactate indicate?

When the body cannot produce energy from glucose (low supply of glucose or O2, 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:

Impaired tissue perfusion (shock, ischemia)

Sepsis: could be from shock or impaired O2 utilization at the cellular level (toxins from the invading organism)

Fluid Therapy

IV Fluid is a DRUG

Indication of IV Fluid:

1-Replace Deficit (Resuscitation)

Fluids of choice: normal saline (in case of metabolic alkalosis) and Ringer’s Lactate (in trauma or metabolic acidosis)

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 0.5–1 mEq/kg/day and glucose requirement is 100–150g/day dextrose

D5 in ¹/2 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 may be hypertonic, isotonic, or hypotonic (the latter is the most common) and it may occurs in the setting of hypervolemia, euvolemia, or hypovolemia)

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

In asymptomatic patient with very low Na: restrict fluid

If chronic and symptomatic: correct it, but to avoid cerebral demylination, 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

Treatment

First calculate water deficit

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

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

Administer ¹/2 of the calculated deficit over a 24-hr period, and then administer the rest over a 24– 48-hr period. The Na correction rate of 0.5 mEq/ hr prevents cerebral edema (8–10 mEq/day)

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 (EKG) 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: 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, aldacton) 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 EKG; and if there are changes or the level is > 6.5 mEq, give 10cc 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 Ca (ionized) < 2.1 mmol/L

Etiology: fluid resuscitation, hypomagnesemia, and pancreatitis are common

Treatment

Treat the underlying cause then replace Ca

Give oral Ca replacement for asymptomatic patients

When Ca < 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 Ca (ionized) > 2.5 mmol/L

Etiology: hyperparathyroidism (out-patient) and malignancy (in-patient)

Treatment

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): [90 mg over 24 hrs]. The effect will peaks after 48–72 hrs

Magnesium (Mg)

Hypomagnesemia

Defined as Mg < 50 mmol/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)

Phosphate

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

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-gama, and nitric oxide

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

Sepsis reduces protein synthesis

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: O2 consumption and CO2 production (respiratory quotient RQ)

Body measurement: body weight and skin folds

Biochemical measurement: albumin, 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)

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

What to Administer: TPN vs. 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

Maintains gut mucosa integrity and reduces bacterial translocation in burn, trauma, 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 × weight in kg) + (5.003 × height in cm) → (6.775 × age in years)

For female: 655.1 + (9.563 × weight in kg) + (1.850 × height in cm) → (4.676 × 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)

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 use

Gastrostomy is placed for long-term 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 × 30 = 2100 kcal

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

Calories from lipid (20% of total calories):

(2100 × 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 × 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:

Stop TPN

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

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 CO2 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), 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

MONITORING AND CARE

Cardiac Monitoring and Care

Myocardiac Infarction (MI) Monitoring

Tachycardia is a potent inducer of MI

Immediately re-start B-blocker postoperatively

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

Blood pressure (BP) Monitoring, Central venous pressure (CVP) +/– pulmonary artery catheter

Major Predictors of Perioperative Cardiovascular Risk

Recent MI (within 7 days to 1 month; if occurred in < 7 days, it is called acute MI)

Decompensated CHF (S3 gallop) and unstable or severe angina

Significant arrhythmia (complete heart block and ventricular arrhythmia)

Severe valve diseases (aortic stenosis)

Pulmonary Monitoring and Care

Continuous O2 monitoring

The cornerstones of pulmonary therapy are good pain control and early mobilization +/– chest physiotherapy

Neurological Monitoring and Care

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 computerized tomography scan (CT scan) of the head

Daily wake-up is important to prevent accumulation of sedation

Delirium is associated with poor outcome

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

Steroid and paralytic agents are risk factors

Renal Monitoring and Care

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

Good fluid resuscitation is the most important preventive measure of acute renal failure postoperatively and after CT contrast examination

N-acetylcystein given 24 hrs before and after CT reduces the risk

GI Monitoring and Care

Stress ulcer prophylaxis and early enteral feeding are essentials

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

Hematological Monitoring and Care

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 heparin 6 hours prior to surgery, then resume it 6 hrs after surgery without bolusing

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 Monitoring and Care

Good glucose control (10–18 mmol/L) is associated with reduction in mortality as well as a decrease in ARF, infection, and polyneuropathy

Note: Avoid tight glucose control (4.5–6 mmol/L), as such over-control may result in hypoglycemia and its complications

Administer a perioperative stress dose for patients on chronic steroid

Patients taking 5 mg per day or more for more than 2 wks within the past year are considered at risk of adrenal insufficiency

Administer 100 mg of hydrocortisone intravenously on induction; then allow the patients to start back on their own, prescribed doses

Infectious Disease Monitoring and Care

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

PERIOPERATIVE COMPLICATIONS

Nervous System

Delirium and Psychosis

Delirium 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 lidocain

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 PCO2 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

Respiratory System

General

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

Assess high-risk patients by room air arterial blood gas 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

Atelectasis

The most common postoperative pulmonary complication, and the most common cause of fever in the first 48 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 —specifically, ventilator-associated (VAP) or from aspiration (oropharynx flora or gastric content)

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, PaO2/FiO2 < 300 and wedge pressure < 18 mmHg

Acute Respiratory Distress Syndrome (ARDS)

The same criteria for acute lung injury but with a PaO2/FiO2 ratio of < 200 (instead of 300)

Pulmonary Embolism (PE) and DVT

General

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, EKG, 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

Un-fractionated heparin: given 5000 units every 8hrs

For high-risk patients: 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

Cardiovascular System

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

New recommendation is to wait > 4–6 weeks post-MI for elective surgery

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

Prevention

Identify patients with major high risk like

Recent MI (within the past month)

Unstable angina

Decompensated heart failure

Severe valve disease (aortic stenosis)

Significant arrhythmia (AV block, ventricular)

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 electrocardiogram (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

Valvulopathy 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)

Amoxacillin 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

Gastrointestinal System

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 tear sare 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

Stomal 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 lowerrecurrence 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

Peristoma 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 you surgical techniques

Incision: 2-cm circular skin incision, 4 fingerbreadth 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 pseudomembraneous 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 is 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:

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

Emergency surgery, Arterial supply

Kinking (tension), Inflammation and Irradiation

Neoplasm and Glucocorticoid 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), Amoxacillin/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

Outcome

Mortality ranges form 1% to > 30% in diffuse suppurative peritonitis

Table 1: Types of antibiotics

Urinary System

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 Renal Failure

General: defined as an acute reduction in urine output

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

Endocrine System

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: O2, 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 × 0.6 × (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

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

Wound Complications

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, followed by pneumonia

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, 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: inadequate hemostasis, tissue trauma, dead space, foreign body, and/ or use of a drain

Microbiology

Staphylococcus (most common)

Coagulase positive S. aureus then Coagulase negative S. epidermidis (the most common cause of nosocomial bacteremia)

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

Bacteroids: metronidazole, clindamycin, and B-lactemase 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

Fluconaozle is the first line for candida albican. However, other canadida species are resistant to fluconazole; therefore, gasifungin 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):

Staphyloccus, streptococcus, E. coli, and anaerobes

Closteridium 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 flagyl

Clindamycin or vancomycin for patients with penicillin allergy

Administer 30–60 min. (at the beginning of anesthesia) 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, and gentle tissue handling

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 occuring 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, meropenem), triple, or even quadruple (adding vancomycin) 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 (appedicular 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 (abdmominal 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

Nutrition

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

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

ELDERLY PATIENTS

Preoperative Assessment of

Function

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

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

Exercise tolerance: most sensitive predictor

Cognition

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

Nutrition

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

Preoperative Work Up

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

Urine analysis, CXR, and EKG

Perioperative Monitoring and Care

Cardiovascular system

Cardiac disease is the most common co-morbid condition and the leading cause of death

Normal vitals provide false sense of security (often drugs effect results)

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 O2 delivery by maintaining a higher Hb level (above 90)

Respiratory system

Chronic lower respiratory disease is the fourth leading cause of death

Respiratory complication is the most common postoperative complication in elderly patients

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

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 GFR is common

Serum creatinine may be misleading due to reduction in muscle mass; therefore, 24-hr urine collection for creatinine clearance is the most accurate tool

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

Perioperative nutritional supplementation may be needed

Abnormal glucose metabolism is present in 20% of patients older than 60

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 in response to skin incision in 50% of patients. The higher the MAC the less potent agent

Isoflurane is the most commonly used agent

IV Agents

Induction agent

Thiopental, ketamine, propofol, etomidate, and midazolam

Opioids: reduce the MAC of inhalation agent, blunt the tachycardia and HTN during intubation, provide analgesia, and produce hypnosis and amnesia 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 overdose are numbness/tingling of tongue or lips, metallic taste, lightheadedness, or visual disturbance

Types: peripheral nerve block, epidural, and spinal

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 oversedation 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)

Type II (autosomal dominant, dysfunctional factor)

Type III (autosomal recessive, complete absence)

Diagnosis: prolonged PTT and bleeding time with normal PT

Treatment

Preoperative level should be > 50% for few days

Type I: DDAVP

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

Hemophilia A (VIII) and B (IX)

Etiology: X-linked recessive disorder

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

Presentation: large hematoma or hemoarthroses, and rarely mucosal bleeding

Diagnosis: prolonged PTT with normal PT and low in specific factors

Treatment

Preoperative infusion to keep level >30% for minor surgery and >80% for major surgery

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 vW factors 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 (cephalosporine, 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; it’s 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)

Hepatic and Renal Dysfunction

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

Uremia can cause platelet dysfunction (decreaseed 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; rhFVII 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 persistent 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)

Assess intraoperative and preoperative medication

Review compatibility of intraoperative transfusion

Treatment

Treat the underlying cause by ligating the bleeding vessel and correcting coagulopathy, FFP, DDAVP and/or platelet transfusion

Postoperative Bleeding

Etiology

Anatomic or structural bleeding

Thrombocytopenia (the most common cause is infection, followed by medications)

Platelet dysfunction (ASA, Plavix®)

DIC and unrecognized hereditary coagulation disorder

Medication (heparin causing HIT, NSAIDS, and ASA)

Vitamin K deficiency (nutritional) and liver/kidney failure

Antithrombotic Medications in the Perioperative Period

Patient with low risk of thrombosis

These patients have uncomplicated A. fib., biological valves, DVT in > 3months

Stop warfarin 5 days before surgery and resume when hemostasis achieved; NO need for bridging with heparin

Patient with high risk of thrombosis

These patients have complicated A. fib., DVT < 3months, mechanical valves, antiphospholipid syndrome, or active cancer

Stop warfarin 5 days before surgery and bridge it with LMWH or UFH; then hold warfarin for 24 hrs, LMWH or UFH for 6 hrs, before surgery

Resume LMWH or UFH 6–24 hrs postoperatively; when hemostasis is achieved, then begin warfarin

Urgent reverse effect of warfarin

Use IV vitamin K (takes 12–24 hrs to work)

When more rapid correction is needed, administer FFP

For patient on UFH: protamine IV (1 mg per 100 U of UFH, max. rate is 50 mg over 10 min. and max. dose is 100 mg)

Heparin-Induced Thrombocytopenia (HIT)

General: May happen in up to 5% of patients within 4–5 days (type II) from heparin exposure (could be IV, SQ, or even a flush of the IV line) or even within 24 hrs (type I)

Etiology

Mechanism: Anti PF4/heparin IgG antibodies

Risk factor: Heparin duration > 1wk, UFH, Female, history of recent surgery

Presentation

Thrombosis in > 50% (both venous and arterial but venous is more); bleeding is very rare

Necrotic lesion at injection site (specific), adrenal necrosis, and DIC

Diagnosis

Rule out other causes of thrombocytopenia

> 50% drop in platelet count

EIA specific for IgG (HIT antibodies) with sensitivity of 99%, which leads to overdiagnosis and Anti-PF4

Washed platelet activation assay (> 50% serotonin release) is not that sensitive

Always perform lower extremities U/S to rule out DVT

Treatment

Stop all sources of heparin

DO NOT give warfarin (risk of limb gangrene during the acute phase)

DO NOT transfuse platelet unless patient is bleeding

Anticoagulation occurs even in the absence of thrombosis (once confirmed HIT, you should anticoagulate with heparin alternative)

Danaparoid: ATIII dependent → inhibit Xa and thrombin

Lepirudin: hirudin (leech saliva) recombinant, thrombin inhibitor, cleared by the kidney (need adjustment in renal failure patients)

Argatroban: thrombin inhibitor, recommended in renal failure patient (cleared by the liver)

Warfarin: as long-term