! "

-sum total of abnormalities of all organ systems and their interactions that determine the outcome of an operation
-estimation using Goldman’s cardiac risk index
-risk of surgical cardiac death:
-no previous MI: 1.0-1.2%
-MI > 6 months: 6.0%
-MI (transmural) < 3 months: 16-37%
-predisposing factors for perioperative cardiac death:
1. infarction within 6 months
2. congestive heart failure
3. arrhythmias
4. aortic stenosis
5. emergency or major surgery
6. age greater than 70 years
7. poor medical condition
-ECG and hematocrit level are significant
-stress test indicated to identify patients at risk
-positive if any or all of the following:
-ST depression > 0.2 mV, inadequate heart rate response to stress, or hypotension
-delay surgery (if possible) to > 6 months after MI
-angioplasty or CABG may be necessary before any major surgical procedure
-treat CHF and a-fib
( &
-risk factors:
1. smoking
2. obesity
3. advanced age
4. industrial exposure
5. PCO2 > 45 mmHg diffusion defect
6. abnormal PFTs:
-FVC < 70% predicted
-FEV1 < 2.0L or < 70% predicted
-PEFR < 200 L/min
-FEV1/FVC < 65%
7. PAP > 30 mmHg
-exercise oxygen consumption (prior to thoracotomy) (VO2) > 20 ml/kg/min less likely to have post-op pulmonary
-8 weeks smoking cessation prior to surgery beneficial
#)$ *
-serum abnormalities of BUN and Cr are not manifest until > 75-90% of renal reserve lost
-creatinine clearance (ml/min) = [1.23 x weight (140-age)]/creatinine in umol/L
-correct reversible causes: infection, uncontrolled hypertension, obstruction, and dehydration
-peritoneal, hemodialysis, or continuous ultrafiltration occasionally required
#+$ *
-patients with cirrhosis
-Child-Pugh criteria: based on presence of ascites, bilirubin, encephalopathy, nutritional status, albumin
-class A < 5%; B 5-10%; C 20-50% mortality following non-cardiac surgery
-generally die of high-output CV failure and low peripheral resistance
-see Table 11-4
-measures that can be taken:
-abstinence from alcohol important prior to elective procedures
-improve protein tolerance by use of branched-chain amino acid
-control ascites:
-spironolactone and lasix combined with fluid restriction to 1500 ml/day
-limit sodium to 2g/day
& see Chap. 3
. */*
-difficult to assess
-severely malnourished patient:
-weight loss > 15% over previous 3-4 months
-serum albumin < 3.0 g/dL
-energy to injected skin-test antigens
-serum transferring level < 200 mg/dL
-if severely malnourished, then enteral or parenteral (only if severe) nutrition for 4-5 days preop
-normalize retinol binding protein, thyroxin-binding prealbumin, and transferring
#0$ !
&# 1
-no definite guidelines
-see appendix
2 * 2
-lack of metabolically effective circulating insulin
-deficient utilization of glucose by peripheral tissues
-increased output of glucose by liver
-increased fatty acids ketones urine
-glycosuria osmotic diuresis loss of sodium and potassium
-anaesthetic agents can cause an exaggerated hyperglycemic epinephrine response and an increased
resistance to exogenously administered insulin
-stress of operation aggravates hyperglycemia
-epinephrine: glycogenolysis
-glucocorticoid: mobilized protein, anti-insulin effect
-growth hormone
-DM pts should have preference on operative schedule to minimize effects of fasting and ketosis
-mild DM frequently do not require insulin; dietary control sufficient
-pts using OHA should continue their use until day before operation
Insulin Therapy:
-see appendix for protocols
-IV hydration, insulin therapy, and electrolyte replacement (potassium)
-need for potassium usually does not exceed 80 mEq
Nonketotic Hyperglycemic Hyperosmolar Coma:
-relatively uncommon
-usually occurs in elderly diabetic or nondiabetic obese patients and those receiving TPN
-treat with large amounts of hypotonic solutions and intravenous insulin (est dose of 10 U)
-disorder of normal body thermoregulation
-controlled by anterior hypothalamus
-?protective mechanism to combat infection
-all pyrogens evoke common mediator IL-1 (endogenous pyrogen)
-alters activity of temperature-sensitive neurons raises set-point
-vasoconstriction chills, shivering
increased body temperature
Perioperative Fever:
-fever in the immediate postoperative period usually is not serious, is not very high, and is self-limited
-usually ascribed to atelectasis
Malignant Hyperthermia:
-incidence ~ 1/100000 general anaesthetic procedures
-succinylcholine, halothanes metabolic acidosis and electrolyte imbalances
-hypercalcemia, hypotonicity, hyperthermia (~40OC), oxygen denaturation, hypercapnia, cardiac
-treat with dantrolene IV 1 mg/kg, repeat to total dose of 10 mg/kg prn
-supportive measures; ventilation/oxygenation, treatment of possible myoglobinuria
Fever within 24 Hours:
-usually due to atelectasis or failure to clear pulmonary secretions
-unnecessary to do extensive tests at this point
-if high fevers with rigours, hypotension, and changes in mentation: consider severe wound complications
such as necrotizing fasciitis or intestinal leak
Fever at 24-48 Hours:
-usually respiratory complications
-catheter related problems - UTI
-inspect wound for cellulitis, necrotizing fasciitis, or clostridia myositis
Fever after 48-72 Hours:
-most common cause of fever after 72h is wound infection
-also suspect UTI
-less common infections: pneumonitis, acute cholecystitis, idiopathic postoperative pancreatitis
-drug allergy
-candidiasis may complicate IV TPN tx with amphotericin B
-fever after 1 week leaking anastomosis, abscess, deep wound infection
Predisposing Factors:
-staphylococcus aureus most frequently involved offending organism
-enteric organisms in bowel surgery; other less common pathogens: enterococci, Psedomonas, Proteus,
-hemolytic strep responsible for 3% of wound infections
Classification of Operative Wounds
Wound Description
Nontraumatic, uninfected operative wounds
in which the respiratory, alimentary, or
genitourinary tract is not entered. Usually
closed without drains
Respiratory, alimentary, or genitourinary
tract is entered with only minimal
Fresh traumatic wounds; wounds with a
major break in sterile technique; wounds
encountering non-purulent inflammation;
wounds made in or near contaminated skin
Purulent infection is encountered
Factors: -type of operative wound
-remote infection
-duration of operation:
-others (see Table 11-9)
Incidence of
15-24 years (4.7%); > 65 years (10%)
not an independent risk factor when adjusted to age
increase rates from 7 to 16%
doubles rate
< 30 min (3.6%); > 6 hours (18%)
-skin preparation:
-bowel preparation:
-prophylactic antibiotics
-maintenance of temperature:
-meticulous technique:
-appropriate drainage
-clipping (2% infection rate) preferred over shaving (5%) of hair
-clear liquids, cathartics, antibiotic regimens
-warming blankets, warm fluids
-gentle handling of tissue, hemostasis
Clinical Manifestations:
-infections usually evident between 5th and 8th POD; may manifest after weeks if pt on antibiotics
-necrotizing fasciitis or clostridia myositis can occur within 24 hours
-open incision and pack wound with gauze
-cellulitis and edema add antibiotics; Gram stain may help guide treatment
-if hemolytic strep penicillin for 1 week
-clostridia myositis/necrotizing fasciitis surgical debridement
-Fournier’s gangrene: necrotizing fasciitis of perineum or groin in diabetic patients
-30-70% mortality rate
-inadequate hemostasis
-provide good culture medium for bacteria
-early haematomas return to OR ligate responsible vessel primary closure of wound
-late haematomas manage patient expectantly with hope that haematoma has not become contaminated
% *
-lymph collections
-aspiration and pressure dressings
-continuous closed-suction drainage
% . *1
* *
-< 45ya: 1.3%; > 45ya: 5.4%
-generally caused by a technical factor
-contributory factors:
-malnutrition, hypoproteinemia, morbid obesity, malignancy with immunologic deficiency, uraemia,
diabetes, coughing with increased abdominal pressure, remote infection
-local factors: hemorrhage, infection, excessive suture material, poor technique
-monofilament sutures have lower incidence of disruption than braided sutures
-vitamin C deficiency: 8x increase in wound dehiscence
-zinc deficiency associated with poor healing
-steroids interfere with wound healing; use vitamin A to counteract these effects
-chemotherapeutic agents inhibit wound healing
-usually wait 1-2 weeks post-op before chemotherapy started
-radiation causes obliteration of small vasculature and fibrosis
Clinical Manifestations:
-salmon-coloured fluid draining from wound at 4th or 5th POD (85% of the time)
-depends on pt’s condition
-if no evisceration non-operative treatment with sterile occlusive wound dressing and binder
-evisceration moist sterile towels applied and pt returned to OR
-perioperative broad-spectrum antibiotics should be given
( **
-requires release of alpha-adrenergic receptors in SMC of bladder neck and urethra and parasympathetic stimulation
to contract bladder
-stress, pain, spinal anaesthesia, and various anorectal reflexes conspire to increase alpha-adrenergic stimulation
-if retention urinary catheter used
* *
-inadequate resuscitation: -sympathetics decreases renal blood flow; RAA system will shunt blood away
from afferent arterioles
-drug toxicity: aminoglycosides, vancomycin, amphotericin B, high doses of penicillin G or sulfonamides
-see Table 11-12 for other nephrotoxic drugs
Pathophysiology of Renal Dysfunction:
-BUN/Cr 20:1
-commonly observed with dehydration
-hepatorenal syndrome:
-two mechanisms: hypovolemia (type I) and maldistribution of blood flow (type II)
-Type I: deficiency in intravascular volume secondary to blockage of liver outflow ascites
-Type II: failing liver, elevated bilirubin, other stigmata of cirrhosis; CO and low PVR
-kidneys are normal; recovery is rare and depends on recovery of intrinsic liver disease
Intrinsic Damage:
-acute tubular necrosis:
-most common cause in surgical setting is renal perfusion d/t prolonged and sustained
hypotension (from sepsis, blood los, hypovolemia, dehydration, or myocardial infarction)
-kidney tries to maintain glomerular blood flow afferent dilatation and efferent
constriction of arterioles
-perceived hypoperfusion
angiotensin by RAA system afferent constriction
- sympathetics
norepinephrine afferent constriction
-this results in tubular ischemic and hypoperfusion of renal cortex ATN
-myoglobinuria and transfusion reaction (free Hb) may complicate renal injury
-other causes:
-radiocontrast dyes with dehydration
-atheromatous embolic during aortic vascular surgery
-clamping of renal artery
Postrenal Failure:
-ureteral clots or stones; BPH
Prevention of Acute Renal Failure:
-chronic UTI treat with Abx
-BPH TURP or balloon dilation
-chronic renal impairment ensure adequate hydration
-in low flow states, mannitol, bicarbonate, and diuresis induced by furosemide should be used
-mannitol increases renal corticla blood flow and produces an osmotic diuresis
-oliguria with u/o of 0.4-0.5 cc/kg/h in adult
-anuria: uncommon; usually from ATN as a result of renal artery thrombosis or obstructive uropathy
-fractional excretion of sodium (FENa) = [UNa / PNa] / [UCr/PCr]
-if > 1% intrinsic renal damage
-UNa < 10 mEq/L prerenal cause or intrinsic liver disease
-intrinsic UNa > 40 mEq/L, FENa > 3%
-if diagnosis is uncertain:
-volume challenge if suspect hypovolemia
-once adequate volume status established furosemide (20-40 mg) to improve u/o
-stop nephrotoxic drugs
-established renal failure:
-treat hyperkalemia: infusion of calcium, hypertonic dextrose solution, and insulin then resins
-maintenance of nutrition in patients with ATN: enterally or parenterally
-IV “Giordano-Giovannetti diet” of essential AA and hypertonic dextrose, with minimum
of fat, decreases mortality in patients with ATN
-dialysis for critical ionic excesses, volume overload, or BUN concentration > 80-100 mg/dl
-VC and FRC may be reduced after upper abdominal surgery (50-60% and 30% respectively)
-postoperative pain alters mechanics of respiration
-closing volume (lung volume at which airway closure is first detectable) decreases in the postoperative
-other physiologic causes of insufficiency: diffusion defects, abnormalities in V/Q, reduction in CO with
persistent shunt, alterations in Hb level and persistent shun, and shunting that is anatomic or related to
Predisposing Factors:
Cardiac dz:
-must abstain at least 8 weeks to achieve any demonstrable benefit
-must look at physiologic age rather than chronological age
-related to underlying pulmonary dysfunction characteristic of this patient population
-decreased FRC d/t chest wall compliance
-ensure adequate pain control
-use gastrostomy tube rather than NG found to statistically decrease incidence of
respiratory complications
-beware of pulmonary edema in CHF patiens
-collapse of alveoli resulting from anaesthesia, diaphragmatic dysfunction, postoperative incisional pain, and patient
-prevention is key:
-coughing and deep breathing, chest physiotherapy, incentive spirometry,
-intermittent positive pressure breathing, and CPAP
-medication for prophylaxis:
-expectorants: provide more liquid secretions
-detergents and mucolytic solutions: alter surface tension of secretions and render their elimination more
-bronchodilators: eliminate bronchospasm
-third most common nosocomial infection (after wound and UTI)
-pathogens include Psueudomonas, Serratia, Klebsiella, Proteus, Enterobacter, Streptococcus
-use of H2-blockers may breakdown acid barrier, allowing overgrowth and colonization of the stomach by intestinal
flora (gram negatives)
Clinical Manifestations:
-fever, productive cough, dyspnea, pleuritic chest pain, and purulent sputum
-if hypotensive, consider gram negative pneumonia
-cultures obtained via routine ETT suctioning have little predictive benefit in correctly identifying the
pathogen responsible for noscomial pneumonia
-empiric therapy with aminoglycoside and antipseudomonal penicillin initiated until definitive culture
results obtained (via BAL ideally)
-most likely setting is during emergency induction of anaesthesia, particularly in pts with GERD or hiatal hernia
Clinical Manifestations:
-presence of gastric contents in mouth followed by wheezing, hypoxia, bronchorrhea, and cyanosis
-CXR: progression of local damage and infiltration accute respiratory failure results
-causes chemical pneumonitis that results in bacterial colonization with subsequent development of
-prevention: empty stomach and neutralization of gastric contents
-suction then ETT to complete clearance of tracheobronchial tree
( %*
-pulmonary-capillary hydrostatic pressure exceeds plasma oncotic pressure
-most common causes: fluid overload or myocardial insufficiency secondary to MI
-others: sepsis, valvular dysfunction, neurogenic stimulation, and hepatic failure
-increased capillary permeability:
-sepsis, ARDS, acute pancreatitis
Clinical Manifestations:
-two peak phases:
-during resuscitation if too aggressive with fluid replacement
-post-operative when fluid mobilization occurs
-rales, distended neck veins, cyanosis, peripheral pitting edema
-CXR: vascular redistribution, septal lines (Kerley’s B lines), peribronchial and perivascular cuffing
-depends on inciting cause
-for overload:
-pulmonary catheter may aid diagnosis and management
-PAWP 18-25 mmHg; CI decreased with increased PVR
-if PAWP normal or low, look for other causes
-ECG look for evidence of pump failure
-treat with diuretics, IV nitroglycerin ( venous capacitance and preload)
-dobutamine or amrinone may improve cardiac output
-consider afterload reduction with nitroprusside if above maneuvers fail to produce a sufficient CI
( %
-fat embolism extremely common pathologic finding after trauma
-26% in patients with single fracture to 44% in patients with multiple fractures
-fat embolism syndrome with pulmonary dysfunction, coagulopathy, and neurologic disturbances associated with
increased circulating fat globules is ncommon
-long bone fractures with release of marrow fat into circulation
Clinical Manifestations:
-respiratory insufficiency
-CXR shows characteristic bilateral alveolar infiltrates
-may evolve into ARDS
-CNS involvement in 86% confusion and disorientation with eventual progression to coma
-characteristic petechial rash occurs in axillae, neck , and skin folds
-fat globules in urine not specific for fat embolism syndrome
-associated findings:
-unexplained drop in hct, thrombocytopenia, hypocalcemia, and hypoalbuminemia
-immobilize any long bone fracture
-early surgical fixation decreases incidence of pulmonary complications of fat embolism
-oxygenation and supportive measures
* *
( %
*# . $
-pt incapable of maintaining adequate oxygenation, adequate ventilation, adequate tissue delivery, or some
combination of these defects
-syndrome that includes:
-lung injury, acute in nature
-bilateral infiltrates on frontal chest radiograph
-PaO2/FIO2 < 200
-PCWP < 19 mmHg with no evidence of CHF
-may be due to specific single cause or may represent endpoint of a poorly understood pathway with a common final
denominator of lung damage and subsequent decompensation of oxygenation and ventilation
Etiology and Pathophysiology:
-abnormal cytokine response to injury:
-activation of complement cascade, activtionof thromboxane-leukotrienes pathway, disorders in
NO production, degranulation of neutrophils, production of increased permeability factors by
transudation of fluid and reactive materials into alveoli
-causes V/Q mismatch
-CXR shows “whiteout”; CT scan demonstrate regional changes in lung function
-volutrauma: maldistribution of inspired tidal volume secondary to PPV and the heterogeneous nature of
lung injury in ARDS
-overdistention of alveolus beyond its normal maximum
-reduce volutrauma:
-early use of PEEP adjusted to the inflection point (as seen on pressure-volume curve)
-pressure-limited ventilation with plateau pressures less than 35 cmH2O
-permissive hypercapnia
-use of inhalational NO
-PEEP has remained the mainstay of treatment of ARDS
-recruits collapsed alveolar units
-attenuates lung injury associated with PPV
-may prevent loss of FRC and prevent alveolar collapse at end-expiration
-permissive hypercapnia limits potentially detrimental effects of increased peak airway pressures, the
number of breaths necessary per minute, which reduces the risk of barotrauma and volutrauma
-inhalation of NO at mall doses has reduced pulmonary hypertension and improved oxygenation in a
variety of patients
-newer modalities using partial liquid ventilation (PLV) and perfluorocarbon-assisted gas exchange
-mortality from perioperative MI ranges from 54% to 89%
-presence of coronary artery disease: risk of perioperative MI increased from 0.1-0.7% to 1.1%
-patients over 40: infarction rate is 1.8%
-previous MI: infarction rate 27% (within 3 months); 11% (b/n 3 and 6 months); 5% (> 6 months)
Identification of the Patient at Risk:
-Goldman index
-look for cardiac signs, symptoms and risk factors
Clinical Manifestations:
-most cases occur on operative day or during first 3 PODs
-most important precipitating factor is shock risk of coronary thrombosis and myocardial ischemic
-chest pain only in 27% of patients b/c may be masked by narcotics
-may manifest as a sudden appearance of shock, dyspnea, cyanosis, tachycardia, arrhythmia, or CHF
-evaluate with ECG, serial cardiac enzymes, ABG (rule out respiratory causes)
-optimize CHF (digitalization for pts with enlarged hearts)
-treat anemia
-optimize fluid and electrolyte balance
-continue beta-blockers until morning of operation
-operation after 6 months of an MI
-regulation of BP important
-avoid hypoxia, hypotension, haemorrhage, dehydration, electrolyte disturbance and arrhythmias
-+/- monitoring in ICU
-pain relief: morphine and sedation
-+/- heparin, ASA; nitro and beta-blockers
-hypoxia relief: oxygen
-shock treated by vasopressor agents
-early emergency cardiac catheterization, angioplasty, or stenting may reverse an evolving MI
1( 1
-sinus tachycardia (not an arrhythmia) is the most common disturbance of rhythm, followed by PVC and sinoatrial
-intrinsic cardiac disease
-perioperative release of catecholamines d/t stress or pain
-organ manipulation that stimulates reflex response
-electrolyte abnormalities and metabolic disturbances:
-hypokalemia PACs and PVCs
-hyperkalemia conduction abnormalities
QT interval ventricular arhythmias
-hypercalcemia bardycardia and heart block
-cardiac medications:
-digitalis toxicity supraventricular-atrial flutter with varying block, PVCs, VT or VF
-antihypertensive meds sinus bardycardia or induction block
-anaesthetic agents:
-halothanes ventricular dysrhythmias
-parasympathetic stimulation (neostigmine, physostigmine, succinylcholine) bardycardia
-other factors:
-hypercapnia may suppress sinoatrial node function ectopic pacemaker or aberrant reentry
-thyrotoxicosis atrial fibrillation
Management of Preexisting Arrhythmias:
-digoxin for patients with supraventricular tachycardia
-reversible causes, such as electrolyte disturbances, drug toxicity, hypoxia, etc. should be controlled
-cardiac pacing for significant conduction defects:
-third degree AV block
-Mobitz II block
-sick sinus syndrome
Management of New-onset Arrhythmias:
-P waves present supraventricular origin
-variable morphology ectopic focus, MAT or SVT
-P waves absent A-fib
-QRS narrow supraventricular origin
-QRS wide ventricular origin or supraventricular with aberrant conduction, conduction block
-Acute tachyarrhythmias with hypotension cardioversion (100
-Symptomatic bradycardia 0.5mg atropine IV q5min to max of 0.04 mg/kg
-consider transcutaneous pacing
Sinus Tachycardia:
-find and treat cause: pain, hypovolemia, hypoxia, acidosis, sepsis, CHF, hypoperfusion, hypercapnia
Paraoxysmal Supraventricular Tachycardia:
-re-entry tachycardia
-rates between 150 and 250 bpm
-primary treatment with
-adenosine 6 mg IV; repeat with 12 mg after 1-2 min
-then verapamil 2-5 mg IV with second dose after 15-30 min
-may consider cardioversion
Atrial Fibrillation:
-lack of “atrial kick” may result in 10-15% decrease in cardiac output
-thyrotoxicosis, valvular heart disease, hypertension, CAD, PE, MI
-common after pneumonectomy
-cardioversion if hemodynamically unstable
-anticoagulate if long standing A-fib
-control rate (eg. with CCB, BB) and rhythm
Sustained Supraventricular Tachycardias:
-may be a result of digitalis toxicity
-obtain serum potassium and digitalis levels
Atrial Flutter:
-if unstable cardioversion
-digitalis used to maintain heart rate once controlled
Ventricular Tachycardia and Fibrillation:
-if pulseless precordial thump and immediate defibrillation at 200 J
-(review ACLS protocols)
( * *
Preoperative Hypertension:
-preoperative hypertension that is untreated or poorly controlled does increase the risk of perioperative
blood pressure lability, which may result in increased incidence of stroke, TIA, arrhythmias, post-op MI,
and possibly post-op renal failure
-postpone operation until hypertension controlled if:
-previous hypertension with diastolic pressure > 110
-new-onset hypertension
-sudden increases in hypertension
-recent deterioration in critical end-organ status
-delay operation in patients with mild or moderate hypertension with:
-ECG changes of MI or ischemic
-new-onset dysrhythmias
-emergence of LVH on ECG
-new onset or unstable angina
-CHF, whether established or new
-recent neurological deficit
-new onset of high-grade hypertensive retinopathy
-continue antihypertensive medications until day of operation
Postoperative Hypertension:
-systolic pressures > 200 mmHg result in bleeding from suture line, haemorrhagic cerebral infarction,
myocardial ischemic or infarction, and acute renal failure
-~ 80% of post-op HTN episodes occur within first 3 h of emergence form anaesthesia
-d/t ETT, inadequate analgesia, acute bladder distention, fluid overload
-tracheal stimulation, hypothermia, hypercapnia, hypoxemia
-if uncontrollable sodium nitroprusside or labetalol is given
-late post-op:
-d/t hypervolemia 2o fluid mobilization into intravascular space, inadequate analgesia, or failure to
resume previous antihypertensive medications
( *
Lupus Anticoagulant Factor (Anticardiolipin Syndrome):
-antibodies that interfere with in vitro PTT by prolonging phospholipid-dependent clotting factors
-increased risk of arterial and venous thrombosis
-patients normally do not require anticoagulation therapy
-those undergoing major procedures should receive prophylactic anticoagulation therapy and mechanical
Heparin-Induced Thrombocytopenia:
-form of consumptive platelet activation
-not dose dependent
-mechanism: autoantibody formation directed toward heparin and platelet surface antigens
-mild: occurs 2-4 days after heparin exposure
-severe: 6-12 days after exposure and associated with thrombosis
-arterial thrombosis common
-significant mortality rate
-phlegmasia cerulea dolens amputation rate up to 30%
-treatment: stop heparin; +/- surgical thrombectomy; Greenfield filter, anticoagulation with warfarin
1* *% 1
Antithrombin-III Deficiency:
-AT-III the most important inhibitor of coagulation
-inactivates thrombin, Xa, IXa, XIa, plasmin, kallikrein, XIIa
-deficiency is autosomal dominant
-recurrent thrombosis in 60%; pulmonary embolus in 40%
-treatment: heparin; if OR FFP to raise level of AT-III
Protein C Deficiency:
-Protein C: vit K-dependent inhibitor of procoagulant system
-inactivates V and VIII
-seen in 4-5% of patients < 45y with unexplained venous thrombosis
-deficiency is autosomal dominant: (CRM-: lack of protein; CRM+: dysfunctional protein)
-significant when serum activity < 70%
-treatment: warfarin
Protein S Deficiency:
-Protein S: vit K-dependent; produced by hepatocytes and megakaryocyte
-cofactor for Protein C
-significant when serum activity < 60%
-associated with high mortality related mainly of primary disease
-75% of pts are > 70y
-causes: poor oral hygiene, dehydration, use of anticholinergic agents, lack of oral intake
-staphylococci infection via probable transductal inoculation of parotid gland
-routes of spread for suppurative parotitis:
-downward into deep fascial planes of the neck
-backward into external auditory canal
-outward into skin of face
Clinical Manifestations:
-swollen tender parotid
-may progress rapidly to severe cellulitis on affected side of face and neck
-may require tracheotomy if airway compromised
-prophylaxis: adequate hydration, good oral hygiene
-start with broad spectrum Abx against staph; take C+S of pus
-surgical drainage; should not be delayed beyond 5th day
-mortality approximated 20%, but his was frequently related to the patient’s basic disease
3 7*
-small bowel normally does not manifest ileus post-op, because it continues to function throughout and after
-tube feedings may start almost immediately after operation
-if inflammation or several anastomoses in small bowel 24h ileus might be experienced
-gastric ileus: 24-48h
-colonic ileus: 3-5 days
-caused by:
-surgical manipulation, inflammation, peritonitis, blood in peritonem
-blood in retroperitoneum
-hypokalemia, hypocalcemia, hyponatremia, hypomagnesaemia
-opiates and phenothiazine
-correct underlying disorder, if any; mostly supportive treatment
-long tube decompression
-measure serum albumin prolonged ileus in hypoalbuminemic patients
-12.5g q8-12h to raise albumin > 3.0 mg/dL often results in return of bowel function
* &
General Considerations:
-factors that increase likelihood of anastomotic leakage:
-emergency procedures, poorly prepared patients, inadequately resuscitated patients, prolonged
intraoperative hypotension, hypothermia
-etiological factors: poor surgical technique, distal obstruction, inadequate proximal decompression
Duodenal Stump Blowout:
-disastrous complication with a high mortality
-complications: peritonitis, subhepatic abscess, pancreatitis, sepsis, establishment of an external fistula wit
fluid, and electrolyte abnormalities
-most likely to occur between 2nd and 7th POD
-adequate drainage required: incision below (R)CM and insertion of large sump catheter
-fluid and electrolyte therapy, TPN instituted
Intestinal Leaks and Fistulas:
Leaks: -fever, leukocytosis, unexplained ileus in absence of intestinal obstruction, complicated post-op course
-if patient is in jeopardy, sepsis uncontrolled, no effective drainage abdomen re-explored
-anastomosis must be resected and redone
-if hemodynamically unstable separation of both ends and diversion should be done
Fistula: -increased wound pain and redness/drainage on POD #4-5
-usually result from operations involving inflammatory bowel disease, cancer, or lysis of adhesions
-allow fistula to close spontaneously
Therapy of an Established Fistula:
-five phases: stabilization, identification and diagnosis, decision, operation, healing
1. Stabilization:
-resuscitation using crystalloids, RBC, and albumin
-Abx only if septic
-sump-type drain placed around skin; skin protected with Stomadheisve and ion exchange paste to keep
pH acidic and prevent activation of pancreatic enzymes that require basic pH
-TPN: 5-6% AA, 15-25% dextrose, 20% fat
-nutrition can be monitored with RBP, TBP, transferring
-enteral feeds may be attempted but they must be supplemented with TPN
2. Identification and Diagnosis:
-obtain fistulogram/sinogram
-degree of bowel continuity, size and depth of defect, presence of distal obstruction, nature of bowel
adjacent to fistula, presence of large abscess
-fistulas unlikely to close spontaneously:
-ileal, gastric, fistulas at ligament of Treitz
-total anastomotic disruption; partial disruption with adjacent abscess; lateral fistula with distal
obstruction; fistula in strictured intestine; end fistula with no distal communication
-local sepsis or systematic sepsis
-spontaneous closure usually within 5 weeks of adequate nutrition support in a patient w/o sepsis
3. Decision:
-somatostatin used to promote closure
-if short-turnover protein levels are increasing, the serum albumin concentration is approaching 3.0 g/dl,
and the patient is maintaining the albumin level without infusions of exogenous albumin, operation can
take place
-failure to maintain or increase in levels of transferring, retinol-binding protein, and thyroxin-binding
prealbumin indicative of mortality
4. Operation:
-mortality ~10-11% if operated during first 10 days or after 4 months; ~20% between 10 days and 4months
-resection and end-to-end anastomosis; protection with omentum onlay
-for duodenal fistula: vagotomy and gastrojejunostomy, feeding jejunostomy and gastrostomy, area of
fistula drained
-chronic pancreatic fistula:
-excise fistula down to pancreas, identify leak, distal pancreatectoy and splenectomy
-Roux-en-Y anastomosis can be used to provide internal drainage for the pancreatic fistula
5. Healing:
-feeding delayed 7-10 days
-difficulties eating:
-lack taste sensation: use zinc sulfate or lactate
-may be necessary to allow alcohol to induce eating
Colocutaneous Fistulas:
-fluid and electrolyte abnormalities and skin digestion are rare, but infectious complications are significant
-percuaneous drainage of intraabdominal abscesses and local care of wound infections
-antibiotics as indicated
-spontaneous closure likely
-persistence if sepsis, distal obstruction, anastomotic dehiscence, Crohn’s disease, or carcinoma present
-lack of spontaneous close by 5 weeks surgical repair
-resection of fistula and affected colonic segment with primary anastomosis and temporary
diversion of the fecal stream by colostomy
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-loss of pyloric valve that normally prevents hyperosmolar material from entering duodenum and small
-d/t pyloroplasty, pyloromyotomy, gastrojejunostomy, gastric resection, Billroth I or II anastomosis
-results in release of vasoactive substances:
-serotonin, bradykinin, substance P, peptides (VIP, pancreatic polypeptide, insulin, glucagon,
neurotensin, enteroglucagon)
-results in decreased plasma volume hypotension; hypokalemia
-early postprandial bloating, borborygmus, cramps, sensation of light-headedness, palpitations,
sweating, hypotension
-eating solids at meal and drinking liquids afterwards diminishes symptoms
-avoid carbohydrates which are more likely to provoke dumping
-in severe cases, long-acting octreotide may oppose some of the action of released peptides and ameliorate
the symptoms
-surgical treatments: conversion of BII to BI; 6 cm reverse loop of jejunum to slow transit of hypertonic
Postvagotomy Diarrhea:
-5-20% of patients have troublesome diarrhea post-truncal vagotomy
-dysmotility or dysfunction of small bowel motility stasis and overgrowth of bacteria,
malabsorption of fat, increased and incoordinate bile flow into small bowel
-treatment difficult:
-antibiotics have little success
-10-cm reversed jejunal loop 100 cm distal to ligament of Treitz has been advocated
Afferent Loop Syndrome:
-syndrome almost always occurs when the afferent loop is anastomosed to the greater curve after a BI
-obstruction of afferent loop from adhesions, kinking, intussusception, volvulus of afferent loop, stomal
ulcer, or obstruction of the efferent limb
-duodenal secretions increases in afferent loop regurgitated into stomach
-haemorrhagic pancreatitis or perforation can occur
-eating is regularly followed by RUQ epigastric distention and pain, borborygmus, and cramps
relieved by projectile vomitus of clear bile that is never mixed with food
-operation require for relief of these symptoms:
-afferent loop is anastomosed into Roux-en-Y efferent loop ~60 cm downstream to prevent reflux
of bile into stomach
-vagotomy to prevent marginal ulcer
Alkaline Reflux Gastritis:
-stomach sensitive to bile; eating associated with burning epigastric pain
-large amounts of bile emanating form afferent loop
-acute and chronic inflammation, evidence of decreased parietal cells, and increase in mucous-secreting
cells, and intestinalization of the gastric glands
-most effective treatment: cholestyramin and sucralfate
-if medically unmanageable: Tanner-19 procedure with vagotomy and long bile-containing loop
anastomosed 60 cm down stream
Nutritional Complications:
-fat malabsorption chronic nutritional deficiency, failure of absorption of fat-soluble vitamins, chronic
bile salt diarrhea
-iron and calcium absorbed primarily in duodenum
-after BII many pts hypocalcemic and iron-deficiency anemic
-loss of intrinsic factor monthly B12 injections required
-may require conversion of BII to BI
Recurrence of Disease:
-complications for ileostomies: ulcerative colitis 4%; Crohn’s disease 30%
-Crohn’s: granulomatous, ulcerations; peristomal fistulas
-ciprofloxacin and metronidazole should be initiated
-no point in resiting stoma recurrence will likely happen again
Stomal Necrosis and Retraction:
-necrosis or retraction superficial to fascia no immediate action required
-necrosis extends below fascia immediate laparotomy and reconstruction of stoma
-retraction below level of fascia immediate laparotomy to prevent further fecal contamination of
peritoneal cavity
Skin Complications:
-usually result of siting and inability to obtain appropriate seal around stoma
-Caraya powder, ion exchange paste, +/- nystatin powder and systemic fluconazole (if yeast) are helpful
-cellulitis requires antibiotics
Stomal Stricture:
-development of serositis in immediate postoperative period
-most common cause of stricture is necrosis or retraction, resulting in mucocutaneous separation, exposure
of the serosa, and subsequent serositis
-tx: stoma separated from skin, skin opening enlarged, new maturation performed
-if stricture at fascial level, fascial opening enlarged
Peristomal Hernias and Prolapse:
-prolapse occurs when there is vigorous peristalsis and insufficient fixation of bowel to underside of
anterior abdominal wall
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* /
* * *
-most common metabolic complication after surgery
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-may result in CNS damage, seizures and death
-secretion of ADH is more prolonged or more intense than after normal operative procedures
-if slight edema and [Na] ~125-130 fluid restriction is all that is required
-if CNS disturbance:
-symptoms not severe mannitol given slowly provokes diuresis of excess water secreted with
minimum of sodium; furosemide can be added
-if severe 3% saline; small increments 50-100 ml over 3-4 hours
-permanent CNS damage can occur if rapid correction of hyponatremia
-prevention: avoid overresuscitation of patients; limit free water
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%4* 2
Thyroid Storm:
-mortality of 10-20%
-occurs in patients with existing thyrotoxicosis that is unrecognized or uncontrolled
-any traumatic event, such as surgery, infection, or embolism, may complicate thyrotoxicosis and provoke
thyroid storm
-once hypotension supervenes, it is a preterminal event
-irreversible cardiac failure usually is the mode of death
-control of catecholamine-induced cardiac symptoms: propranolol IV 1mg/min to max of 10 mg
to control HR
-dobutamine may be necessary
-PTU 200 mg and KI 5-10 gtts given to decrease T3 and T4 release
-hydrocortisone 200 mg IV followed by 100 mg q8h diminishes thyroid hormone release
Myxedema Coma:
-pts with chronic hypothyroidism that is unrecognized or inadequately controlled; provoked by stress of
-inciting factors: trauma, infection, GIB, surgery, narcotics and phenothiazine
-warming, hydration, assisted ventilation
-L-thyroxine 300-500 mg IV then 50-100 mg/d
// * (
-d/t suppression of pituitary-adrenal axis by previous administration of steroids or destruction or exhaustion of
adrenal glands
-in patients with carcinoma, bilateral adrenal metastasis may occur
-unexplained hypotension, fever, abdominal pain, light-headedness, weakness, palpitations, mental status
changes, nausea, and vomiting
-lab findings:
-hypoglycemia, hyponatremia, occasionally hyperkalemia
-measure serum cortisol and initiate treatment
-hydrocortisone 200 mg IV
-hypotension should resolve in 1-2h if dx is correct
-400 mg hydrocortisone in divided doses over 24h should b given if hypotension not resolved
-most common cause is pre-existing liver disease
-cirrhosis, alcoholic hepatitis, fatty infiltration
-general anaesthesia should be avoided in patients with established liver dz:
-portal vein’s contribution is diminished and hepatic artery supplies at least 50% of hepatic flow
-splanchnic vasoconstriction of hepatic artery markedly decreases hepatic flow
-therefore, regional or epidural anaesthetic is preferred
-liver failure usually on 3rd or 5th POD
-somnolence, jaundice, u/o, ascites
-treatable reversible causes:
-hypovolemia, hypokalemia, hypomagnesaemia, GIB, constipation, remote infection
-must r/o SBP
-correct lytes, administration of neomycin, cathartic, or lactulose, and provision of nutritional support
-enteral feeds preferred:
-modified low aromatic, high branched-chain amino acid formulation
-hepatorenal syndrome type II can complicate hepatic failure; if liver does not recover post-op death
-delirium (20%), depression (9%), dementia (3%), functional psychosis (2%) of elderly post-op patients
Clinical Manifestations:
-manifestations are extremely variable
-delirium: occurs most commonly in elderly patients and those who are immobilized for long periods
-depressive reactions: pt characteristically uncooperative or recovery may be impeded by listlessness,
anorexia, and disinterest
-suicide a major risk in pts with depressive reaction
-paranoid psychotic disorder
-efforts should be directed at removing toxic causes of the acute brain syndrome, removing unnecessary
stimuli without isolating the patient, and providing psychologic or pharmacologic tranquillization
-consultation with psychiatry is indicated in the case of any acute and severe emotional disturbance
* *
/. *
-delirium usually follows operation within 48h but may be delayed
-hyperactivity with irritability, delusions, hallucinations, restlessness, and agitation
-cause is multifactorial
-Haldol 2-15 mg PO bid or 1-5 mg IV followed by 5-10 mg/h may help agitation
-prophylactic medication with lorazepam should be administered in the perioperative period to patients with severe
alcoholic histories who are candidates for DTs
.* *
-characteristically occurs late in the post-op period
-use of SSRIs are useful
-very yound gan old patients are particularly vulnerable to the development of psychiatric complications after
surgical treatment
Pediatric Surgery:
-severe anxiety states may be precipitated by the shock of operation
-emotional needs must be attended to
-maturity is important and decreases post-op anxiety reactions
Surgery in the Aged:
-more prone to become emotionally disturbed when confronted with new situations, esp. if inadequate
comprehension and generalized feeling of insecurity
Gynecologic and Breast Surgery:
-high incidence of depression, anxiety and sexual difficulties
-contact with other mastectomy patients expedites psychologic rehabilitation
-the more the procedure antedates menopause, the greater the likelihood of associated psychologic
disturbance (ie. hysterectomy)
Cancer Surgery:
-two major threats: disease and extensive surgical treatment
-depression is related to an anticipated interference with valued activities
-tendency toward seclusion, withdrawal, and nonparticipation
-depression frequent
Cardiac Surgery:
-serious psychiatric disturbances observed with considerable frequency afte mitral valvulotomy and openheart surgery
-manifestations usually after initial lucid interval of 3-5 days; resolve shortly after transfer from CICU to
-postoperative incapacitation and increased time on heart-lung machine are factors increasing the
likelihood of delirium ?organic brain damage from operation
Dialysis and Transplantation:
-suicide rate is 300 times greater in dialysis and transplantation patients
-uraemia, debilitating disease, and the undergoing of repeated procedures are contributing factors