! "

!
"
-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
complications
-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
.
3
2 * 2
$
4
Pathophysiology:
-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
Management:
-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
Ketoacidosis:
-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)
!
Pathophysiology:
-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
dysrhythmia
-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:
-thrombophlebitis
-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
5
5
.
%
4
/*
Predisposing Factors:
-staphylococcus aureus most frequently involved offending organism
-enteric organisms in bowel surgery; other less common pathogens: enterococci, Psedomonas, Proteus,
Klebsiella
-hemolytic strep responsible for 3% of wound infections
Classification of Operative Wounds
Class
Wound Description
I
Clean
Nontraumatic, uninfected operative wounds
in which the respiratory, alimentary, or
genitourinary tract is not entered. Usually
closed without drains
1.5-3.9%
II
Clean-contaminated
Respiratory, alimentary, or genitourinary
tract is entered with only minimal
contamination
3-4%
III
Contaminated
Fresh traumatic wounds; wounds with a
major break in sterile technique; wounds
encountering non-purulent inflammation;
wounds made in or near contaminated skin
7.4-8.5%
IV
Dirty
Purulent infection is encountered
28-40%
Factors: -type of operative wound
-age:
-diabetes:
-steroids:
-obesity:
-remote infection
-duration of operation:
-malnutrition
-others (see Table 11-9)
Examples
Incidence of
Infection
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%)
Prevention:
-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
Management:
-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
5
%
*
-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
5
% *
-lymph collections
-aspiration and pressure dressings
-continuous closed-suction drainage
5
% . *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)
Treatment:
-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
4
4
( **
-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
* *
*
Etiology:
-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:
Prerenal:
-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)
-mechanism:
-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
Manifestations:
-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%
Management:
-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
4
Pathophysiology:
-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
period
-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
atelectasis
Predisposing Factors:
Smoking:
Age:
Obesity:
COPD:
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
positioning
-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
likely
-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
Management:
-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
pneumonia
Management:
-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
Management:
-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
-?ARDS
-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
2
( %
*
-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
Pathophysiology:
-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
Management:
-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
macrophages
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
Management:
-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
(PAGE)
.
4(
4
%
/
-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)
Management:
-pre-operative:
-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
-intra-operative:
-regulation of BP important
-avoid hypoxia, hypotension, haemorrhage, dehydration, electrolyte disturbance and arrhythmias
-treatment:
-+/- 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
arrhythmia
Etiology:
-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
-hypocalcemia
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
mechanisms
-thyrotoxicosis atrial fibrillation
-pheochromocytoma
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:
-ECG:
-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
360J)
-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
-causes:
-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
3
6
*%
( *
2*
*
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
prophylaxis
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
2
.
%*
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
Management:
-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
Prognosis:
-mortality approximated 20%, but his was frequently related to the patient’s basic disease
4
*
%
3 7*
2
-small bowel normally does not manifest ileus post-op, because it continues to function throughout and after
operation
-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
-treatment:
-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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*
Dumping:
-loss of pyloric valve that normally prevents hyperosmolar material from entering duodenum and small
bowel
-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
-symptoms:
-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
solution
Postvagotomy Diarrhea:
-5-20% of patients have troublesome diarrhea post-truncal vagotomy
-factors:
-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
gastrectomy
-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
-symptoms:
-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
4
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3
4
* /
* * *
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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
-management:
-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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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
-tx:
-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
operation
-inciting factors: trauma, infection, GIB, surgery, narcotics and phenothiazine
-tx:
-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
-symptoms:
-unexplained hypotension, fever, abdominal pain, light-headedness, weakness, palpitations, mental status
changes, nausea, and vomiting
-lab findings:
-hypoglycemia, hyponatremia, occasionally hyperkalemia
-tx:
-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
8*
*
-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
-tx:
-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
4
-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
Management:
-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
.*
* *
%
1*
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-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
ward
-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