Perioperative & Orthopaedic Medicine: Preventing Dangerous Blood Clots

1. 1. 1. Thromboprophylaxis‌ 2. #### Thromboembolic disease
2. Common orthopaedic complication
3. Thrombosis: clotting at improper site
4. Embolism: clot that migrates
5. Most clinically silent but can be fatal
6. Complications of thromboembolic disease:
7. Postthrombotic syndrome: chronic venous insufficiency
8. Venous hypertension (HTN)
9. Chronic skin issue with swelling, pain
10. Pigmentation, induration, ulceration
11. Recurrent deep venous thrombosis (DVT): risk four to eight times higher after first DVT
12. Pulmonary embolism (PE)
13. Pathophysiology (Virchow triad) ( Fig. 1.51)
14. Endothelial damage: trauma or surgery
15. Exposes collagen—triggers platelets
16. Platelets—three roles:
17. Adhesion and activation
18. Secretion of prothrombotic mediators
19. Aggregation of many platelets
20. Stasis: allows bonds of clotting proteins and cells
21. Immobility: pain, stroke, paralysis
22. Blood viscosity: polycythemia, cancer, estrogen
23. Decreased inflow: tourniquet, vascular disease
24. Decreased outflow: venous scarring, CHF
25. Hypercoagulability
26. Clotting cascade’s final product is thrombin
27. Converts soluble fibrinogen to insoluble fibrin
28. Risk factors and epidemiology
29. Reported risks of thromboembolic disease vary by:
30. Definitions: asymptomatic versus symptomatic
31. Location
32. Distal: those below popliteal space have very low PE risk
33. Proximal: those above popliteal space have higher PE risk
34. Patient-specific risks factors ( Fig. 1.52)
35. Prior thromboembolic disease a strong risk factor
36. Risk increases exponentially with age (>40 years) ( Fig. 1.53)
37. Genetic factors—thrombophilias
38. Decreased anticlotting factors
39. Antithrombin III, protein C, protein S deficiencies

40. Increased clotting factors or factor activity

41. Factor V Leiden

42. Mutated factor V not inactivated as effectively by activated protein C, so clotting process remains active for longer than normal

43. Elevated factor VIII
44. Hyperhomocysteinemia
45. Prothrombin G20210A (factor II mutation)
    
    
    FIG. 1.51 Left, Electromicrograph panel (A through E). (A) Scanning electron micrograph (SEM) of free platelets. (B) SEM of platelet adhesion. (C) SEM of platelet activation. (D) Transmission electron micrograph of aggregating platelets. 1, Platelet before secretion; 2 and 3, platelets secreting contents of granules; 4, collagen of endothelium. (E) SEM of fibrin mesh encasing colorized red blood cells. Right, Illustration panel (A through H) showing venous thromboembolus formation. (A) Stasis. (B) Fibrin formation. (C) Clot retraction. (D) Propagation. (E–H) Continuation of this process until the vessel is effectively occluded.
    From Miller MD, Thompson SR, editors: DeLee and Drez’s orthopaedic sports
    medicine: principles and practice, ed 4, Philadelphia, 2014, Saunders; platelet electron micrographs courtesy James G. White, MD, Department of Laboratory Medicine and Pathology, University of Minnesota School of Medicine; Miller MD
    et al: Review of orthopaedics, ed 6, Philadelphia, 2012, Saunders; and Simon SR, editor: Orthopaedic basic science, Rosemont, IL, 1994, American Academy of Orthopaedic Surgeons, p 492.
    
    FIG. 1.52 Genetic (primary) disorders (table on lef t) and secondary hypercoagulable states (figure on right ).
    Data from Ginsberg MA: Venous thromboembolism. In Hoffman R et al, editors: Hematology: basic principles and practice, ed 4, Philadelphia, 2005, Churchill Livingstone, pp 2225–2236; Perry SL, Ortel TL: Clinical and laboratory evaluation of thrombophilia, Clin Chest Med 24:153–170, 2003; and Schafer AI: Thrombotic disorders: hypercoagulable states. In Goldman L, Ausiello D, editors: Cecil textbook of medicine, ed 22, Philadelphia, 2004, Saunders, pp 1082–1087.
    
    FIG. 1.53 Top, The three primary influences of thromboembolic disease (Virchow triad). Bottom, The relative risks of various patient conditions; note that age has an exponentially increasing risk.
    Composite from Miller MD, Thompson SR, editors: DeLee and Drez’s orthopaedic sports medicine: principles and practice, ed 3, Philadelphia, 2014, Saunders; and data from Anderson FAJr et al: Apopulation-based perspective of the hospital incidence and case-fatality rates of deep vein thrombosis and pulmonary embolism. The Worcester DVT Study, Arch Intern Med 151:933–938, 1991.
46. Procedure-specific factors ( Fig. 1.54)
47. PE risk lower with distal procedures versus hip procedures
48. Risk higher with longer procedures
49. Total knee arthroplasty (TKA) has higher total DVT risk but lower PE risk
50. Risk with hip fracture is higher than that with THA.
51. Diagnosis
52. Clinical diagnosis favors assessment of risk factors.
53. Physical exam is unreliable: most cases are asymptomatic.
54. DVTs can cause calf pain, palpable cords, swelling.
55. 50% with classic signs have no DVT according to studies
    
    --- FIG. 1.54 Rates of symptomatic thromboembolism in orthopaedic sports medicine. From DeHart M: Deep venous thrombosis and pulmonary embolism. In Miller MD, Thompson SR, editors: DeLee and Drez’s orthopaedic sports medicine: principles and practice, ed 4, Philadelphia, 2014, Saunders, p 207.
56. 50% with venogram positive for clo t have normal physical findings
57. PEs: most asymptomatic
58. Signs/symptoms include pleuritic chest pain, dyspnea, tachypnea
59. Saddle emboli can manifest as death.
60. Laboratory studies
61. D -dimer studies not helpful after injury/surger y but negative result rules out significant clot.
62. ECG: rule out MI
63. Nonspecific findings; most common finding is sinus tachycardia.
64. Radiologic studies ( Fig. 1.55)
65. Venogram—best for distal (below popliteal) lesions (clinical relevance?)
66. Duplex compression ultrasound—most practical
67. Noninvasive, easily repeatable bedside test
68. Finding of “noncompressible vein ” about 95% sensitive/specific
69. Guidelines strongly against routin e duplex screening
70. Chest x-ray
71. Early findings: usually normal, “oligemia,” or prominent hilum ( Fig.
    1.56B)
72. Late findings: wedge or platelike atelectasis (see Fig. 1.56C)
73. Spiral CT angiography—best for suspected PE
74. Ventilation-perfusion (
    
    ) scan—most helpful for dye-sensitive patients
75. Thromboembolic prophylaxis
76. Preventing DVTs has been shown to be possible, although whether such prevention avoids death is unproven.
77. Guidelines vary in their recommendations ( Fig. 1.57).
78. Prophylaxis recommended for all patients undergoing arthroplasty.
79. Those undergoing THA may benefit from extended treatment (≈30 days).
80. For patients without risk-related conditions, prophylaxis is not recommended for
81. Upper extremity procedures, arthroscopic procedures, surgery for isolated fractures at knee and below
82. Mechanical measures
83. Early mobilization
84. Graduated elastic hose—not sufficient alone
85. Intermittent pneumatic compression devices (IPCDs)
86. Stimulate fibrinolytic system
87. Low bleeding risks
88. Grade IC by 2012 American College of Chest Physicians (ACCP) guidelines
89. Continuous passive motion (CPM) of no benefit
90. Pharmacologic prophylaxis:
91. Surgical Care Improvement Project (SCIP) quality measures require DVT prophylaxis.

92. Aspirin

93. Irreversibly binds and inactivates COX in platelets, thereby reducing thromboxane A 2

94. Weakest: Use of IPCD encouraged
    
    
    FIG. 1.55 Top left to right, Venogram showing deep vein thrombosis). Intraluminal filling defects (arrows) seen on two or more views of a venogram.
    The left and middle images are at the knee, and the right image is at the hip. Middle , Doppler ultrasound for proximal DVT in femoral vein thrombosis. (A) Longitudinal view shows presence of flow ( light blue ) in the more superficial vein over an occlusive thrombus ( dark gray ). (B) A transverse view without compression shows an open superficial vein, appearing as a black oval ( white arrow ) and a thrombosed deeper vein
    as a dark gray circle with an echogenic center ( red arrow ). (C) A transverse view with compression shows the flattened compressible superficial vein ( white arrow ) and the unchanged noncompressible thrombosed deeper vein ( red arrow ). Bottom left, Spiral CT pulmonary angiography. (A) Large pulmonary embolism ( arrows ). (B) Normal CT. Right images, high probability
    
    scan showing full lung fields on ventilation scan (upper) and multiple areas lacking tracer on the perfusion scan (lower) . ant, Anterior; LAO, left anterior oblique; post, posterior; RPO, right posterior oblique. DVT panel from Jackson JE, Hemingway AP: Principles, techniques and complications of angiography. In Grainger RG, editor: Grainger & Allison’s diagnostic radiology: a textbook of medical imaging, _ed 4, Philadelphia, 2011, Churchill Livingstone. Original images courtesy Austin Radiological Association and Seton Family of Hospitals.
    
    --- FIG. 1.56 Chest radiographs. (A) Diffuse bilateral fluffy patchy infiltrates, worse at bases, are consistent with ARDS (acute respiratory distress syndrome). (B) A focal area of oligemia in the right middle zone (Westermark sign [_white arrow ]) and cutoff of the pulmonary artery in the upper lobe of the right lung are both seen with acute pulmonary embolism. (C) The peripheral wedge-shaped density without air bronchograms at lateral right lung base (Hampton hump [ black arrow ]) develops over time after a pulmonary embolism. B from Krishnan AS, Barrett T: Images in clinical medicine: Westermark sign in pulmonary embolism, N Engl J Med 366:e16, 2012; C from Patel UB et al: Radiographic features of pulmonary embolism: Hampton hump, Postgrad Med J 90:420–421, 2014.
    
    --- FIG. 1.57 Recommendations on prevention of VTE in hip and knee arthroplasty. Hx, history; US, ultrasonography. 3. Low bleeding risk: Should be considered for patients at higher risk for bleeding.
95. Warfarin (Coumadin)
96. Prevents vitamin K γ-carboxylation in liver
97. Inhibits factors II, VII, IX, X, and proteins C and S
98. Vitamin K and fresh frozen plasma can reverse
99. Multiple reactions with drugs and diet
100. Must be monitored with international normalized ratio (INR; goal, 2–3)

101. Heparin

102. Activates antithrombin III (ATIII), which then inactivates factor Xa and thrombin

103. Protamine sulfate can reverse
104. Short half-life: 2 hours
105. High bleeding rate in arthroplasty
106. Binds platelets—heparin-induced thrombocytopenia
107. Low-molecular-weight heparin (LMWH)
108. Reversibly inhibits factor Xa through ATIII and factor II
109. Protamine sulfate can reverse
110. No monitoring needed
111. Less heparin-induced thrombocytopenia
112. Higher risk for bleeding than with
     warfarin

113. Fondaparinux

114. Irreversibly but indirectly inhibits factor X through ATIII

115. Synthetic pentasaccharide
116. No monitoring
117. No antidote
118. Higher risk for bleeding than with LMWH

119. Rivaroxaban

120. Direct Xa inhibitor

121. Oral drug
122. Higher risk for bleeding than with LMWH
123. Hirudin
124. Direct thrombin (IIa) inhibitor
125. Intramuscular and oral (dabigatran) versions
126. No antidote
127. Inferior vena cava (IVC) filter use: controversial
128. Should be considered in following conditions:
129. Contraindication to prophylaxis
130. Cerebral bleed/trauma
131. Spine surgery
132. Prior complication of prophylaxis
133. Treatment of thromboembolic disease
134. Pharmacologic treatment
135. Prolonged therapy often recommended
136. Approximately 3 months after DVT, approximately 12 months after PE
137. Early mobilization— no bed rest
138. Risk of dislodgment less than risk of more clots in these high-risk patients
139. Graduated elastic compression hose for 2 years
140. May prevent postthrombotic syndrome
141. Thrombolytics, thrombectomy, embolectomy controversial
142. Special venous thromboembolism (VTE) situations
143. Isolated calf thrombosis smaller than 5 cm rarely needs treatment.
144. Follow with serial ultrasound scans.
145. Upper extremity blood clot in athlete
146. “Effort thrombosis” (Paget-Schroetter syndrome)
147. Axillary–subclavian vein thrombosis
148. Complaints
149. Pain, swelling
150. Dilated veins
151. Feeling of heaviness
152. Diagnosis: duplex ultrasound
153. Treatment: thoracic outlet decompression should be considered

Perioperative Disease and Comorbidities

1. Orthopaedic surgeons who evaluate their patients with care preoperatively can be rewarded with fewer perioperative problems.

2. Goals include finding correctable issues and identifying risks to provide accurate risk/benefit assessment for proper consent.

3. Cardiac issues

4. Coronary artery disease (CAD): leading cause in those older than 35 years
5. Leading cause of cardiac death in young sports population: hypertrophic cardiomyopathy
6. American College of Cardiology/American Heart Association (ACC/AHA) elements for assessing risk
7. Clinical risk factors in perioperative cardiac risk
8. Major predictors
9. Unstable/severe angina, recent MI (<6 weeks)
10. Worsening or new-onset CHF
11. Arrhythmias
12. Atrioventricular (AV) block
13. Symptomatic ventricular dysrhythmia: bradycardia (<30
    beats/min), tachycardia (>100 beats/min)
14. Severe aortic stenosis or symptomatic mitral stenosis
15. Other
16. Prior ischemic heart disease
17. Prior CHF
18. Prior stroke/ TIA
19. Diabetes
20. Renal insufficiency (creatine >2 mg/dL)
21. Functional exercise capacity—measured in metabolic equivalents (METs)
22. MET: 3.5 mL O2 uptake/kg/min
23. Perioperative risk elevated if unable to meet 4-MET demand
24. Walk up flight of steps or hill (= 4 METs)
25. Heavy work around house (>4 METs)
26. Can patient walk four blocks or climb two flights of stairs?
27. Surgery-specific risk:
28. High risk (>5% risk of death/MI)
29. Aortic, major or peripheral vascular procedures

30. Intermediate risk (1%–5% risk of death/MI)

31. Orthopaedic, ENT, abdominal/thoracic or procedures

32. Low risk (<1% risk of death/MI)—usually do not need further clearance

33. Ambulatory surgery, endoscopic or superficial procedures

34. Shock

35. Twelve-lead ECG if:
36. CAD and intermediate-risk procedure
37. One clinical risk factor and intermediate-risk procedure
38. Noninvasive evaluation of left ventricular function if:
39. Three or more clinical risk factors and intermediate-risk procedure
40. Dyspnea of unknown origin
41. CHF with worsening dyspnea without testing in 12 months
42. β-Blockers and statins should be continued around the time of surgery.
43. Acetylsalicylic acid (ASA) should be stopped 7 days prior to surgery.
44. Cardiology consultation should be considered for patients taking other agents (clopidogrel, prasugrel).
45. Risk of stent thrombosis balanced with that of surgical bleed
46. Cardiovascular collapse with hypotension, followed by impaired tissue perfusion and cellular hypoxia. May be a result of orthopaedic pathology or a complication of surgery.
47. Metabolic consequence
48. O2 is unavailable—no oxidative phosphorylation
49. Cells shift to anaerobic metabolism and glycolysis
50. Pyruvate is converted to lactate—metabolic acidosis

51. Lactate—indirect marker of tissue hypoperfusion

52. Best measures of adequate resuscitation

53. Clinical measure of organ function: urine output more than 30 mL/h

54. Laboratory measure: serum lactate less than 2.5 mg/dL

55. Types of shock
56. Neurogenic shock
57. High spinal cord injury (also anesthetic accidents)
58. Loss of sympathetic tone and of vasomotor tone of peripheral arterial bed
59. Bradycardia, hypotension, warm extremities
60. Treatment: vasoconstrictors and volume
61. Septic shock (vasogenic)
62. Number one cause of ICU death
63. Mortality 50%
64. Bacterial toxins stimulate cytokine storm.
65. Examples: gram-negative lipopolysaccharides
66. Toxic shock superantigen
67. Inflammatory mediators cause endothelial dysfunction and peripheral vasodilation
68. Treatment
69. Cardiogenic shock
70. Bad pump
71. Identification and treatment of infections
72. Prompt resection of dead tissue
73. Appropriate antibiotics
74. Extensive MI, arrhythmias
75. Blocked pump (obstructive shock)
76. Massive “saddle” pulmonary embolism
77. Tension pneumothorax
78. Decreased lung sounds, hypertympany, tracheal deviation
79. Treated with needle decompression followed by tube thoracostomy
80. Cardiac tamponade
81. Beck triad: hypotension, muffled heart sounds, neck vein distension
82. Hypovolemic shock
83. Pulsus paradoxus
84. Decreased systolic BP with inspiration
85. Treatment: pericardiocentesis
86. Most common shock of trauma
87. Volume loss from bleeds or burns
88. “Third spacing” also a cause
89. Neuroendocrine response: save heart and brain
90. Peripheral vasoconstriction
91. BP may be normal
92. Pale, cold, clammy extremities
93. Percentage of blood loss key to symptoms/signs
94. Class I: up to 15% blood volume loss
95. Vital signs can be maintained.
96. Pulse below 100 beats/min
97. Class II: 15%–30% blood volume loss
98. Tachycardia (>100 beats/min), orthostatic
99. Anxious
100. Increased diastolic BP
101. Class III: 30%–40% blood volume loss
102. Decreased systolic BP
103. Oliguria
104. Confusion, mental status changes
105. Class IV: more than 40% blood volume loss
106. Life threatening; patient is obtunded
107. Narrowed pulse pressure
108. Immeasurable diastolic BP
109. Treatment

110. Perioperative pulmonary issues

111. First, ABCs of resuscitation: then, bleeding must be stopped.
112. Blood products make better resuscitation fluids than saline.
113. Higher in cases that involve thorax such as scoliosis
114. Highest in patients with prior disease
115. Spinal/epidural anesthesia favored over general
116. Medical treatment should be maximized around surgery.
117. COPD
118. Symptomatic COPD: anticholinergic inhalers (ipratropium)
119. May require corticosteroids
120. Asthma
121. Presence of wheezes or shortness of breath: β-agonist inhalers (albuterol)
122. Perioperative oral steroids safe
123. Systemic glucocorticoid should be considered if forced expiratory volume in 1 minute (FEV1) or peak expiratory flow rate (PEFR) is below 80% predicted values/personal best.
124. Postoperative atelectasis
125. Like the associated cough, the workup is usually nonproductive.
126. Deep breathing/incentive spirometry—equally effective
127. Postoperative pneumonia takes up to 5 days to manifest.
128. Productive cough, fever/chills, increased WBC count
129. Radiograph: pulmonary infiltrates
130. Smoking cessation improves outcomes
131. Patients should stop 6–8 weeks preoperatively.
132. Nicotine supplements do no harm to wound.
133. Fewer pulmonary complications
134. Smokers have six times more pulmonary complications.
135. Fewer wound healing issues and wound infections
136. Lower nonunion rate
137. Shoulder, neck, and thoracic pain in smokers
138. Prompts careful evaluation of lung fields

139. Superior sulcus tumor (Pancoast tumor)

140. Acute respiratory distress syndrome (ARDS)

141. Intrinsic atrophy of hand—C8–T1

142. Pulmonary failure due to edema (see Fig. 1.56A)
143. Pathophysiology
144. Complement pathway activated
145. Increased pulmonary capillary permeability
146. Intravascular fluid floods alveoli
147. Results
148. Hypoxia, pulmonary HTN
149. Right heart failure
150. 50% mortality
151. Etiology
152. Blunt chest trauma, aspiration, pneumonia, sepsis
153. Shock, burns, smoke inhalation, near drowning
154. Orthopaedic: Long-bone trauma
155. Clinical symptoms
156. Tachypnea, dyspnea, hypoxia, decreased lung compliance
157. PaO 2 /FIO 2 ratio below 200
158. Imaging
159. Radiographs: diffuse bilateral infiltrates, “snowstorm”
160. CT: ground glass appearance
161. Treatment
162. Prompt diagnosis and treatment of musculoskeletal infections
163. Prompt treatment of long-bone fractures
164. Ventilation with positive end-expiratory pressure (PEEP)
165. 100% O2

166. Fat emboli syndrome—classic clinical triad

167. Petechial rash: fat to skin
168. Neurologic symptoms: fat to brain
169. Mental status changes: confusion, stupor
170. Rigidity, convulsions, coma
171. Pulmonary collapse: fat showers lung
172. ARDS: hypoxia, tachypnea, dyspnea
173. Associated with long-bone fractures

174. Bleeding and blood products

175. Bleeding complications can be avoided through preoperative identification of risk.
176. Common inherited bleeding disorders
177. Von Willebrand disease: autosomal dominant
178. Most common genetic coagulation disorder
179. Von Willebrand factor dysfunction
180. Binds platelets to endothelium
181. Carrier for factor VIII
182. Treatment: desmopressin

183. Hemophilia A (VIII): X-linked recessive

184. Hemophilia B (IX) Christmas disease: X-linked recessive
185. Medicines/supplements that should be stopped prior to surgery
186. Platelet-inhibitor drugs (aspirin, clopidogrel, prasugrel, NSAIDs)
187. Drugs that cause thrombocytopenia
188. Penicillin, quinine, heparin, LMWH
189. Anticoagulants (see earlier discussion on DVT)
190. Supplements
191. Fish oil, omega-3 fatty acids, vitamin E
192. Garlic, ginger, Ginkgo biloba
193. Dong quai, feverfew
194. Diseases associated with increased bleeding
195. Chronic renal disease—uremia causes platelet dysfunction
196. Chronic liver failure—decreased liver proteins of clotting cascade
197. Techniques to avoid blood loss at surgery
198. Tourniquets: tissue effect relates to time and pressure
199. Used no longer than 2 hours
200. Time to restoration of equilibrium
201. 5 minutes after 90 minutes of use
202. 15 minutes after 3 hours
203. Prolonged use can cause tissue damage.
204. Nerve damage compressive (not ischemic)
205. Electromyography: subclinical abnormalities in 70% with routine use
206. Slight increase in pain
207. Wider tourniquets distribute forces
208. Pad underneath prevents skin blisters in TKA
209. Lowest pressure needed for effect should be used
210. 100–150 mm Hg above systolic BP
211. 200 mm Hg upper extremity
212. 250 mm Hg lower extremity
213. Tranexamic acid
214. Synthetic lysine analogue; acts on fibrinolytic system
215. Competitive inhibitor of plasminogen activation
216. Reduces blood loss with no increase in DVT.
217. Temperature
218. Mild hypothermia increases bleeding time and blood loss.
219. Intraoperative “cell saver” may be cost-effective if:
220. About 1000 mL of blood loss is expected
221. Recovery of 1 or more unit of blood is anticipated.
222. Techniques not yet found to be effective or cost-effective
223. Bipolar sealant, topical sealants, autologous donation
224. Reinfusion systems, routine transfusions over 8 g/dL Hb
225. Preoperative techniques to address anemia
226. Oral iron 30–45 days preoperatively
227. Vitamin C increases iron absorbtion
228. Folate and vitamin B12 deficiency also a source of anemia
229. Erythropoietin if preoperative Hb below 13
230. Transfusions
231. Ratio of 1:1:1 blood product resuscitation is superior to saline fluid
232. Preoperative Hb most significant predictor of need
233. Various guidelines for when to transfuse
234. Hb less than 6 g/dL: transfusion
235. Hb 7–8 g/dL: transfusion of postoperative patients
236. Hb 8–10 g/dL: transfusion of symptomatic patients
237. Restrictive transfusion strategies
238. Lower 30-day mortality trend
239. Lower infection risk trend
240. Greatest benefits to orthopaedic patients
241. No difference in functional recovery
242. Transfusions risks
243. Leading risk: transfusion of wrong blood to patient
244. Occurs in 1 in 10,000 to 1 in 20,000 RBC units transfused
245. Transfusion reactions
246. Febrile nonhemolytic transfusion reaction
247. Most common
248. 1–6 hours post-transfusion
249. From leukocyte cytokines released from stored cells
250. Leukoreduction decreases incidence
251. Acute hemolytic transfusion reaction
252. Medical emergency
253. ABO incompatibility
254. IgM anti-A and anti-B,
     which fix complement
255. Rapid intravascular hemolysis
256. Classic triad: fever, flank pain, red/brown urine (rare)
257. Can cause disseminated intravascular coagulation (DIC), shock, and acute renal failure (ARF) due to acute tubular necrosis (ATN)
258. Positive direct antiglobulin (Coombs) test result
259. Delayed hemolytic transfusion reactions
260. Reexposure to previous antigen (i.e., Rh or Kidd)
261. History of pregnancy, prior transfusion, transplantation
262. 3–30 days post-transfusion
263. Anemia, mild elevation of unconjugated bilirubin, spherocytosis
264. Anaphylactic reactions: about 1 in 20,000
265. Rapid hypotension, angioedema
266. Shock, respiratory distress
267. Frequently involve anti-IgA and IgE antibodies
268. Treatment: cessation of transfusions, ABCs of resuscitation, epinephrine
269. Urticarial reactions: about 1%–3%
270. Mast cell/basophils release of histamine—hives
271. Infectious risks
272. Bacterial: 0.2 per million packed red blood cell (PRBC) units transfused
273. Gram-positive organisms
274. Cryophilic organisms: Yersinia, Pseudomonas
275. HTLV—approximately 1 in 2 million

276. Renal and urologic issues

277. HIV—approximately 1 in 2 million
278. Hepatitis C—approximately 1 in 2 million
279. Hepatitis B—approximately 1 in 250,000
280. ARF (acute kidney injury [AKI])
281. Edema, HTN, urinary output less than 30 mL/hour (<0.5 mL/kg/h)
282. Laboratory findings: creatinine increased over 1.5 times baseline
283. Hyperkalemia can be fatal.
284. For blood potassium level more than
     5.5 mmp/L, dialysis should be considered.
285. Prerenal renal failure (most common ARF): decreased kidney perfusion
286. Hypovolemia/hypotension from blood loss
287. Intrinsic renal failure
288. ATN: most frequent intrinsic ARF
289. Ischemia, sepsis, nephrotoxic drugs
290. Myoglobin from rhabdomyolysis
291. Acute interstitial nephritis (AIN): fever, eosinophils in blood/urine
292. Glomerular disease: hematuria, proteinuria, HTN, edema
293. SLE, poststreptococcal, IgA nephropathy, hepatorenal
294. Postrenal ARF: obstruction
295. Chronic kidney disease (CKD)
296. Definition: GFR below 60 mL/min per 1.73 m2 or urine albumin loss greater than 30 mg/day
297. Retained phosphate and secondary to hyperparathyroidism
298. Causes increased extraskeletal calcification
299. High perioperative complications
300. Increased cardiovascular risk
301. Hyperkalemia and fluid adjustments
302. Increased bleeding complications
303. Poor BP control
304. Higher infection rates
305. Higher complications/revisions
306. Higher morbidity
307. Perioperative urinary retention
308. Outflow obstructions: benign prostatic hypertrophy (BPH) in men (common)
309. Bladder muscle (detrusor) compromise
310. Overdistention
311. Excess fluid/long procedures
312. Neurogenic
313. Spinal trauma, tumor, stroke, diabetes
314. “Neurogenic” atonic bladder
315. Medications
316. Anticholinergic and sympathomimetic drugs
317. Opioids, antidepressants, pseudoephedrine, diphenhydramine
318. Can cause postrenal ARF (AKI)
319. Associated with higher rates of urinary tract infections
320. Increased 2-year mortality after hip fracture
321. Treatment
322. α-Blockers—tamsulosin 0.4 mg/day
323. Bladder ultrasound if no voiding by 3–4 hours
324. If ultrasound shows more than 400–600 mL, in-and-out (IO) urinary catheter should be used.
325. Trauma patient—no catheter if bloody meatus or scrotal hematoma present
326. Perioperative UTI
327. “Irritative symptoms”: dysuria, urgency, frequency
328. Account for 30%–40% of hospital-acquired infections
329. Most common organisms: Escherichia coli and Enterococcus
330. Diagnosis
331. If symptoms, urinalysis and culture/sensitivity testing
332. WBCs (leukocyte esterase positive)
333. Bacterial count over 103 CFU/mL, treated preoperatively
334. Treatment
335. Antibiotics for gram-negative organisms
336. Trimethoprim-sulfamethoxazole or fluoroquinolone
     1.** GI motility disorders ( ** Fig. 1.58)
337. 1.5% of hip/knee arthroplasties
338. Common presentation
339. Abdominal pain
340. Distension
341. Nausea with or without vomiting
342. Prevention
343. Chewing gum: vagal (parasympathetic stimulation)
344. Early mobility
345. Spinal (sympathetic block)
346. Limiting dose and length of IV opioids
347. Postoperative adynamic ileus
348. Gut autonomic nerve imbalance:
349. More common in spine (≈7%) and joint arthroplasty (≈1%)
350. X-rays: dilated small and large bowel (see Fig. 1.58A)
351. Treatment: nothing by mouth status, nasogastric tube
352. Electrolyte control
353. Cessation of narcotics
354. Superior mesenteric artery (SMA) syndrome (cast syndrome)
355. Occlusion of duodenum by SMA
356. Orthopaedic causes
357. Hip spica cast
358. Following scoliosis surgery
359. Following THA with severe hip flexion contracture
360. Following traumatic quadriplegia
361. Also found in patients with rapid, large weight loss
362. X-rays: distended stomach and upper duodenum (see Fig. 1.58B )
363. CT
364. Aortomesenteric artery angle less than 25 degrees
365. Aortomesenteric distance less than 8 mm
366. Treatment: nothing by mouth status, nasogastric tube
367. Acute colonic pseudoobstruction (Ogilvie syndrome)
368. Large bowel dilation
369. Abdominal distension the prominent symptom
370. Colonic perforation should be avoided.
371. Risk factors
372. Elderly or male patient
373. Previous bowel surgery
374. Diabetes, hypothyroidism
375. Electrolyte disorders
376. Radiographic findings
377. Distended transverse and descending colon and cecum (see Fig. 1.58C)
378. Colonic diameter more than 10 cm risks perforation.
379. Treatment
380. Nothing by mouth status
381. Neostigmine
382. Colonic decompression
383. Pseudomembranous colitis: potentially fatal diarrhea
384. Most common antibiotic-associated colitis
385. Change in colon flora favors Clostridium difficile
386. Makes enterotoxin-A and cytotoxin-B
387. Many antibiotics
388. Clindamycin, fluoroquinolones
389. Penicillins and cephalosporins
390. Can become severe fulminant colitis
391. Toxic megacolon and perforations
392. Risk factors
393. Elderly hospitalized patient
394. Severe illness
395. Antibiotic use
396. Proton pump inhibitor use
397. Diagnosis
398. Watery diarrhea with fever
399. Leukocytosis, lower abdominal pain
400. Laboratory findings
401. WBC count more than 15,000 cells/µL
402. Stool specimen should be tested for C. difficile
     toxin
403. PCR or ELISA
404. KUB (kidney, ureter, bladder) (plain abdominal) radiograph
405. Toxic megacolon: greater than 7 cm
406. Thumbprinting (see Fig. 1.58D)
407. Treatment
408. Oral metronidazole
409. Oral vancomycin (IV will not work)
410. Fidaxomicin
411. Colectomy if unresponsive and severe
412. Megacolon, WBC count more than 20,000 cells/µL

413. Perioperative hepatic issues

414. Liver failure: critical for producing proteins and metabolizing toxins
415. Laboratory findings
416. Increased aspartate aminotransferase (AST), alanine aminotransferase (ALT), and bilirubin
417. INR above 1.5, low platelets (<150,000 cells/µL)
418. Acute—most commonly viral and drug induced
419. Acetaminophen—number one cause in United States
420. Other toxins: alcohol, occupational, mushrooms
421. Viral hepatitis
422. Chronic—cirrhosis is end-stage fibrosis of liver
423. Common: hepatitis (B, C), alcoholism, hemochromatosis
424. Classifications can be helpful to estimate risks
425. Child classification—most widely used
426. Based on laboratory results and physical examination
427. Model for End-Stage Liver Disease (MELD) score ( http://www.mayoclinic.org/medical-professionals/model-end-stage-liver-disease/meld-model )
428. Formula based on bilirubin, INR, creatinine
429. Studies highlight mortality at 90 days relative to MELD score
430. <9: about 2% mortality
431. 10–19: about 6% mortality
432. 20–29: about 20% mortality
433. 30–39: about 53% mortality

434. 40: about 71% mortality

435. Complication rates from surgery are extremely high.
436. In patients undergoing arthroplasty, MELD score above 10 predicted
437. Three times the complication rate
438. Four times the rate death

439. Perioperative CNS issues

440. Stroke
441. Rare (0.2% of joint arthroplasties)
442. Mortality roughly 25% at 1 year
443. Ischemic more common than hemorrhagic
444. Risk factors
445. Advanced age, CVA, TIA
446. MI, coronary artery bypass graft, atrial fibrillation, or ECG rhythm abnormality
447. Left ventricular dysfunction
448. Cardiac valvular disease
449. General anesthesia higher risk than regional
450. Diagnosis: head CT or MRI
451. Treatment: ABCs of resuscitation, hospitalist/neurology consultation
452. Delirium: approximately 40% in patients with hip fractures
453. Fluctuating levels of consciousness
454. Impairment of memory and attention
455. Disorientation, hallucinations, agitation
456. Associated with increased length of stay
457. Decubitus ulcers, failure to regain function
458. Feeding issues, urinary incontinence
459. Mortality and nursing home placement
460. Risk factors
461. Older patients
462. History of prior postoperative confusion
463. History of alcohol abuse
464. Acute surgery more than elective
     
     --- FIG. 1.58 Perioperative gastrointestinal mobility radiographs. (A) Dilated loops of both small bowel and large bowel consistent with ileus. (B) Characteristic dilation with air-fluid levels in the stomach and right-sided upper duodenum, seen in mesenteric artery syndrome (cast syndrome). (C) Isolated dilation of the large bowel seen in acute colonic pseudoobstruction (Ogilvie syndrome). (D) Dilated loops of both small and large bowel in a patient with watery diarrhea after antibiotic use. Wide, thickened, transverse bands of nodular colon wall replace normal haustral folds (thumbprinting), as seen in pseudomembranous colitis. A and C from Nelson JD et al: Acute colonic pseudo-obstruction [Ogilvie syndrome] after arthroplasty in the lower extremity, J Bone Joint Surg Am 88:604–610, 2006; B from Tidjane Aet al: [Superior mesenteric artery syndrome: rare but think about it], [article in French] Pan Afr Med J 17:47, 2014; and D from Thomas Aet al: “Thumbprinting,” Intern Med J 40:666, 2010.
465. Night-time surgery
466. Long duration of anesthesia
467. Intraoperative pressures below 80 mm Hg
468. Use of meperidine (Demerol)
469. Diagnosis: anemia ruled out, infection, electrolyte issues
470. Treatment
471. O2 saturation above 95%, systolic BP above 90 mm
     Hg
472. Correction of medical issues
473. Family/friends
474. Medications for sedation: used with caution
475. Restraints as last resort

476. Special anesthesia issues

477. Obstructive sleep apnea (OSA)
478. Intermittent hypercapnia and hypoxia
479. Decreased CO2-induced respiratory drive
480. Extreme sensitivity to opioids
481. Leads to
482. Pulmonary HTN
483. Cardiac arrhythmias
484. GERD (reflux) directly related to BMI
485. Delayed gastric emptying
486. Increased risks for aspiration/intubation
487. Higher risk for complications (2–4 times greater)
488. Respiratory failure, ICU transfers, increased length of stay
489. Increased postoperative O2
     desaturation
490. Increased intubation, aspiration pneumonia, ARDS
491. Increased MI, arrhythmias (atrial fibrillation)
492. Screening tools: STOP-BANG ( Fig. 1.59)
493. S noring, t ired, o bserved apnea, p
     ressure (HTN)
     B MI over 35, a ge older than 50 years, n eck circumference larger than 40 cm, g ender male
494. Five or more factors present—high risk of severe OSA
495. Best practices
496. Initiation or continuation of CPAP use
497. More than 2 weeks of preoperative CPAP
     improved HTN, O2 saturation, apneic events
498. Pulmonary HTN: in 20%–40% of patients with OSA
499. Preoperative serum bicarbonate predicts hypoxia in OSA
500. Chronic respiratory acidosis
501. Site of service (American Society of Anesthesiology consensus statement)
502. Malignant hyperthermia
503. Ambulatory surgery under local/regional— lower risk
504. Avoid procedures requiring opioids— greater risk
505. Comorbid conditions must be optimized for outpatient surgery.
506. HTN, arrhythmias, CHF, cardiovascular disease, and metabolic syndrome

507. Metabolic syndrome = obesity, hypertension, hypercholesterolem dyslipidemia, and insulin resistance

508. Avoidance of flat supine position; sitting position opens airway.

509. Autosomal dominant genetic defect of T-tubule of sarcoplasmic reticulum

510. Ryanodine receptor defect (RYR1)
511. Dihydropyridine receptors (DHP)

512. Triggered by volatile anesthetics and succinylcholine

513. Creates an uncontrolled release of Ca2+
514. Sustained muscular contraction (masseter rigidity)

515. Increased end-tidal CO 2

516. Earliest and most sensitive sign

517. Mixed respiratory and metabolic alkalosis
518. Hyperthermia is classic but occurs later.
519. Muscle damage
520. Myoglobin from rhabdomyolysis can cause ARF.
521. Elevated creatine kinase
522. Hyperkalemia can lead to ventricular arrhythmias.
523. Treatment with dantrolene
524. Decreases intracellular Ca2+
525. Stabilizes sarcoplasmic reticulum
526. Treatment of high serum potassium
527. Hydration
528. Cooling