THESE CARDS WAS PREPARED BY
Page 1 of 217
DR.MAZEN AL SOHAIBANI. King Fahad Medical City –Ryadh - Saudi Arabia He was kind enough to share them with his residents. They describe the important points-anesthetic concerns- in most common anesthesia topics, to help you prepare for the vaiva/case scenario exam.I hope that you will find them helpful in your exam as well as in your clinical works as it was for me. A:airway. B:breathing/respiaratory system C:circulation/heart condition. D:drugs. M:metabolic concerns..lytes/glucose/ABG..etc. G:gastrointestinal system.
THA Page 2 of 217 Usually elderly Pt If a revision blood loss and it takes longer Epidural or GA Look for the cause of arthritis # due to CV disease (syncope) avascular necrosis due steroids, infarction (sickle cell disease) Spinal Vs GA less risk of PE with spinal and blood loss A, B, C look under elderly, and other co-existing diseases Consider Autologus blood donation Lab: ECG, CBC….. depend on the co-existing diseases If suspect a difficult A/W GA, due to position Intra-op: risk of PE (cement, BM, fat) consider art-line in Pt with CV disease Post-op: need to anticoagulated, pain epidural or PCA DDx of circulatory collapse intra-op: PE, MI, total spinal, anaphylaxis
Thalassemia Page 3 of 217 Ethnic: Mediterranean, African-American, middle east and Asian -thalassemia o major (homozygote) (Cooley’s anemia) severe, need treatment o intermediate (hetro) o minor (hetro) o manifest after 1st year of life, when Hb F disappears. -thalassemia o 4 genes for the -chain synthesis o 1 gene deletion silent carrier. o 2 genes deletion mild microcytic anemia. o 3 genes deletion severe hemolytic anemia. o 4 genes deletion hydrps fetalis GI absorption of iron and with multi-Tx iron overload hemochromatosis . treatment : o Tx and folate in mild form o Multi Tx and iron chelating agent in the severe form o Splenectomy
The Myotonias Page 4 of 217 delayed relaxation of skeletal muscle after voluntary contraction, myotonic contracture is not relieved by regional, NDMR, or deep GA. Relaxation may be induced by infiltration of the muscle with local anesthetic. caused by genetic abnormalities that produce defects in sodium or chloride channels or proteins which alter ion channel function in muscle cells giving drugs that Na influx into the cell and delay return of membrane excitability,like quinine, tocainide, or mexilitene, may relax myotonic contracture. Myotonic Dystrophy (Steinert's Disease) is the most common form of the myotonias and the most severe. AD inherited disorder (1 in 8000), S/S during the 2nd and 3rd decades of life. clinical features associated with myotonic dystrophy: muscle degeneration, cataracts, premature balding, DM, thyroid dysfunction, adrenal insufficiency, gonadal atrophy, cardiac conduction abnormalities. Cardiac abnormalities LV diastolic dysfunction, cardiac failure is rare. o AV block , A.fib, or flutter, ventricular dysrhythmias. o 1st -degree AV block may actually precede the onset of clinical symptoms o Sudden death may be a result of the abrupt onset of 3rd -degree AV block.
Thoracic trauma: Page 5 of 217 ACLS, and in addition to other injuries Heart and major vessels Chest wall flail chest > 3 ribs# need intubation with PEEP Esophageal Diaphragm initially no S/S then CXR diagnostic Lung parenchyma contusion Tracheal, bronchial injury with blunt trauma Pt may have stridor, wheezing, dyspnea S: subQ emphysema, pneumomediastinum, air leak, loss of expiratory volume Due to association with other injury, mainly c-spine DLT is difficult to insert so consider other option If chest tube drain >1L initially or >200ml/h open When putting a C-line have it in the same side of the chest injury Always be careful with PPV which can worse the hemodynamic with tamponade, and convert a pneumo to a tension pneumo Complication of chest injury empyema, recurrent pneumo, persistence air leak, BPF
TOF Page 6 of 217 Most common cyanotic CHD, F=M VSD, RVH, overriding aorta, RVOTO(sub, valvular, supra) 70% have bicuspid aortic valve, 10% LAD from RCA CXR: pul vascular marking, Rt aortic arch, ECG: RAD, RVH Tet spells: hypercyanotic attaches peak 2-6 m, by age 6y ferq & severity Initiated by feeding, crying, defecation Any thing that PVR or SVR tet spells (PO2, PCO2, acidosis) Rt to Lt shunt S/S: clubbing, cyanosis, polycythemia Pre-op: avoid dehydration, and don’t upset them Hemodynamic goals: o Preload o R/R slow and sinus o cont o SVR o PVR A N/A
TOF, obst Page 7 of 217 Corrected TOF, not risk, and no special precautions May have a residual or recur VSD, or pul outflow tract obstruction All TOF need Echo for that reason 12-ECG may have arrhythmias, or conduction abnormality after the repair So for residual defect manage as TOF hemodynamic Goals: o preload o R/R slightly maintain sinus o Cont maintain, or slightly o Afterload maintain, avoid sudden in SVR No spinal early epidural is desirable, may PVR Consider art-line
Tonsillectomy and Adenoidectomy Page 8 of 217 Peds considerations Indication: recurrent tonsillitis, OSA, abscess A tonsils size(0-+4(75%)), A/W obstruction wheezing , stridor B OSA with snoring, O2 sat, cor pulmonale, chest retraction and RR C CHD need Abx prophylaxis, Rt heart failure ECG, CXR, Echo D over counter meds may contain ASA Induction normal Intra-op avoid NSAID’s , give zofran and decadron Post-op: o N&V, dehydration, pain, bleeding see other card o Pul edema due to relief of the obstruction frothy pink secretion in the ETT, sat, wheezing, RR o DDx anaphylaxis , CHF, volume overload, ARDS, aspiration o Mx supportive ETT, PPV with PEEP, O2 , diuretics o Usually subsided with in 24 hrs
Transplanted heart Page 9 of 217 High risk of infection mainly cholecystitis The efferent denervation is permanent, while some may retain afferent innervations The response to exercise in normal heart is by HR, in a transplanted heart it’s by SV, with little and delayed in HR They are preload dependent ECG may shows both donor and recipient P waves No vagal input No bradycardia But they response to stress(hypoxia, PCO2) by HR but it’s delayed Premature CAD, with in 3 yrs, mainly without angina, if they have Aff pain The main symptom is dyspnea C altered response to stress, and drugs, CAD, maintain preload D atropine and pancuronium No effect, Neostgmine may slow HR, Norepi -effect, Adenosine effect, in addition to the side effect of immunosuppressant drugs, may need stress dose steroids, and Abx coverage M adrenal suppression, glucose intolerance Heme anemia, thrombocytopenia
Trauma in pregnancy Page 10 of 217 Blunt Closed head injury is the major cause of death Other risks: o Uterine rupture o Placenta Abruption o Fetal injury o Spleen and liver rupture Penetrating GSW, stabbing Burn Same rule of nines apply to pregnant Pt With inhalation injury CO poisoning the fetus has a higher affinity to CO than the mother Apply the same ATLS, maintain LUD Have fetal US done, and continue FHR monitor
TURP-TURB: Page 11 of 217 Distilled H2O hemolysis not used any more Sorbitol converted to fructose hyperglycemia, and to lactate acidosis, also well cause osmotic diuresis and dehydration Glycine(inhibitory neurotransmitter) transit blindness ammonia encephalopathy TURP Syndrome:( water intoxication syndrome) S/S mild (restlessness, nausea, SOB, or dizziness) to severe (seizures, coma, HTN, bradycardia, or CV collapse). In the awake patient: a classic triad of symptoms in both SBP and DBP associated with an in pulse pressure, HR, and mental status changes. Volume overload Lt heart failure pul edema CNS S/S due to both the type of irrigation and the severity of in serum Na Management: o ABC, 100% O2, intubate o Notify the surgeon to terminate the procedure o Consider DDx: over-sedation hypercarbia, hypoxia, Anaphylactic reaction if CV collapse, diabetic coma o 12 leads ECG, and invasive monitoring art line, CVP
Tylenol overdose Page 12 of 217 A single dose of 10-15g can produce liver injury, 25g fulminant hepatic failure Ingestion even a lower dose with alcohol the chance of hepatic failure Tylenol normally detoxified by conjugation to glutathione, but with overdose glutathione depleted metabolized by P-450 to a toxic compound First few hr after N&V, RUQ pain with or without obtundation After 24h symptom disappear and Pt looks well 24-72h liver failure appear, with possible ATN, and cardiotoxicity Poor prognosis with Phos, coaglupathy, encephalopathy and acidosis bilirubin correlate with survival Management: o ABC o Mucomyst, with best result if given 12-20h after ingestion o Roughly 150mg/kg over 15min, then 50mg/kg over 4h then 100mg/kg over 16h o Look at the nomogram
Ulcerative Colitis A may have Ankylosing spondylitis difficult A/W, with S/S bowel obstruction RSI B possible restrictive lung disease with ank-spond C AR, hypovolemia D steroids (stress dose) M electrolytes imbalance, K , metabolic acidosis, albumin, adrenal insufficiency G obstruction, perforation
Page 13 of 217
Upper Ext nerve injury: Page 14 of 217 Ulnar: sensation over the 4th and 5th fingers Muscle wasting, unable to grip a paper between fingers Median: Loss of skin sensation over the lateral 3 ½ of the palm of the hand Weakness of wrist flexion, when making a fist the index and middle finger remain straight, also loss of thumb flexion Radial: If the injury at the axilla unable to extend the forearm (triceps) If in the spiral groove wrist drop MCN: Loss of arm flexion (biceps), loss of sensation over the lateral aspect of the forearm Axillary N Loss of skin sensation over the lower ½ of the deltoid muscle, with weakness of arm abduction
URTI Page 15 of 217 Need to distinguish from allergic rhinitis incidence of croup, bronchospasm, and laryngospasm If emergency or urgent surgery proceed, and anticipate the above problems If elective, and < 1yr postponed If elective, >1 yr temp postponed Elective > 1yr normal temp P/E purulent secretion, LRTI postponed = = = = clear proceed to surgery How long to postponed for, if too long, the child may end up with another episode of URTI, So 2-4 wks is reasonable
Uterine Rupture Risk see box 37-1 chestnut Mainly fetal distress and bleeding A & B onst C hypovolemic shock, hypotension Heme bleeding, anemia Mx See abruption card Basically same management they come for stat C/S due fetal distress
Page 16 of 217
VAE: Page 17 of 217 When the surgical field > 5cm above the Rt atrium. 40-50% in the sitting position, if known PFO, avoid sitting position Dx. By TEE the most sensitive then pericardial doppler, placed in the Rt sternal border 3rd to 6th intercostal space, which detect 0.25ml of air Miller all Pt going for N.surgery in sitting position need to have CVP Mx: 100% O2 Notify the surgeon, flood the surgical field with saline gauze Wax the bone edges Compress the jugular vein Head down Aspirate through the CVP D/C N2O, and PEEP which may cause paradoxical embolism
von Willebrand's Disease Page 18 of 217 AD, 3types I, II, III(very rare), group O blood have 20-30% less vWF Prolonged bleeding time, N PT and PTT I (70-80%) vWF, IIA also function abnormal, IIB they have thrombocytopenia which aggravated by giving DDAVP (C/I). Pregnancy vWF Rx DDAVP 0.3ug/kg 1hr prior to surgery. DDAVP may cause fibrinolysis by releasing t-PA so consider giving TXA Cryo have vWF , recombinant Vwf. Hematology consult, Possible HIV + Do gentle intubation, avoid blind suctioning, avoid Regional anesthesia
VSD Page 19 of 217 Rare in adult , with S/S depend on the size, and PVR, the larger, and the lower PVR more severe symptom small asymptomatic, load pansystolic murmur Lt sternal border, with normal ECG and CXR mod also asymptomatic, with biventricular enlargement on CXR large when pul blood flow > systemic, S/S early as 4 wks, Lt Rt change to Rt Lt cyanosis hemodynamic goals: o Preload o R/R N and sinus o Cont slight o Afterload o PVR Pre-op Abx prophylaxis A N/A B pul edema C shunt, CHF, low forward CO
White Cell–Related Transfusion Reactions Page 20 of 217 Febrile Reactions: antibodies to the HLAs after multiple Tx, 1% of all RBC transfusions. the patient experiences a temp of more than 1°C within 4 hrs of a blood Tx and defervesces within 48 hours.may also develop chills, respiratory distress, anxiety, headache, myalgias, nausea, and a nonproductive cough. Febrile reactions can be treated with acetaminophen should be distinguished from a hemolytic transfusion reaction (direct Coombs test) Graft-versus-Host Disease (GVHD) the donor lymphocytes may become engrafted, proliferate, and establish an immune response against the recipient. Patients at risk for GVHD include organ transplant recipients, neonates who have undergone a blood-exchange Tx, and patients immunocompromised by many other disease processes. GVHD typically progresses rapidly to pancytopenia, and the fatality rate is very high Also when a genetic relationship exists between the donor and the recipient GVHD has been reported with the transfusion of whole blood, packed RBCs, granulocytes, platelets, and fresh, not frozen, plasma. It has not occurred following transfusion of FFP, cryoprecipitate, or frozen RBCs
Wilms tumor Page 21 of 217 A delayed G. emptying RSI B lung mets, chemo, and radiotherapy effect C HTN, severe if both kidneys involved CHF, renin secretion D chemo R hyperaldosternism(2nd) K H severe anemia, low PLT, acquired vWD possible need F VIII concentrate M art,and central line Lab X-match, Lytes CBC other upper body IV access Potential intra-op problem IVC obstruction CO Tumor in the IVC embolic phenomena Post-op ICU backup mazen h o m e
m a z e n o f f i c e
,
AAA Elective Page 22 of 217 Long procedure, large fluid shift, and high risk of blood loss A N/A B potential COPD C CAD, HTN, Renal border line function In the pre-op evaluation: concentrate on cardiac function with detailed H/P and work up Lab: CBC-D, BUN, creat, Lytes, Mg, ECG, CXR, PFT, ABG, Echo if available Consider optimizing any medical condition pre-op by meds, consultation, and further evaluation. X-match for at least 6 U of blood, have FFP ready Consider Epidural to do it as a combined technique Have the cell saver in the room, IV worming device, with blood set Lines: Big 14G peripheral IV, Art line, CVP/PAC, bear hugger Monitors: standard + 5 leads ECG, Foley, temp, art-line, CVP/PAC, TEE Induction: routine, modify on cardiac status Before induction have inotrops and vasodilators ready to go
Abruptio placenta Page 23 of 217 Risk with cocaine abuse, smoking, trauma, previous abruption, age Most common cause of DIC, risk ante-postpartum hemorrhage, fetal hypoxia The bleeding could be concealed, and can have 2500ml of blood DDx placenta previa, uterine rupture A obst B obst C hypovolemic shock, Heme anemia, coaglupathy DIC R ARF from both shock, and DIC Fetus Demise, hypoxia, Mx: Depend on the severity, usually partial managed conservative with bed rest ABC, RSI, GI prophylaxis, induction with Ketamine, LUD Lab CBC, Lytes, BUN, creat, PT, PTT, fibrinogen, D-dimer , X-match Monitor Art line, CVP/PAC, fetal monitoring , large IV Synto may not work atony consider ergot, hemoabt(PGF2), may end up need hysterectomy
Achondroplasia: A potential difficult A/W, foramen Magnum Stenosis Avoid neck extension , OSA B Kyphoscoliosis Restrictive lung disease C Cor-pulmonale, pul HTN CNS hydrocephalus, possible ICP, central sleep apnea Lab CXR, C-spine, CT, MRI base of the skull, PFT, ECG, Echo, in addition to the regular blood work
Page 24 of 217
Acromegaly Page 25 of 217 99% from pituitary adenoma A large tongue , epiglottis, large nose difficult intubation and mask fitting Need FOI, possible vocal cord paralysis, and subglottic stenosis smaller ETT, and potential post-op A/W obstruction B OSA C HTN, Cardiomegaly, cardiomyopathy, arrhythmias, CHF, hemodynamic instability (ECG, CXR, Echo) D steroids for other pituitary problems N neuropathy (document), adenoma effect ? pressure vision M DM, hyperthyroid, Position nerve compression Monitors art line
ACT Page 26 of 217 Mainly for depression, possible difficult to obtain an accurate medical history C/I: Pheo, pregnancy, recent CVA and MI, SOL with ICP, and long bone # The main effect is on the CVS: o Initial PSN effect with hypotension and bradycardia, even arrest o Followed by intense SNS activation with HTN, tachycardia, arrhythmias and ICP and IOP Review the old anesthetic record for the dose, and any problems may had happened Also review all Pt med (TCA, MAOI) avoid indirect sympathomimetics, also be careful when direct acting drugs exaggerated response Monitors standard CAS monitors, consider invasive monitoring in sick Pt Pt with pacemaker or AICD not C/I have the magnet in the room, know what is the program
Acute liver dysfunction Page 27 of 217 M&M Postponed if not an emergency History of alcohol, drugs, exposure to toxins at work A LOC B hypoxia, hyperventilation, V/Q mismatch D altered drug metabolism M lytes abnormalities Renal impairment CNS encephalopathy Heme coags abnormalities Avoid sedation pre-op Correct coags pre-op Intra-op avoid hypoxemia, and hypotension both hepatic blood flow
Acute pericarditis, and effusion Page 28 of 217 Most common cause is viral infection Post-MI Dressler Syndrome S/S diffuse chest pain, with diffuse ST-elevation in ECG pericardial leads, with sinus tachy, chest exam friction rub. Consider Echo, if suspected effusion or tamponade Normal pericardial fluid 20-30 ml, o In chronic effusion the pericardium can accommodate up to 1000 ml, without S/S of tamponade o But in acute effusion as low as 200 ml can give symptoms
Adrenal Insufficiency (Addison disease): Page 29 of 217 Need 90% destruction of the adrenal gland to produce symptoms primary (Addison's disease) is idiopathic adrenal insufficiency due to autoimmune destruction. causes both a gluco and a mineralocorticoid deficiency. Hashimoto's thyroiditis in association with autoimmune adrenal insufficiency is termed Schmidt's syndrome. Other: bacterial or fungal infections, metastatic cancer, sepsis and hemorrhage. Secondary: anterior pituitary fails to secrete sufficient quantities of ACTH. from tumor, infection, surgical ablation, or radiation therapy.( less severe S/S, aldosterone is maintained S/S Wt loss, muscle weakness, BP, abd/back pain due bleeding, N&V, hyperpigmenation in primary only Dx by ACTH stim test
Adult with repaired CHD Page 30 of 217 Type of CHD, When, What, and Where, (Repair) Understand the physiology of the repair Residue, Sequelae, and the complication of the repair. Follow up with cardiologist, recent Echo, if not ask for one Discuss the case with a college who knows more about CHD(peds cardiac anesthetist) The Need for SBE prophylaxis High risk for arrhythmia (pads on) for pacing, cardioversion, or shock Have inotrops support ready. In case of shunt be meticulous about air in the IV, use saline instead of air for epidurals. In case of pulmonary HTN have NO in the room
AI Well tolerated in pregnancy hemodynamic Goals: o preload maintain, LUD o R/R slightly maintain sinus o Cont maintain, avoid cardiodepressant o Afterlaod Epidural is good
Page 31 of 217
Airway foreign body Page 32 of 217 Emergency and potential life threatening In addition to peds consideration Brief H/P AMPLE, depend on the Severity of the symptoms and hypoxemia may consider CXR( most are radiolucent), but may see atelectasis Do inhalation induction with Sevo, Avoid PPV, minimal support if needed Assess the eye for depth (see later) The dilemma Full stomach Vs need of maintaining spontaneous Ventilation Once the eye in stage III do direct laryngoscopy Lidocaine spray May give IV bolus of propofol upon the removal of the foreign body Consider a dose of decadron , and racemic Epi
Airway laser surgery:
Page 33 of 217
Risk for both the patient and OR personal Knew what is the indication papiloma, stenosis, neoplasm PFT, flow volume loop, CT The airway is shared with the surgeon close communication Eyeglasses and laser mask, Pt eyes closed, covered with wet gauzes, and metal shields, cover the exposed skin with wet towels Consider glyco pre-med Use laser-metal ETT, and fill the cuff with NS with methylene blue Avoid N2O, use the lowest FiO2 possible < 40%, other Jet ventilation Pt need to be completely paralyzed In case of airway fire remove ETT, have 60 cc syringe filled with NS ready, after controlling the fire asses the airway damage, and ongoing fire, avoid high Fi02 initially till you make sure that there is no ongoing fire direct laryngoscope, bronchoscope with possible lavage and CXR, reintubate with new ETT, keep intubated, Abx, and steroids ICU post-op CO2 laser only 0.01 mm penetration less bleeding and edema post-op With Nd-YAG laser deeper penetration, and risk of air embolism The metal-ETT are bigger than the PVC tubes so use one size smaller
Equations alveolar gas equation:
Shunt equation
ventilation–perfusion ratio (VQI),is determined as follows:
Page 34 of 217
Amniotic fluid embolism Page 35 of 217 Catastrophic event with high mortality rate 86% A LOC, obst B hypoxia, pul edema C cardiopul collapse, RV failure D D/C synto Heme DIC, hemorrhage R ARF CNS seizure Mx: ABC, 100% O2, Large IV,LUD, Lab as abruption, last thing to do CPB (case report) If Pt survive ICU
Amphetamines For management same as cocaine A&B obst C HTN arrhythmias, tachycardia D MAC with acute intoxication, while chronic MAC CNS seizure Obst risk of abruption R. anesthesia severe hypotension, with possible arrest Ecstasy: serotonin and dopamine level C HTN arrhythmia H DIC, MSK rhabdomyolysis M+R lytes abnormality, ARF Fetus toxicity Mx
Page 36 of 217
Amyloidosis: Page 37 of 217 Extracellular deposition of amyloid type protein A macrogolssia, tracheal stenosis (smaller ETT) B pul edema from CHF C arrhythmias, restrictive myopathy, CHF, autonomic dysfunction Renal CRF, nephritic syndrome Heme Factor X deficiency Lab/DI: CBC, lytes, BUN, Creat, CXR, PFT/ flow volume loop, ABG, ECG, ECHO, coags Monitoring: CAS, Art-line, CVP/PAC, TEE Avoid Regional if coagulopathic The main goal intra-op is to maintain U/O, avoid any nephro-toxic drugs Have an ICU backup
Amyotrophic Lateral Sclerosis (ALS) Page 38 of 217 Degenerative disease of the CNS with involvement of both UMN and LMN S/S Asymmetric weakness, reflex, fasciculation and muscle atrophy A bulbar involvement Aspiration mod RSI B respiratory failure C D Sux C/I, sensitivity to NDMR, M abnormal glucose and Ca metabolism, with thyroid dysfunction Do Regional technique better If GA: Mod RSI, ICU post-op
Anesthesia for organ donation: Page 39 of 217 COMMON PHYSIOLOGIC DERANGEMENTS AFTER BRAIN DEATH Condition Cause Hypotension Hypovolemia (DI; hemorrhage) Neurogenic shock Hypoxemia
Neurogenic pul edema, Pul contusion, Pneumonia Gastric aspiration, Fluid overload
Hypothermia
Hypothalamic infarction, Exposure
Dysrhythmia (especially bradycardia)
Intracranial injury or herniation, Hypothermia Hypoxia, Electrolyte abnormality Myocardial contusion, ischemia Avoid vasopressors may cause visceral ischemia Consider using low dose Dopamine if needed They are atropine resistance Consider use NDMR due to somatic spinal reflex No need for GA, for BP consider use vasodilators
Anesthesia For The Geriatric Patient Page 40 of 217 physiological reserve of all organs Common diseases with aging are Sleep apnea, COPD, CAD, HTN, arrhythmias, DM, arthritis, Alzheimer A stiff neck B CC, CV, V/Q mismatch, response to hypoxia and hypercarbia C diastolic dysfunction, HTN, CAD, arrhythmias, CHF D Vd, with both hepatic and renal clearance, MAC, sensitivity to narcotics and sedatives M DM, Na, heat production with more prone to hypothermia GI/hep gastric empting, hepatic mass and blood flow Renal GFR, Na losing , drugs clearance, risk of volume overload CNS Alzheimer, dementia, stiff ligament difficult epidural/spinal heme anemia Always IV wormer, bear hugger, and consider invasive monitoring
Aneurysm Page 41 of 217 F>M, usually present with SAH Aneurismal SAH classification by Hunt & Hess and WFNS to estimate the surgical risk and outcome WFNS Grade GCS Scale* Motor Deficit I 15 Absent II 13–14 Absent III 13–14 Present IV 7–12 Present or absent V 3–6 Present or absent A LOC B pul edema C HTN, ECG changes ST, T, QT, U role out IHD M lytes disturbance, SIADH, DI, pituitary dysfunction Classic S/S: headache, N&V, photophobia, LOC Lab: CBC, Lytes, BUN, Creat, CXR, ECG, review CT/MRI, X-match Induction as Supratentorial May need controlled hypotension, unless they do temporary clipping
Ankylosing spondylitis Page 42 of 217 M>F, 20-30 y.o, -ve rheumatoid factor, HLA-B27 is +ve in 90% of Pts S/S: back pain and stiffness improve with exercise, lumber disc degeneration, sacroilitis A; Spines: limitation in the movement of all the spines, with risk of C5-C7 #, possible difficult intubation , TMJ involvement, Cricoarytenoid involvement (rare) B: restrictive lung disease, chest wall compliance and VC, consider PFT C: Aortitis with AI, CHF due to cardiomyopathy, dysrhythmias secondary to cardiac conduction system involvement. Renal risk of RF Drugs: anti-inflammatory drugs Better to extubate awake Intervertebral ligament calcification, difficult to perform neuraxial block by midline approach, ? C/I if pt have peripheral neuropathy.
Aortic Regurgitation Page 43 of 217 Chronic: rheumatic disease, hypertensive and atherosclerotic diseases, cystic medial necrosis with or without other features of Marfan's syndrome, connective tissue diseases including Reiter's syndrome and ankylosing spondylitis, luetic (syphilitic) aortitis, Acute: infective endocarditis, nonpenetrating trauma, ascending aortic aneurysm dissection Pathogenesis Chronic: LV volume overload LV dilationLVH eccentric hypertrophy LVEDV but LVEDP still normal over time LVEDP Acute: severe AR LV volume overload, but without time for LV dilation,HR is the only comp mechanism to maintain forward CO, LVEDP and LAP rapidly, with pul congestion. History: chronic AR usually remain asymptomatic for years. Early symptoms include a sensation pounding in the chest, palpitations, or head pounding. Exertional dyspnea may be the first manifestation of LV decompensation, with later development of orthopnea and PND. Symptoms of more advanced disease include angina pectoris, which may be nocturnal, and eventually symptoms of right-sided CHF with ascites and peripheral edema. Prognosis worsens with the onset of symptoms; mortality rate is estimated to be more than 10% per year among patients with severe AR and angina pectoris and more than 20% per year among patients with symptoms of CHF. Acute severe AR Patients typically exhibit symptoms referable to the underlying disease, including fever with infective endocarditis, and chest or back pain with aortic dissection.
Aortic Stenosis Page 44 of 217 Valvular AS should be distinguished from nonvalvular forms of LV outflow obstruction, including congenital supravalvular stenosis and subvalvular membrane, ridge or tunnel stenosis, and dynamic subvalvular LV outflow obstruction in HOCM The normal AVA is 2.5-3.5 cm2. AS is not usually of hemodynamic significance until the valve area is to 25% of normal. mild 1.5 to 3.0 cm2, moderate 1.0 to 1.5 cm2, severe <1.0 cm2. With normal CO, severe AS mean transvalvular pressure gradient 50 mm Hg. Transvalvular gradients are affected by flow, so patients may have low gradients despite severe AS if there is LV systolic dysfunction. therapeutic decisions typically are based on the presence of symptoms in the setting of significant aortic stenosis, categorization of disease as mild, moderate, or severe is of lesser clinical importance. Etiology congenital (bicuspid), rheumatic, or senile degenerative (calcific) in origin. History long latent period >30 yrs The three classic symptoms associated with aortic stenosis are dyspnea, angina pectoris, and syncope. (life expectancy < 5 yrs) Dyspnea due to in LVDP, LA, and pulmonary venous pressures. Angina occurs without CAD resulting from O2 demand from LV mass and intracavitary pressures in the setting of a fixed blood supply and from coronary flow due to progressive outflow obstruction. Syncope may be caused by peripheral vasodilation with exertion, with in peripheral oxygen requirement in the setting of a fixed CO.
Appendectomy In older Pt consider other and possible catastrophic problem (AAA) A full stomach (RSI) C dehydration, with intravascular volume GI Vomiting, full stomach M Lytes abnormalities, acid base disturbance Other could be septic Lab CBC-D, lytes, BUN, Creat, ABG Pain PCA
APR For rectal Ca, with possible bowel obstruction Usually in elderly with other co morbidities With bowel prep fluid deficit hypotension upon induction A RSI (b. obstruction) C hypovolemia, elderly Position lithotomy, jackknife Monitors CAS, art line, temp, foley Pain PCA, epidural
Page 45 of 217
Arnold chiari malformation Page 46 of 217 It’s one of the chiari malformation it’s type II associated with myelomeningocele present for posterior fossa decompression and repair of myelomeningocele and insertion of shunt on of the main issue is position during induction due to myelomeningocele, may put a donut where the defect is in the hall, if big may have to the induction in lateral position then turn prone A potential difficult airway, due to hydrocephalus awake intubation B vocal cords paralysis trach, resp depression due to post fossa compression C bradycardia CNS the defects, and CN palsy position as above
AS Page 47 of 217 Mild well tolerated Mod/severe not well tolerated hemodynamic Goals: o preload maintain, LUD, treat hypovolemia aggressively o R/R slightly maintain sinus treat arrhythmia aggressively o Cont maintain, avoid cardiodepressant o Afterlaod , avoid sudden in SVR Need are-line, CVP/PAC risk of arrhythmia with insertion, to maintain PCWP =18 GA opioids, mix kitamine/STP Have the crash cart in the room, pads on the Pt ASD: 3 types: ostium secundum @ foramen ovale
Asthma: Page 48 of 217 H/P: how bad is the asthma? Severity? Frequency? Any hospital or ICU admission in the past, if yes when was the last one, how he/she manage the asthma at home, or need ER visit, Exam: V/S, A/E , wheezing Review PFT results pre-post bronchodilators, and optimize pre-op If Pt is steroids (PO) dependent asthma consider steroids coverage peri-op Pre-med -agonist, Anticholenergics, Induction: IV Lidocaine, avoid STP, intubate deep, may consider LMA Maintenance: avoid any histamine releasing drugs, Emergence: consider extubate deep, IV Lidocaine pre-extubation Consider regional anesthesia to avoid intubation
Autonomic hyperreflexia: Page 49 of 217 Post spinal cord injury above T-7 70-75%, following the resolution of spinal shock, 2-3 weeks after injury Stimulation below the level of transection Severe HTN with bradycardia A potential difficult A/W, unstable C-spine, aspiration risk (FOI), (RSI) B respiratory reserve and volumes, risk of aspiration, pneumonia, PE, respiratory failure PFT, ABG, post-op vent (ICU) C hyperreflexia, orthostatic hypotension, assess the volume status. ECG, D (Sux C/I), have anti-HTN ready (Niprid) N. stimulator show resistance N deficit Neuraxial best is a good choice but may be difficult to assess the level of the block too high, or too low Hyper-reflexia may happen post-op due to bladder or rectal distension. Sequelae CV collapse, arrhythmias, pul edema, stroke, seizure, death
AVM: Page 50 of 217 M>F, 10-40yrs S/S parenchymal hemorrhage, SAH, Sz, motor/sens deficit In Peds Vein of Galen AVM hydrocephalus + high output cardiac failure A LOC B aspiration during Sz C CHF CNS Sz, LOC, ICP Pt may have (NPPB) normal perfusion pressure breakthrough cerebral hyperperfusion with normal CPP o Rx: diuretics, hypervent, mild hypothermia, N-low MAP, high dose STP The rest of management like Aneurysm High risk of bleeding blood in the room
Airway laser surgery: Page 51 of 217 Risk for both the patient and OR personal Knew what is the indication papiloma, stenosis, neoplasm PFT, flow volume loop, CT The airway is shared with the surgeon close communication Eyeglasses, Pt eyes closed, covered with wet gauzes, and metal shields Consider glyco pre-med Use laser-metal ETT, and fill the cuff with NS with methylene blue Avoid N2O, use the lowest FiO2 possible, other Jet ventilation Pt need to be completely paralyzed In case of airway fire remove ETT, have 60 cc syringe filled with NS ready, after controlling the fire asses the airway damage direct laryngoscope, bronchoscope with possible lavage and CXR, reintubate with new ETT consider ICU post-op
EEG FREQUENCY RANGES Page 52 of 217 Delta rhythm (0–3 Hz) Deep sleep, deep anesthesia, or pathologic states (e.g., brain tumors, hypoxia, metabolic encephalopathy) Theta rhythm (4–7 Hz) Sleep and anesthesia in adults, hyperventilation in awake children and young adults Alpha rhythm (8–13 Hz) Resting, awake adult with eyes closed; predominantly seen in occipital leads Beta rhythm (>13 Hz) Mental activity, light anesthesia
Hyponatremia < 130 Page 53 of 217 or in serum Na & in ECV & PV, so it’s result from excess or deficit of water total body Na regulated by aldosterone and ANP, where serum [Na] by ADH S/S depend on the rate and severity of of Na: loss of apatite, N&V, cramps, weakness, LOC, coma and seizure Acute CNS S/S is due to cerebral edema What is the serum osmolality see figure Cerebral salt wasting syndrome, mediated by BNP, independent of SIADH, risk head trauma, tumor, SAH, and infection SIADH see other card Rx < 120 with 3% NS @ 1-2 ml/kg/hr to serum Na 1-2 mEq/l/hr only for few hrs, not more than 25 mEq/l/48 hrs Rapid correction abrupt brain dehydration central pontine myelinolysis mild (transient behavioral disturbances or seizures) to severe (including pseudobulbar palsy and quadriparesis).Within 3 to 4 weeks of the clinical onset of the syndrome, areas of demyelination are apparent on MRI, risk factors (alcoholism, poor nutritional status, liver disease, burns, and hypokalemia) , cerebral hemorrhage and CHF Once serum Na > 120 fluid restriction is enough , Also treat the underlying causes To calculate the net water loss necessary to [Na+] in hyponatremia, use the following equation: Current [Na+] × current TBW = desired [Na+] × desired TBW TBW= 0.6x wt
INDICATIONS FOR ONE-LUNG VENTILATION ABSOLUTE 1. Isolation of each lung to prevent contamination of a healthy lung a. Infection (abscess, infected cyst) b. Massive hemorrhage 2. Control of distribution of ventilation to only one lung a. Bronchopleural fistula b. Bronchopleural cutaneous fistula c. Unilateral cyst or bullae d. Major bronchial disruption or trauma 3. Unilateral lung lavage 4. Video-assisted thoracoscopic surgery RELATIVE 1. Surgical exposure—high priority a. Thoracic aortic aneurysm b. Pneumonectomy c. Upper lobectomy 2. Surgical exposure—low priority a. Esophageal surgery b. Middle and lower lobectomy c. Thoracoscopy under general anesthesia
Page 54 of 217
Omphalocele and Gastroschisis Page 55 of 217 o Impaired blood supply to the herniated organs, and intestinal obstruction o Major intravascular fluid shift and dehydration full-strength balanced salt solution o Hypothermia and hypoglycemia A possible difficult airway Beckwith-Wiedemann syndrome consists of mental retardation, hypoglycemia, congenital heart disease, a large tongue, and an omphalocele. B respiratory failure C CHD in 20% of infants with omphalocele. Induction: NG aspirate gastric content then RSI , need large IV , possible central, and arterial line Post-op keep intubated
Stroke & TIA: Page 56 of 217 Hemorrhagic or ischemic Etiology: Atherosclerosis, embolic MI, A.fib, VHD, post-op CEA, trauma, severe HTN A LOC, loss of A/W reflux (RSI) B hypoventilation C HTN, CAD, VHD, A.fib, arrhythmias ECG, Echo D anti-PLT, ASA, coumadin N LOC Peri-op Avoid swinging in BP, and hyperglycemia With chronic HTN the cerebral autoregulation curve shifted to the Rt
Bioterrorism Page 57 of 217 Use of nerve gases which are a potent Ach.esterase inhibitor and cause a cholinergic crisis A mass casualty with both physical trauma and gas intoxication Healthy soldiers Vs civilian with different age groups and other comorbidities The amount, duration and the rout of exposure are the major determine of the clinical course of intoxication Exposure to vapor gives respiratory symptoms (SOB, wheezing, bronchorrhea) with rapid cardiopulmonary collapse (muscarinic effect) Where dermal exposure slow, and gradual S/S local muscle twitches and fasciculation (nicotinic effect) then resp failure, also carry more risk to the health care personal with direct contact All the nerve gases causes irreversible inhibition to AchE in both central and peripheral NS The key point in the management is to give the antidote ASAP, and protect the health care personal
BKA Page 58 of 217 For PVD, DM, gangrene, trauma, tumor Most of the Pt with major co-morbidities e.g. CAD, PVD, DM, COPD, CVA, Sepsis, CRF, H/P standard + depend on the co-morbidities Lab also as above Options: GA Vs spinal/epidural may the incidence of phantom limb pain, but look for C/I monitors standard + depend on the above co-morbidities Position risk of ischemic necrosis (pads) EBL 250 ml The use of tourniquet bleeding, but be aware of risk thrombus embolization PE Post-op pain(epidural, nerve block, PCA), DVT (S/C heparin), MI, CVA, infection, bleeding
BPF and Empyema Page 59 of 217 Causes: after pulmonary resection for carcinoma, traumatic rupture of a bronchus or bulla ( barotrauma or PEEP), penetrating chest wound, or spontaneous drainage into the bronchial tree of an empyema cavity or lung cyst PPV contamination of the healthy lung, loss of air with alveolar ventilation and CO2 retention, and potential tension Pneumothorax In case of empyema with BPF drain the empyema under LA with chest tube under suction, then do a CXR, then may fix the BPF under GA GA options ( the main target is to avoid PPV) o Awake intubation with DLT o Gas induction and maintaining spontaneous ventilation o RSI Keep FiO2 always 1, and avoid N2O For non-surgical management: DLT and resting the affected lung, or use of HFJV Keep a high index of suspicion for tension Pneumothorax
Brain death Page 60 of 217 ―irreversible cessation of all function of the entire brain, including the cortex and brain stem, determined in accordance with accepted medical standards‖ CRITERIA FOR THE DIAGNOSIS OF BRAIN DEATH: LOSS OF CEREBRAL CORTICAL FUNCTION o No spontaneous movement o Unresponsive to external stimuli LOSS OF BRAIN STEM FUNCTION o Absent respiratory reflex (apnea test) o Absent cranial nerve reflexes (Gag or cough reflex to suction) o Pupillary light reflex ( no pupil constriction) o Corneal reflex ( no blinking with corneal touch) o Oculocephalic reflex ( doll’s eyes) o Oculovestibular reflex (cold caloric test) o Atropine resistance SUPPORTING STUDIES o Electroencephalography
Brain metabolism and physiology: Page 61 of 217 In adult:O2 3.5 ml/100g/min& 5.5 mg/100g/min of glucose, peds 5.5 ml O2 the autoregulation is abolished by trauma and hypoxia CSF from the choroids plexus and absorbed by the arachnoid villi, volume 100-150 ml, rate of production and absorption 0.3-0.4 ml/min, with production by Lasix and acetazolamide Enf production and resistance to absorption, Iso 0/ resistance ICP N= 10 mmHg, ICP CPP, and herniation All volatile agents CBF with return to baseline in 3 hrs, with CMRO2 All volatile agents and kitamine cause cerebral vasodilation, except N2O N2O cause CBF w/out dilation, and no change in CMRO2 All IV drugs cause CBF and CMRO2
Bronchiectasis: Page 62 of 217 Localized irreversible dilation of bronchus May have COPD, and restrictive component And may associated with other condition so look of other underlying disease: aspergillosis, HIV, R. arthritis If Pt present to OR with active pul infection postponed Sx, and give Abx therapy Lab: PFT, ABG, CXR pneumonia Pt may present with hymoptysis required arterial embolization, or resection of the affected segment Consider DLT to isolate the affect lung Need pre-op Abx
Carcinoid Tumors Page 63 of 217 GI is the most common source, 50% appendix, 25% in the ileum(the source of metastatic tumors), also from the lung, hormones secreted by nonmetastatic tumors reach the liver by portal vein and are usually inactivated there. once metastases to the liver, the hormones secreted by the hepatic metastases may have direct access to the systemic circulation, to produce the S/S of the carcinoid syndrome Could be a manifestation of MEN I, Release Serotonin, Histamine, Kinins Symptoms: cutaneous flushing, abd pain, V, diarrhea, HTN, hypotension, bronchospasm, and hyperglycemia A N/A, Gentle induction, avoid sux, STP B bronchospasm, endobronchial tumor obstruction C Rt side disease myocardial fibrosis TR, PR, consider CVP, art line sympathomimetic drugs can trigger mediator release from carcinoid tumors D Give antihistamines, avoid drugs that can cause histamine release octreotide 10-100 ug IV M Dehydration due to diarrhea, and vasoconstriction , hyperglycemia Intra-op
Cardiac herniation Page 64 of 217 An emergency and life threatening with mortality 50% With pneumonectomy, in the 1st few hrs or few days later Pathophysiology: o twisting of the SVC (SVC syndrome), o twisting IVC (cardiovascular collapse), o twisting distal trachea (wheezing), o twisting pulmonary veins (pulmonary edema), o pericardial constriction of the heart (myocardial ischemia and ventricular arrhythmia) Risks: o Events that intrapleural pressure in the (ventilated) hemithorax or that intrapleural pressure in the surgical (empty) hemithorax may predispose the patient to cardiac herniation. o Placing the patient with the empty hemithorax in a dependent o Use of high levels of pressure and volume during mechanical ventilation of the remaining lung can push the heart into the empty hemithorax. And coughing
Cardiac Risk* Stratification for Noncardiac Surgical Procedures Page 65 of 217 High (Reported cardiac risk often greater than 5%) · Emergent major operations, particularly in the elderly · Aortic and other major vascular surgery · Peripheral vascular surgery · Anticipated prolonged surgical procedures associated with large fluid shifts and/or blood loss Intermediate (Reported cardiac risk generally less than 5%) · Carotid endarterectomy · Head and neck surgery · Intraperitoneal and intrathoracic surgery · Orthopedic surgery · Prostate surgery Low† (Reported cardiac risk generally less than 1%) · Endoscopic procedures · Superficial procedure · Cataract surgery · Breast surgery *Combined incidence of cardiac death and nonfatal myocardial infarction. †Do not generally require further preoperative cardiac testing.
CAROTID ENDARTERECTOMY Page 66 of 217 Pre-op: H/P Lab: CBC, Lytes, BUN, creat, Glucose, ECG, PFT if needed A N/A B possible smoker COPD C CAD, HTN (need to well controlled pre-op) M DM CNS neurological deficit Regional (deep, superficial cervical plexus) Vs GA same out come Induction: anticipate fluctuation of BP Maintenance: Iso neuro-protection, Keep BP 20% higher, monitor blood glucose, LA infiltration over the carotid sinus, give heparin 100u/kg Monitors: standard+ 5leads ECG, Art-line, in cardiac Pt consider TEE, Emergence: early to assess for nay neuro deficit Post-op potential problems: new neuro deficit back to OR or Angio, hemodynamic instability mainly HTN, bleeding with hematoma formation which may compromise the Airway Back to the OR, 100% O2 have difficult airway
Canadian Cardiovascular Society Functional Classification of Angina Pectoris Page 67 of 217 Class Definition Specific Activity Scale I Ordinary physical activity, (eg, walking and climbing stairs) does not cause angina; angina occurs with strenuous, rapid, or prolonged exertion at work or recreation. Ability to ski, play basketball, light jog (5 mph), or shovel snow without angina II Slight limitation of ordinary activity; angina occurs on walking or climbing stairs rapidly; walking uphill; walking or stair climbing after meals, in cold, in wind, or under emotional stress; or only during the few hours after awakening; when walking > 2 blocks on level ground; or when climbing more than 1 flight of stairs at a normal pace and in normal conditions. Ability to garden, rake, roller skate, walk at 4 mph on level ground, and have sexual intercourse without stopping III Marked limitation of ordinary physical activity; angina occurs on walking 1 to 2 blocks on level ground or climbing 1 flight of stairs at a normal pace in normal conditions. Ability to shower or dress without stopping, walk 2.5 mph, bowl, make a bed, and play golf IV Inability to perform any physical activity without discomfort; anginal symptoms may be present at rest. Inability to perform activities requiring 2 or fewer metabolic equivalents (METs) without angina
Cesarean Section Page 68 of 217 Depend if elective/urgent Vs stat Always have the room ready: Anesthesia machine checked, A/W equipment ready, Emergency drugs ready Always ask for blood for any bleeding case Elective/urgent: Enough time to evaluate Pt, H/P as routine obstetric Hx, and anesthetic Hx with physical exam mainly the A/W, chest, edema …..+ review lab, obstetric consideration Obtain informed consent from the Pt for neuroaxial block, with risk/benefit discussion, if not C/I for the block. Pre-meds GI, other if indicated e.g. asthma, anxiety, endocarditis, steroids IV at least 1.5 -2.0 L of fluids O2, Pre-block V/S If using hyperbaric L.A lie the Pt down very quickly + LUD, repeat BP Inform the Pt that if she feel sick to tell me right way (BP) Examine the block by asking the surgeon to use a teeth forceps As soon as the baby out give synto 5 U then 20 U in the bag For spinal: 10.5 mg marcaine hyperbaric, 20 ug fentanyl, 150 ug epimorph
CHF: Page 69 of 217 Causes: IHD, VHD, CHD, Cardiomyopathy, HTN, pul HTN Hallmark: CO, VEDP, SVR, metabolic acidosis Could be Sys Vs Dias, Rt or Lt S/S: SOBOE, orthopnea, PND, exercise tolerance P/E: crackles,S3 gallop, JVP, hepatosplenomegaly, ascites, peripheral edema Rx that proven to improve outcome: ACEI, -blocker, spironlactone Rx that improve symptom: Dig, and loop diuretics Other antiarrhythmics, anticoag, vasodilators Other modality: biventricular pacing, AICD Assess using NYHA functional capacity I no limitation with normal activity, and no symptom II slight limitation with normal activity, symptomatic III marked limitation with normal activity, comfortable at rest, les the normal activity produce symptom VI severe limitation, symptomatic at rest Pre-op: postponed if decompensated, Cardiology consult to optimize Workup: CBC, Lytes, Chem, 12-ECG, CXR, review Echo
Lab and Clinical Criteria for Estimating Hepatic Reserve (Child-PughPage 70 of 217 Classification) CRITERIA CLASS A CLASS B CLASS C Serum bilirubin mg/100 mL <2.0 2.0–3.0 >3.0 Serum albumin g/100 mL
>3.5
3.0–3.5
Ascites
None
Easily controlled
Encephalopathy
None
Minimal
Advanced
Excellent
Good
Poor
1–4
4–6
>6
5%
10%
50%
Nutrition Prothrombin time (sec > control) Surgical risk mortality rate
<3.0 Not easily controlled
Chronic constrictive pericarditis Page 71 of 217 It resemble tamponade in impede diasolic pressure, venous pressure, and stroke volume Causes: idiopathic, CRF, radiation, R. arthritis, and post-heart S/S: arrhythmias A.fib and flutter, kussmaul sign exaggerationin CVP with inspiration, pulsus paradoxes but less than tamponade CXR: calcification over the pericardium. ECG: voltage of QRS, inverted T-waves Rx surgical pericardiotomy Anesthesia Mx o Preload maintain, and avoid , since they’re preload dependent o Cont maintain, avoid cardio-depressant drugs o Rate: avoid sudden HR o Afterload maintain, avoid sudden drop in SVR, since limited CO o Avoid all histamine releasing drugs o Art-line, PAC, CVP at least
Clinical Predictors of Increased Perioperative Cardiovascular Risk (Myocardial Page 72 of 217 Infarction, Heart Failure, Death) Major Unstable coronary syndromes · Acute or recent myocardial infarction* with evidence of important ischemic risk by clinical symptoms or noninvasive study · Unstable or severe† angina (Canadian class III or IV)‡ Decompensated heart failure Significant arrhythmias · High-grade atrioventricular block · Symptomatic ventricular arrhythmias in the presence of underlying heart disease · Supraventricular arrhythmias with uncontrolled ventricular rate Severe valvular disease Intermediate Mild angina pectoris (Canadian class I or II) Previous myocardial infarction by history or pathological Q waves Compensated or prior heart failure Diabetes mellitus (particularly insulin-dependent) Renal insufficiency
Coarctation of the Aorta Page 73 of 217 If corrected no special precautions Arm-leg different < 20mmHg good outcome Uncorrected high risk of LV failure, aortic rupture or dissection, endocarditis High mortality rate, risk of offspring CHD Risk of having bicuspid aortic valve, aneurysm of circle of Willis Measure Rt Vs Lt side BP, and upper Vs lower BP Need Echo and 12-ECG hemodynamic Goals: o preload o R/R slightly maintain sinus o Cont maintain, avoid cardiodepressant o Afterload maintain, avoid sudden in SVR Avoid Regional GA is better tolerated for C/S Monitors Art-line, CVP, Ephedrine and dopamine are the best choice since they have choronotropic effect
Cocaine abuse Page 74 of 217 Affect three main neurotransmitters Norepi, Serotonin and dopamine Can present like PIH with HTN, edema, proteinuria A B aspiration, bronchspasm, pneumothorax, pneumomediasinum C MI, HTN, arrhythmias Renal ARF Heme thrombocytopenia, DIC, anemia Hepatic failure, rupture CNS seizure, ICH, SAH, CVA fetus UP blood flow, cross placenta The main problem is severe HTN with induction, So consider NTG, hydralazin with induction, avoid pure -blockers alone may get unopposed -effect, with risk of coronary vasospasm Regional OK, be aware of severe hypotension with spinal,and ephedrine is not a good choice(not work) Neo better
Coma/LOC Page 75 of 217 Management: o ABC o Monitors o Give thiamine 100 mg IV, Dextrose 50g IV o Lab: ABG, ECG, chemostrip, lytes, BUN, creat, CBC-D, LFT, coagulation profile, urine analysis, blood/urine for toxicology and drugs level DDx: o CNS pathology: tumor, trauma, seizure disorder, aneurysm, AVM o Infection: meningitis, encephalitis, sepsis o Metabolic: hypoglycemia, DKA, HONKC, uremia, hepatic encephalopathy , acidosis o Respiratory: hypoxia, hypercarbia o Overdose: EtOH, drugs(opioids, TCA, Cocaine, Tylenol,…..) H/P AMPLE, VS, Neuro GCS, lateralization, pupils,
COMPARISON OF MYASTHENIC SYNDROME ANDMYASTHENIA Page 76 of 217 GRAVIS Myasthenic Syndrome Myasthenia Gravis Manifestations Proximal limb weakness Extraocular, bulbar and (arms > legs) facial muscle weakness Exercise improves with strength Fatigue with exercise Muscle pain common Muscle pain uncommon Reflexes absent or Reflexes normal Gender pathology Response to muscle relaxants
Male > female Small cell carcinoma of the lung Sensitive to Sux and NDMR
Poor response to anticholinesterases
Female > male Thymoma Resistant to Sux Sensitive to NDMR Good response to anticholinesterases
Congenital Diaphragmatic Hernia Page 77 of 217 95% Lt side neonatal and premature consideration A insert NGT , keep suction B hypoplastic lung RDS, risk of pneumothorax with PPV, keep Airway pressure < 20-30 cmH2O, and avoid lung expansion after hernia repair, neonate could be on NO or ECMO, N2O is C/I, keep 100% O2 C 15% CHD R renal abnormality N neuro abnormality Congenital lobar emphysema o LUL most common o Emergency and potential life threatening A ? B resp failure, ball valve avoid PPV, cyanosis, N2O C/I, 100% O2 C mediastinal shift hemodynamic instability , 20% CHD Lab X-match Induction gas induction, with spontaneous breathing
COPD Page 78 of 217 A airway reactivity bronchospasm B risk of hypoxia, hypercarbia, bronchospasm, and PPC: atelectasis, pneumonia, respiratory failure, smoking C cor pulmonale, RV failure, pul HTN D avoid STP, sensitivity to resp depressant drugs Heme polycythemia Lytes PPC with: FEV1/FVC < 70%, FEF25-75 <50%, FVC< 75%, with respiratory failure more likely if FEV1 <50%, PaCO2 > 50 H/P: smoking, wheezing, coughing, sputum amount and color, exercise tolerance, home O2, A/E bilaterally, wheezing, crackles, JVP, peripheral edema, cyanosis With smoking risk of CAD Lab: CXR, ABG, PFT, ECG, CBC-D, lytes, BUN, creat For PFT do pre and post bronchodilators Optimize the Pt pre-op: smoking cessation, bronchodilators(-agonist, steroids, anticholenergic) , consider Abx therapy Pt may need O2 supplement pre-op if PaO2<60, cor pulmonale, Hct >55
Coronary Artery Disease— Myocardial Infarction Anatomic Site Leads ECG Changes Inferior II, III, aVF Q, ST, T Lateral I, aVL, V5–V6 Q, ST, T Anterior I, aVL, V1–V4 Q, ST, T Anteroseptal V1–V4 Q, ST, T
Electrolyte Disturbances Ca2+ Rate <100 Rhythm Regular PR interval Normal QT interval
Ca2+ <100 Regular Normal/
K+ <100 Regular Normal T flat/U wave
Page 79 of 217
Coronary Artery Right Left circumflex Left LAD
K+ <100 Regular Normal T peaked QT
Craniosynostosis: Page 80 of 217 May associated with other syndrome Crouzon’s syndrome (MH) Main issues: difficult A/W, massive blood loss, VAE, ICP A possible difficult A/W maxillary hypoplasia, large tongue, micrognethia Awake FOI, multi masks and blads B tracheal stenosis, tracheomalacia, OSA C CHD ASD, TOF, PDA D Avoid ketamine and sux M lytes abnormality N ICP, seizure disorder, mental retardation Have a big IV access, blood in the OR If only one suture short procedure, if > 1 , long with risk of bleeding so need art line, CVP, IV wormer , bear hugger, Foley cath If involve below the orbit A/W swelling keep intubated post-op (ICU) till the swelling subsided
Creutzfeldt - Jakob disease Page 81 of 217 human spongiform encephalopathies. The other two diseases in this group are kuru and Gerstmann-Straussler syndrome. Pathologically, these disorders are characterized by vacuolation of brain tissue and neuronal loss. caused by an unusual infectious agent—a prion. A prion is a small proteinaceous infectious agent. Prions are resistant to alcohol, formalin, ionizing radiation, proteases, and nucleases, but can be inactivated by heat (autoclaving), phenol, detergents, and extremes of pH. incubation time is long (years) The typical clinical characteristics include subacute dementia, myoclonus, and EEG changes. Management of Anesthesia Because of the transmissibility of the disease, appropriate precautions should be taken to protect other patients and health care providers. A prone to aspirate gastric impaired swallowing function and decreased activity of laryngeal reflexes. C autonomic dysfunction abnormal CV responses to anesthesia and vasoactive drugs. DBecause lower motor neuron dysfunction succinylcholine should be avoided.
Crohn's Disease Page 82 of 217 A RSI for S/S of bowel obstruction B N/A C hypovolemia D Steroids (stress dose), immunosuppressant G obstruction, fatty liver, cirrhosis, perforation R amyloidosis Heme chronic anemia, iron def, vit B12, folate M hypovolemia, K, 3rd space loss, albumin free fraction of drugs MSK arthritis with ROM
Cushing Syndrome :( Glucocorticoid Excess) Page 83 of 217 Cortisol function: 1- maintain BP by converting Norepi epi, 2- antiinflammatory, 3- Na retention, and K excretion, 4- hyperglycemia by gluconeogenesis, and glucose uptake by the cells Exogenous therapy (most common) > 21 days Bilateral adrenal hyperplasia due to ACTH from pituitary adenoma or nonendocrine tumor (lung, kidney, pancreas) A possible difficult A/W, mucosa easily traumatize B OSA C HTN, volume overload D steroids (stress dose), avoid etomidate, titrate NDMR N emotional, psycosis M DM, K, met alk, Addison crisis MSK osteopenia, muscle wasting Immun infection Post bilateral adrenalectomy may need mineralocorticoid replacement in day 5, give 0.05–0.1 mg·day–1 of fludrocortisone
CV diseases in pregnancy Page 84 of 217 Lt Rt shunt e.g. ASD, VSD, PDA are well tolerated in pregnancy The main keys in management for anesthesia are o Avoid air bubble in the IV o For epidural insertion use saline instead of air both due to risk of paradoxical air embolism o Pain catecholamine SVR shunt RV failure o So early epidural is desirable o Slowly titrate the epidural, and avoid spinal sudden SVR convert the shunt to Rt Lt o Give O2 all the time
CVP Waveform Components WAVEFORM
Page 85 of 217
PHASE
MECHANICAL EVENT
a wave
End-diastole
Atrial contraction
c wave
Early systole
v wave h wave x descent
Late systole Mid- to late diastole Mid-systole
Isovolumic ventricular contraction, tricuspid motion toward right atrium Systolic filling of atrium Diastolic plateau Atrial relaxation, descent of the base, systolic collapse
y descent
Early diastole
Early ventricular filling, diastolic collapse
Cyanide toxicity Page 86 of 217 By preventing oxidative phosphorylation cellular hypoxia anaerobic metabolism S/S lactic acidosis, tachyphylaxis to SNP, SvO2, Sz Management: D/C SNP 100% O2 Thiosulfate 150 mg/kg IV administered over 15 minutes (acts as a sulfur donor to convert cyanide to thiocyanate) If severe, with deteriorating hemodynamics and metabolic acidosis slow IV administration of sodium nitrate, 5 mg/kg. ( converts Hb to methemoglobin, which acts as an antidote by converting cyanide to cyanomethemoglobin hydroxocobalamin (vitamin B12a) which binds cyanide to form cyanocobalamin (vitamin B12) can be administered (25 mg/hour IV to a maximum of 100 mg)
Cystic fibrosis: Page 87 of 217 A disease of the exocrine glands: salivary, sweet, GI, pul Rx: chest physio, Abx, bronchodilator, GI enzyme A sinusitis avoid nasal intubation with active nasal infection. B pneumonia, mixed obstructive/restrictive disease, bronchiectasis C cor-pulmonale GI cholelithiasis, pancreatic insufficiency, hepatic dysfunction Heme bleeding disorder Lab: CBC-D, lytes, BUN, creat, coags, CXR, PFT, ECG, Echo if needed Monitors: CAS, art-line Suction the airway before extubation Consider regional block for post-op pain control Encourage chest physio post-op
Deliberate Hypotension: Page 88 of 217 Mainly used to blood loss: aneurysm, AVM, spine Sx, major head and neck The main C/I are: uncontrolled HTN, severe anemia, TIA’s angina, heart failure, resp failure, acidosis, hypoxia, Renal insuff Ass intravascular volume pre-op, and expand it if necessary. Have a target MAP based on awake MAP e.g. 70% of the awake MAP Monitors: Art-line, CVP, SSEP or EEG in brain and spine Sx Choices: o SNP: rapid on/off, risks: pul shunt, ICP, cyanide and thiocyanate toxicity, and rebound HTN, also it’s inhibit PLT aggregation, do not exceed 10ug/kg/min for 10 min, or > 1mg/kg in 2hrs, or 0.5mg/kg in 24hrs, Rx of toxicity: IV thiosulfate, if abnormal renal functionhydroxocobalamin o NTG: less potent, no cyanide problem, but shunt, o Isoflurane: easy titration, CMRO2, o Other: Trimethaphan, Esmolol and Labetalol, Prostaglandin E1, Nicardipine
Diabetes Insipidus Page 89 of 217 from inadequate secretion of ADH (central DI) or resistance on the part of the renal tubules to ADH (nephrogenic DI) Failure to secrete adequate amounts of ADH results in polydipsia, hypernatremia, and a high output of poorly concentrated urine. Etiology due to destruction of the pituitary gland by intracranial trauma, infiltrating lesions, or surgery. management depends on the extent of the hormonal deficiency. During surgery, the patient with complete DI receives an iv infusion of aqueous ADH (100–200 mU·h–1) combined with administration of an isotonic crystalloid solution. The serum sodium and plasma osmolality are measured on a regular basis, and therapeutic changes are made accordingly. ADH also may be given intramuscularly (as vasopressin tannate in oil). DDAVP administered intranasally has prolonged antidiuretic activity (12– 24 hours) and is associated with a low incidence of pressor effects. As a consequence of the large outpouring of ADH in response to surgical stress, patients with a residually functioning gland usually do not need
DIABETES MELLITUS Page 90 of 217 A stiff joint syndrome ―prayer sign,‖, mobility of the AO joint. difficult intubation, FOI, RSI full stomach B N/A C CAD, PVD, cardiomyopathy , silent MI, autonomic neuropathy, risk of post-op MI D metformin associated with lactic acidosis in hypotension, hypoxia GI delayed gastric emptying, full stomach M hypo, hyperglycemia, lytes abnormalities, DKA, hyperosmolar coma Renal renal function CNS neuropathy (positioning), CVA Pre-op: lab: ECG, Lytes, FBS, BUN, creat D/C OHA in AM, consider insulin/D5% infusion peri-op for long cases Document neuropathy pre-op for positioning and regional anesthesia monitoring intra-op, includes 5-leads ECG, Art-line, frequent ABG, or chemosrip for glucose, and in PARR unless it’s an emergency Sx, postponed DKA, and hyperosmoalr coma
Diabetic Ketoacidosis Page 91 of 217 Accumulation of acetoacetate and -hydroxybutyrate ketone bodies are organic acids metabolic acidosis with an unmeasured AG. Provoked by intercurrent illness, trauma, or cessation of insulin therapy. the degree of hyperglycemia does not correlate with the severity of the acidosis. Blood sugar levels are often in the 300–500 mg·dl–1 range. leukocytosis, abdominal pain, GI ileus, and mildly amylase levels are all common in DKA, Pt may Dx as acute abdomen. Treatment Regular insulin 10 units iv bolus followed by an insulin infusion nominally at (blood glucose/150) units·h–1 Isotonic iv fluids as guided by V/S and urine OP; anticipate 4–10 l deficit When urine >0.5 ml·kg–1·h–1, give KCl 10–40 mEq·h–1 (with continuous ECG) When glucose to 250 mg·dl–1, add dextrose 5% at 100 ml·h–1 Consider sodium bicarbonate to correct pH <7.1 When glucose levels below 250 mg·dl–1, glucose should be added to the iv fluid while insulin therapy continues. K replacement is a key concern in patients with DKA, Because of the diuresis, the total body potassium stores are reduced.
DIC
Page 92 of 217
Dilated Cardiomyopathy myocardial contractility systolic dysfunction CO ventricular filling pressure Dilatation of both ventricles MR, TR. Causes: the most common is IHD and alcohol Other causes: o Direct: Toxic :Alcohol, Anthracyclines, Catecholamines, Cobalt, Phenothiazines, Radiation, Uremia, Adriamycin. Infectious:Protozoan (Chagas' disease) Viral (coxsackievirus, other enteroviruses, influenza) Metabolic :Starvation, Thiamine deficiency (beriberi) Genetic, Idiopathic o Indirect Ischemic Large-vessel coronary disease (postinfarction cardiomyopathy) Small-vessel coronary disease Global ischemia (cardiac surgery) Anemia, TTP, Hypersensitivity, Idiopathic myocarditis
Down syndrome: Page 93 of 217 Highly associated with CHD 50%, cyanotic 8%(mainly TOF) A C1-2 subluxation, subglottic stenosis, large tongue difficult intubation, avoid neck extension B C CHD, TOF, CHF, Tet spells, Rt Lt shunt ( be meticulous about air in the IV) M hypothyroidism, hypothermia CNS MR
ECT during pregnancy Obstetric consideration Risk of abortion and premature labor, also risk of bleeding Minimize the amount of drugs as much as possible Use only the drugs that are known to be safe(STP, Sux, NDMR, Opioids, Ketamine, Etomidate) Have an obstetric consultation Beyond the 1st trimester do GA with ETT, RSI, with maintaining LUD Have FHR monitor
EEG FREQUENCY RANGES Page 94 of 217 Delta rhythm (0–3 Hz) Deep sleep, deep anesthesia, or pathologic states (e.g., brain tumors, hypoxia, metabolic encephalopathy) Theta rhythm (4–7 Hz) Sleep and anesthesia in adults, hyperventilation in awake children and young adults Alpha rhythm (8–13 Hz) Resting, awake adult with eyes closed; predominantly seen in occipital leads Beta rhythm (>13 Hz) Mental activity, light anesthesia Effect of anesthesia is depend on the dose. @ low dose frequency @ moderate dose frequency and amplitude @ high dose silent compare to SEP, EEG records the spontaneous brain activity with higher amplitude, while the SEP have a smaller amplitude in response to a specific stimuli.
Ehlers-danlos Syndrome: CTD, abnormal metabolism of type III collagen A avoid A/W traumatization B spontaneous Pneumothorax, Avoid high airway pressure C MR, Arrhythmias, consider SBE prophylaxis Heme bleeding disorder with normal coags profile Anticipated problem bleeding Obstetric premature labor & bleeding Avoid Regional Anesthesia
Page 95 of 217
Eisenmenger Syndrome Chronic Lt Rt shunt changes to Rt Lt Pregnancy S/S due to SVR hypoxia IUGR, demise high rish of thromboembolic event mainly post partum Hemodynamic Goals: o preload maintain, avoid AC compression LUD o R/R maintain normal sinus o Cont maintain, avoid cardiodepressant o Afterload maintain, avoid sudden in SVR o PVR avoid by hypoxia, acidosis, PCO2 Consider inhaled NO, O2 all the time, with pulse oxi Monitors Art-line, PAC/CVP For the 1st stage single shot spinal opioids 2nd stage may consider slow titrating epidural Be aware that they could be anticoagulated For C/S crash cart in the room, with pads on the Pt Epidural have better outcome than GA careful titrate LA
Page 96 of 217
Electric shock and lightning strike Page 97 of 217 Electric shock o Direct effect of the current o Conversion of electric to heat energy Factors determine the nature and severity: magnitude of energy delivered, resistance to current, type of current, current pathway, and duration of contact o Bone and skin have a high resistance o Blood vessels, muscle, nerve have a low resistance o The skin resistance can be by moist and convert a low voltage to a life threatening shock o Alternating current is more dangerous than a direct current o Transthoracic (hand-hand) are more dangerous than vertical ones o VF more common with alternating, while asystole more with direct o Respiratory arrest due to CNS effect (medulla), tetanic contraction of resp muscles, and prolonged paralysis o Consider C-spine precaution, and other injuries o Potential burn to the face early intubation
Cardiac Conditions Associated With Endocarditis Page 98 of 217 Endocarditis prophylaxis recommended High-risk category Prosthetic cardiac valves, including bioprosthetic and homograft valves Previous bacterial endocarditis Complex cyanotic CHD (eg, single ventricle states, TGA, TOF) Surgically constructed systemic pulmonary shunts or conduits Moderate-risk category Most other congenital cardiac malformations (other than above and below) Acquired valvar dysfunction (eg, rheumatic heart disease) Hypertrophic cardiomyopathy Mitral valve prolapse with valvar regurgitation and/or thickened leaflets Endocarditis prophylaxis not recommended Negligible-risk category (no greater risk than the general population) Isolated secundum atrial septal defect Surgical repair of ASD, VSD, or PDA (without residua beyond 6 mo) Previous coronary artery bypass graft surgery Mitral valve prolapse without valvar regurgitation Physiologic, functional, or innocent heart murmurs
Endocarditis Prophylaxis Dental, oral, esophageal, and respiratory o Adult: Ampicillin 2g IV 30 min pre-op o Peds: Ampicillin 50mg/kg within 30 min of starting o Allergy to Amp Clindamycin 600 mg , Peds 20mg/kg GU/GI o High risk: Amp & Gent Adult 2g/ 1.5/kg max 120mg Peds 50mg/kg & 1.5 kg Allergy to Amp Vanco and Gent, 1g for adult and 20mg/kg for peds o Moderate risk: Amp alone Same as above dose Allergy to Amp Vanco also the same dose
Page 99 of 217
Epidermolysis Bullosa Page 100 of 217 inherited or acquired loss of intercellular bridges and separation of the skin layers intradermal fluids accumulation and bulla formation. 3 types o simplex benign o junctional rarely survive beyond early childhood o dystrophic. Systemic manifestations and Anesthetic considerations: o A very fragile m.m bledding & bulla formation with fixation of the tongue difficult intubation use a lot of lubricant on the ETT, and avoid suctioning o skin: very fragile avoid tapes for IV and ETT, avoid tourniquet, BP cuff must be pad with cotton o GI: esophageal stricture malnutrition anemia, cardiomyopathy o CVS: cardiomyopathy and MVP o Lytes: loss of albumin hypovolemia and electrolytes imbalance o Associated diseases: D.M, hypercoagulation, porphyria cutanea tarda, multiple myoloma
Epiglottitis Page 101 of 217 an emergency and life threatening condition 1-7 y.o, most common pathogen is H. influenzae, with incidence due to vaccine The main conflict is difficult airway with risk of aspiration Other DDx is retropharyngeal abscess Rapid onset within 24h, high grade fever, and the kid is sitting foreword, mouth opening and drooling, inspiratory stridor, with toxic appearance Need to managed in the OR, keep the kid with the parents, and do a gas induction without starting an IV, in the presence of the ENT surgeon in the room, and the difficult airway cart in the room Do a gas induction with Sevo, and maintain spontaneous ventilation Use a smaller ETT, and have different sizes ready After Intubation keep sedated and transfer to ICU, and need to be kept intubated for 24-72h, with Abx therapy After intubation risk of pul edema NO NO NO muscle relaxant Give atropine
Epilepsy: Page 102 of 217 H/P: why(pathology: head injury, tumor, CVA, bleeding), frequency, type, last aepisode, S/S of ICP Meds: what, dose, to be taken in AM A N/A B possible frequent aspiration C tuberous sclerosis, drugs effect (cardiotoxicity) D resistance to NDMR with phenytoin, enzyme induction with pentobarb, hepatic toxicity with carbamazepine, other: aplastic anemia, avoid any drugs that may seizure threshold.
Epilepsy surgery Page 103 of 217 Hx type generalized, focal, absence, with, or without Aura Review all meds, mainly anticonvulsant metabolism of NDMR Discuss with the surgeon the anesthetic plan GA Vs sedation with LA May need awake test with speech mapping In case of sedation use a judicious amount of sedation, O2 by NP, and keep communication with Pt all the time In case of A/W obstruction D/C sedation gtt, 100% O2 LMA, ETT In addition to the standard CAS monitoring, if an Art-line needed have in the same side of the lesion e.g. Rt temporal Rt radial art line Avoid any pre-med that may change the seizure threshold, also avoid any long acting anticonvulsant
Ethylene Glycol poisoning Page 104 of 217 Found in: detergent, antifreeze, polish The toxic metabolite Glycolic acid is responsible for the metabolic acidosis with anion gap, and osmolar gap S/S depend on when they present and at which stage: o Stage I (30min-12hr) CNS with hallucination, coma, Sz, tetany o II (12-24hr) Cardioresp HTN, tachycardia, pul edema o III (24-72hr) Renal flank pain, Ca oxalate in the urine Management: o ABC o Lab: CBC-D, Lytes, BUN, creat, EG level, ABG, Osmolality, CXR, ECG o Monitors: ECG, art-line, pulse oxi, Foley cath o ECG QT, Lytes Ca o Gastric lavage o Depend on the serum level of EG whether to give EtOH or not or to start HD
Familial Periodic Paralysis Page 105 of 217 Two forms: hyperkalemic, and hypokalemic, both AD inherited diseases. intermittent, acute episodes of skeletal muscle weakness. Attach may last hours or days. Hyperkalemic Periodic Paralysis. evidence of myotonia as well as episodes of muscle weakness. caused by a sodium channel mutation. Episodes of weakness lasting several hours can occur: during rest after exercise, infusions of KCl, metabolic acidosis, or hypothermia. The weakness may be so severe as to produce respiratory distress. hyperkalemia is often transient, occurring only at the onset of weakness. K levels measured during the episode of weakness may be N or even Treatment consists of a low-K diet and the administration of thiazide diuretics. Consider glucose containing solution pre-op during fasting. Hypokalemic Periodic Paralysis. More common. caused by a calcium channel mutation.
Fat Embolus Syndrome Page 106 of 217 associated with multiple traumatic injuries and surgery for long bone # Risk factors include:male sex, age (20–30 years), hypovolemic shock, intramedullary instrumentation, rheumatoid arthritis, The incidence of FES in isolated long bone fractures is 3–4%, and the mortality rate ranging from 10 to 20%. CRITERIA FOR DIAGNOSIS OF FAT EMBOLUS SYNDROME o MAJOR Axillary/subconjunctival petechiae Hypoxemia (PaO2 < 60 mm Hg; FIO2 < 0.4) CNS depression (disproportionate to hypoxemia) Pulmonary edema o MINOR Tachycardia (>110 beats·min–1) Hyperthermia Retinal fat emboli Urinary fat globules platelets/hematocrit (unexplained)
Flow volume loop
Page 107 of 217
Fluids Page 108 of 217 Blood volume o Preterm 100 ml/kg o Newborn 85 ml/kg o Up to 2y 75 ml/kg o 2-puberty 70 ml/kg Maintenance use the rule 4-2-1, add the deficit using the same rule from NPO and replace it 50% in the first hr, and the rest in the nest 2 hrs Glucose requirement for neonate 4-6 mg/kg/min D10W 100mg/ml of glucose Dehydration o Based on body wt in infant 5% mild, 10% mod, 15% severe o >15 kg 3% mild, 6% mod, 9% severe Clinical signs Mild mod severe Urine anuria Mucosa slight dry Dry parched Fontanel N sunken marked sunken Eye N sunken marked sunken
Gestationl diabetes maternal/fetal M/M, risk of C/S In addition to obstetric consideration A Stiff joint syndrome difficult A/W B C hypovolemia, ANS dysfunction hypotension with R.anesthesia D insulin M hypoglycemia, DKA, HNKC CNS ANS dysfunction, R renal dysfunction Fetus/neonate hypoglycemia, hypothermia, bili, lethargy Lab: CBC-D, Lytes, BUN, Creat, ECG, ABG (PRN) Pre-med GI, Review White classification for DM its according to the severity
Page 109 of 217
Guillian barre’ Syndrome Page 110 of 217 Widespread inflammatory demyelination of peripheral and ANS It’s ascending in nature, LMN involvement ? caused by viral infection GI, flu A full stomach, difficult intubation if TMJ involvement B respiratory involvement C arrhythmia, autonomic dysfunction D NO Sux, (K), sensitivity to NDMR GI bowel obstruction CNS demyelination Pre-op: PFT, ABG, CXR, ECG, CBC, Lytes Before induction have an art-line in place, unpredictable response to intubation and induction, consider CVP, have N. stimulator in place Post-op: continue mech vent (ICU) In Pt with previous disease assess for residual neuropathy, and do PFT In pregnancy premature labor, epidural OK, avoid Spinal severe hypotension
Head and spinal cord injury Page 111 of 217 15% of CO to the brain, with CBF of 50ml/100g/min Pathophysiology: TBI primary injury is due to hematoma, contusion, or DAI, the secondary is an exacerbation of neuronal damage from change in CBF, and systemic factors e.g. BP, hypoxia, severe PCO2, anemia, temp, Sz Hypotension is the most important factor poor prognosis The effect of ICP CPP, and herniation The Autorgulation of CBF is disrupted, but PCO2 reactivity is preserved with in magnitude, it’s very important to maintain SBP > 90 ICP maintain O2, adequate cerebral drain head up, adequate pain/sedation, PCO2 30, mannitol .25-1g/k, hypothermia Anesthesia goals: o Optimize CPP, avoid ischemia, avoid drugs/tech ICP, avoid CMRO2 Exam: GCS, pupils, brainstem reflex, focal/lateralization neuro signs Lab: CT-head, CBC, Coags, Lytes, toxicology screen Induction: RSI, use lido, sux , inline stabilization. Monitors: routine, art line, CVP, ICP, temp
Table 25-4. DERIVED HEMODYNAMIC VARIABLES Name Calculation Units CI CO/BSA l·min–1·m–2 SVR (MAP-CVP/CO) X 80 dyne-cm·s–5 PVR (MPAP-PCWP/CO) X 80 dyne-cm·s–5 Stroke index SI CI/heart rate cc·beat–1·m–2
Page 112 of 217
Left ventricular stroke work index :LVSWI SI X (MAP-PCWP) X 0.0136 g-m·beat–1·m–2 Right ventricular stroke work index :RVSWI SI X (MPAP-CVP) X 0.0136 g-m·beat–1·m–2
Hemophilia Page 113 of 217 A deficient or functionally defective Factor VIII:C. (85%) B (Christmas disease) deficiency or abnormality of Factors IX(14%) C deficiency or abnormality of Factor XI (1%) Both hemophilia A and B are sex-linked recessive disorders, which therefore occur almost exclusively in males. Hemophilia C is an AR disorder that occurs almost exclusively in Ashkenazi Jews Normal concentration of vWF, direct relation between the severity of bleeding and the plasma concentration of the factors CNS bleed is the major cause of death. Lab: PTT, with N PT, with normal BT, Hematology consult Rx factors concentrate VIII, IX and XI, may give Cryo if needed, VIII t1/2 is 12 hrs, IX is 24 hrs, also DDAVP factors release from the endothelium With time type A may develop inhibitors to factor VIII:C , and the dose of factor VIII:C need to be , Possible HIV + Do gentle intubation, avoid blind suctioning, avoid Regional anesthesia
Hepatitis B,C, Page 114 of 217 Depends on the activity and the stage, with Post-op M&M Risk of transmission to OR personal (use needle-less system) A RSI for GI bleeding, B hypoxemia due to shunt, restrictive lung disease, Pul HTN C hyperdynamic circulation, CHF D altered drug pharmacokinetics Heme anemia, PLT, coagulation defect M albumin, lytes abnormality, hypoglycemia, acidosis Renal hepatorenal syndrome GI portal HTN, ascites, upper GI bleed CNS encephalopathy Correct coagulation pre-op (FFP, Cryo, PLT, Vit K) Consider paracentesis pre-op if respiratory compromise Have an ICU consult and back-up bed Lab: CBC-D, BUN, creat, lytes, coags(PT, PTT, fibrinogen), CXR, PFT, ECG, Echo, LFT, ABG
HIV Page 115 of 217 The main considerations are the disease process, side effect of antiviral drugs, and health care personal safety A N/A B PCP, TB, hypoxia, ARDS like, C accelerated CAD, pericarditis, myocarditis, pul HTN, endocarditis, autonomic neuropathy D drugs related side effect neuropathy, pancreatitis, lactic acidosis, and the protease inhibitor may interact with cytochrome P-450 either by induction or inhibition which can sensitivity to BNZ GI esophagitis, diarrhea Heme leukopenia, anemia, ITP Endo DM, adrenal insufficiency CNS demyeliantion neropathy like gullian barre’ syndrome R+ Lytes CRF from sepsis, dehydration, drugs Possible substance abuse cocaine, heroin, opioids , other infection HCV, HBV
HOCM With pregnancy HR and contractility with SVR worsen the obstruction -blockers is the treatment of choice Synto no bolus, give slowly hemodynamic Goals: o preload , LUD o R/R maintain sinus, treat arrhythmia aggressively o Cont , avoid contractility (kitamine) o Afterload , avoid sudden in SVR Neo is the drug of choice if BP Epidural very slow titration With GA risk of CHF
Page 116 of 217
HTN Essential or secondary. With secondary look for the underlying cause: cushing, pheo, …. Postponed if DBP > 110 Continue -blockers, and 2-agonist peri-op D/C ACEI A N/A B N/A C CHF, LVH, PVD, HTN, with labile BP M intravascular volume R renal impairment CNS TIA, CVA, Rt shift of auto regulation curve Hydrate pre-induction Consider Art-line depend on Pt status and the procedure Lab ECG, CBC, Lytes, BUN, creat
Page 117 of 217
Hydrocephalus: Etiology: o Trauma/hemorrhage IVH o Congenital Arnold-chiari malformation o Neoplastic tumor o Post-inflammatory sbscess, meningitis Pt may come for VP, VA, or LP shunt. A impaired A/W reflex aspiration RSI B impaired resp drive ABG C Cushing reflex (brady, HTN) D avoid ketamine and sux N ICP, LOC The rest of management as ICP card
Page 118 of 217
Hyperosmolar Nonketotic Coma Page 119 of 217 In type II (NIDDM) elderly patient with minimal or mild diabetes may present with remarkably high blood glucose levels and profound dehydration. enough endogenous insulin activity to prevent ketosis; even with blood sugar concentrations of 1000 mg·dl–1, they are not in ketoacidosis. it is the combination of an impaired thirst response and mild renal insufficiency that allows the hyperglycemia to develop. The marked hyperosmolarity may lead to coma and seizures, with the increased plasma viscosity producing a tendency to intravascular thrombosis. responds quickly to rehydration and small doses of insulin. One to 2 L of NS, or equivalent, infused over 1–2 hrs if there are no cardiovascular contraindications. Insulin, by bolus or infusion, should be administered. Consider NaHCO3 if severe acidosis With rapid correction of the hyperosmolarity, cerebral edema is a risk, and recovery of mental acuity may be delayed after the blood glucose level and circulating volume have been normalized.
Hyperparathyroidism Page 120 of 217 Primary benign parathyroid adenoma (90% of cases) or hyperplasia (9%) and very rarely to a parathyroid carcinoma, or as part of a (MEN) syndrome. most Pt are hypercalcemic, most are asymptomatic at the time of diagnosis. occurring during pregnancy is associated with a high maternal and fetal morbidity rate (50%), The placenta allows the fetus to concentrate Ca, promoting fetal hypercalcemia and leading to hypoparathyroidism in the newborn. Pregnant women with primary hyperparathyroidism should be treated with surgery. Secondary in parathyroid function as a result of conditions that produce hypocalcemia or hyperphosphatemia.e.g. CRF, malabsorption Tertiary development of hypercalcemia in a patient who has had prolonged secondary hyperparathyroidism that has caused adenomatous changes in the parathyroid gland and PTH production to become autonomous. Surgery is the treatment of choice for the patient with symptomatic disease.
Hyperthyroidism Page 121 of 217 most common etiology is the multinodular diffuse goiter of Graves' disease. between the ages of 20 and 40 years and is predominant in women A potential difficult if large goiter B N/A C hyperdynamic, HTN D Avoid ketamin, and pancuronium M Ca Heme anemia, PLT Consider giving -blockers peri-op, to HR, and the conversion of T4 to T3
Hypertrophic Cardiomyopathy Page 122 of 217 AD, Peak 5th decade of life, F>M, HTN is a common cause, Could associated with LVOFO or without Sport sudden death, Good EF due to hypercontractile state, MR is common Could be dynamic obstruction by the anterior leaflet of the MV during systole systolic anterior motion (SAM). S/S Angina, Syncope, Arrhythmia,CHF A.fib systemic embolism Atrial kick very important A.fib not well tolerated CXR Cardiomegaly ECG LVH Treatment: -blockers 1st choice by HR and contractility outflow obstruction. CCB is other choice. CHF is difficult to treat digoxin contractility obstruction, diuretics hypovolemia obstruction.
Hyponatremia < 130 Page 123 of 217 or in serum Na & in ECV & PV, so it’s result from excess or deficit of water total body Na regulated by aldosterone and ANP, where serum [Na] by ADH S/S depend on the rate and severity of of Na: loss of apatite, N&V, cramps, weakness, LOC, coma and seizure Acute CNS S/S is due to cerebral edema What is the serum osmolality see figure Cerebral salt wasting syndrome, mediated by BNP, independent of SIADH, risk head trauma, tumor, SAH, and infection SIADH see other card Rx < 120 with 3% NS @ 1-2 ml/kg/hr to serum Na 1-2 mEq/l/hr only for few hrs, not more than 25 mEq/l/48 hrs Rapid correction abrupt brain dehydration central pontine myelinolysis mild (transient behavioral disturbances or seizures) to severe (including pseudobulbar palsy and quadriparesis).Within 3 to 4 weeks of the clinical onset of the syndrome, areas of demyelination are apparent on MRI, risk factors (alcoholism, poor nutritional status, liver disease, burns, and hypokalemia) , cerebral hemorrhage and CHF Once serum Na > 120 fluid restriction is enough , Also treat the underlying causes To calculate the net water loss necessary to [Na+] in hyponatremia, use the following equation: Current [Na+] × current TBW = desired [Na+] × desired TBW TBW= 0.6x wt
Hypoparathyroidism Page 124 of 217 underproduction of PTH or resistance of the end-organ tissues to PTH results in hypocalcemia normally: hypocalcemia PTH and 1,25(OH)2D synthesis Ca2+ mobilization from bone, GI absorption, and renal tubule reclamation. most common cause of acquired PTH deficiency is inadvertent removal of the parathyroid glands during thyroid or parathyroid surgery. Other : 131I therapy for thyroid disease, neck trauma, granulomatous disease, or an infiltrating process (malignancy or amyloidosis). Idiopathic is rare and may occur as an isolated disease or as part of an autoimmune polyglandular process (hypothyroidism, adrenal insufficiency). Pseudohypoparathyroidism is an inherited disorder in which parathyroid gland function is normal but the end-organ response to the PTH is deficient. Affected patients have hypocalcemia and hyperphosphatemia. They are characterized by mental retardation, a short stature, obesity, and shortened metacarpals. Chvostek's sign is a contracture of the facial muscle produced by tapping the facial nerve as it passes through the parotid gland.
Hypotension Preload: Hypovolemia Venodilation (spinal) Tamponade Tension Pneumothorax R&R: Too fast and too slow Arrhythmias Other (may affect any component): Electrolytes imbalance Acid-base Hypoxia & hypercarbia
Page 125 of 217
Contractility: Ischemia Valve dysfunction CHF Drugs
Afterload: Drugs Anaphylaxis Sympathectomy Hyperthermia sepsis
Hypothyroidism Page 126 of 217 Hashimoto’s thyroiditis may associated with other autoimmune disease e.g. SLE, RA, DM, hypoparathyroidism, Addison’s disease. May associated with amyloidosis. A goiter altered A/W anatomy, with possible A/W obstruction B OSA, hypoventilation, response to PCO2 and PO2, sensitivity to narcotics, pul edema C bradycardia, CHF, heart block, hypotension, edema GI gastric emptying aspiration M Na, possible SIADH, hypothermia, possible Addison’s disease postponed if severe hypothyroid Pt until at least partially treated. The management of hypothyroid patients with symptomatic CAD has been a subject of particular controversy. In symptomatic patients or unstable patients with cardiac ischemia, thyroid replacement should probably be delayed until after coronary revascularization. Maintain normal body temperature. Consider adrenal insufficiency when intra-op hypotension not responding to fluids and inotrops.
ICP: Page 127 of 217 Normal ICP < 10 mmHg, to convert to cmH2O X by 1.32 A LOC, aspiration risk B resp failure C arrhythmias, hemodynamic instability, MI (ECG, Echo) D avoid sux N ICP, LOC, risk of herniation M DI, SIADH, cerebral salt wasting Monitors: routine, artline, ICP, CVP Mx: 1- hyperventilate PaCO2 25-30 good only for 6 hrs 2- diuretics mannitol 0.25- 1.0 g/kg over 10 min, Lasix 0.5-1.0 mg/kg 3- Steroids need 6-24 hrs to work 4- head elevation 5- Barbiturate 6- CSF drain Avoid neck twisting obstruction of IJ, avoid hyperglycemia Maintain CPP, MAP > 60, avoid PEEP if possible
IHD Page 128 of 217 Apart from atherosclerotic disease, other causes are: collagen vascular disease, sickle cell disease, pheo, PIH, cocaine abuse Avoid ergot, synto OK Need continues sat and ECG monitor Epidural is good prevent catecholamine and hyperventilation which PCO2 coronary vasospasm Neo is a better choice Epidural best for C/S
Immediate Hemolytic Transfusion Reactions Page 129 of 217 Catastrophic and life threatening with mortality 20-60% Hemolysis of the donor RBC ARF, DIC, death Intravascular and extravascular (RES) Antibodies anti-A,B, Kell, Kidd, Lewis, and anti-Duffy Ag-Ab complex activate Hageman factor(XII) kinin bradykinin capillary permeability, also complement histamine , serotonin S/S: fever, chills, N&V, diarrhea, rigor, flushing, hypotension, tachy, chest and abdominal pain Under GA most of S/S are masked only hypotension, tachycardia, bleeding, Hemoglobinuria Management: (keep index of suspicion) o Stop Tx, re-check blood, o 3 main objectives: Maintain BP volume, inotrops Preserve renal function diuretics, alk the urine (NaHCO3) Prevent DIC no specific therapy, maintain BP, prevent stasis o Blood sample should be collected in EDTA tubes for re-X match, direct coombs test ( for definitive diagnosis)
INDICATIONS FOR ONE-LUNG VENTILATION ABSOLUTE 1. Isolation of each lung to prevent contamination of a healthy lung a. Infection (abscess, infected cyst) b. Massive hemorrhage 2. Control of distribution of ventilation to only one lung a. Bronchopleural fistula b. Bronchopleural cutaneous fistula c. Unilateral cyst or bullae d. Major bronchial disruption or trauma 3. Unilateral lung lavage 4. Video-assisted thoracoscopic surgery RELATIVE 1. Surgical exposure—high priority a. Thoracic aortic aneurysm b. Pneumonectomy c. Upper lobectomy 2. Surgical exposure—low priority a. Esophageal surgery b. Middle and lower lobectomy c. Thoracoscopy under general anesthesia
Page 130 of 217
Infratentorial Intracranial Tumors Page 131 of 217 Those tumors produce a mass effect on the brain stem, and ICP by obst hydro A CN involvement + LOC unprotected A/W RSI B Resp depression C brady, HTN, arrhythmias ST-changes , prolonged QT CNS ICP, LOC Position sitting risk of VAE , CV instability in elderly, risk SC compression Prone see other card Monitors as Supratentorial tumors Induction also the same Post-op: o need for continuous CV monitoring 24-48 hrs o HTN is a common problem post-op, need to treated aggressively other wise intracranial bleeding and edema o Manipulation of CN IX, X, XII loss pharyngeal sensation may need to keep intubated
ITP Page 132 of 217 More common in young female, characterize by thrombocytopenia with petechiae, where major cause of mortality is intracranial bleed The main ttt is steroid, if not working splenectomy Consider DDx: TTP, drug induced thrombocytopenia, Connective T disease, HIV, other in preg PIH, DIC, essential thrombocytopenia The main issues with Anesthesia Are o A avoid traumatize the airway o Avoid Regional o Risk of bleeding PLT Tx In Preg antibodies cress the placenta affect the fetus CNS bleed C/S TTP It’s: thrombocytopenia, fever, renal dysfunction, hemolysis, CNS involvement Sz, and jaundice ttt Tx plasma, plasmaphoresis, IVIG, steroids also the same issues as ITP regarding anesthesia
Kidney Tx Page 133 of 217 Of course for CRF A RSI for possible gastroparesis B pul edema if volume overloaded C hyper/hypovolemia, pericardial effusion, pericarditis, arrhythmias D altered drugs pharmacokinetics G Gastroparesis M K, secondary hyperparathyroidism with Ca and phos Heme PLT dysfunction secondary to uremia Lab CBC-D, CXR, ECG, Lytes, BUN, creat, X-match monitorsCAS, Art-line, foley, CVP Goals maximize the renal perfusion at the time of graft reperfusion by maintaining a high BP, intravascular volume, and diuresis with lasix, and mannitol Possible problem Bleeding Post-op pain epidural, PCA
Lower Ext nerve inury: Page 134 of 217 Lumbosacral trunk: Foot drop, with loss of ankle dorsiflexion L5 dermatome loss of sensation lateral leg In obstetric with prolonged labor and difficult vaginal delivery Obturator: Weakness of hip adduction and internal rotation Peroneal N With prolonged lithotomy position At the knee level (injury) foot drop, with no sensory deficit Femoral N: Due to pelvic Sx, prolonged hip flexion, abduction, external rotation during the 2nd stage of labor, as well as lithotomy position Walking OK, but unable to claim stairs, with loss of the patellar reflex Meralgia paresthetica(Lateral femoral cutaneous nerve) tingling, numbness, burning sensation over the lateral thigh resolve spontaneous after giving birth
Ludwig's Angina Page 135 of 217 An emergency and life threatening situation generalized septic cellulitis of the submandibular region occurs after dental extraction, especially of the second or third mandibular molars it’s bilateral, involves 3 fascial spaces: submandibular, submental, and sublingual Early S/S: chills, fever, drooling of saliva, inability to open the mouth, and difficulty in speaking. hemolytic streptococci, aerobic and anaerobic, including gas-forming bacteria The infectious process may spread into the thorax, causing empyema, pericarditis, pericardial effusion, and pulmonary infiltrates, Pneumothorax, necrotizing fasciitis Review the CT/MRI, CXR for Pneumothorax A difficult, difficult A/W B hypoxia, pneumonia, effusion, empyema C dehydration, pericardial effusion, pericarditis Have the ENT surgeon in the room, scrubbed, and the neck is prepped, and the difficult airway cart in the room, consider a reinforced and small size ETT Awake FOI, give glycopyrolate, other option is inhalation induction Post-op keep intubated to ICU until swelling subsided
Lung volumes and capacities
Page 136 of 217
Page 137 of 217 TABLE 30–7. Underestimation of Left Ventricular End-Diastolic Pressure
CONDITION
SITE OF DISCREPANCY
CAUSE OF DISCREPANCY
Decreased left ventricular compliance
Mean LAP
Increased end-diastolic a wave
Aortic regurgitation
LAP a wave
Mitral valve closure prior to enddiastole
Pulmonic regurgitation
PADP
Bidirectional runoff for pulmonary artery flow
Right bundle branch block
PADP
Delayed pulmonic valve opening
Decreased pulmonary vascular bed
PAWP
Obstruction of pulmonary blood flow
Magnesium Page 138 of 217 mainly intracellular, 50% in bone, 25% muscle, and < 1% in the serum. protein-bound (30%), chelated (15%), and ionized (55%) Magnesium is necessary for enzymatic reactions involving DNA and protein synthesis. As a primary regulator or cofactor in many enzyme systems, magnesium is important for the regulation of the Na–K pump, Ca-ATPase enzymes, adenyl cyclase, proton pumps, and slow Ca channels. The distal tubule of the kidney is the major site of magnesium regulation. Hypomagnesemia clinical features of Mg, like Ca neuronal irritability and tetany. can aggravate digoxin toxicity and CHF. S/S: weakness, lethargy, muscle spasms, paresthesias, and depression. When severe seizures, confusion, and coma. CV coronary artery spasm, CHF, dysrhythmias, and hypotension. is associated with K, Na, phos, and Ca. Rarely resulting from inadequate dietary intake, most commonly caused by inadequate GI absorption, excessive Mg losses, or failure of renal Mg conservation. Excessive Mg loss is associated with prolonged nasogastric suctioning, GI or biliary fistulas, and intestinal drains
Magnesium Page 139 of 217 Mainly intracellular, distal tubule is the major site of magnesium regulation Hypomagnesemia Rarely from inadequate dietary intake, most commonly caused by inadequate GI absorption, excessive Mg losses, or failure of renal Mg conservation. Excessive Mg loss is associated with prolonged NGT, gastrointestinal or biliary fistulas, and intestinal drains. A N/A B N/A C arrhythmias, CHF, BP, coronary artery spasm. M may associated with other electrolytes abnormality Rx stop NGT, give Mg Hypermagnesemia Most common cause is iatrogenic, other Addison’s disease, lithium, hypothy S/S depend on Mg level Hypotension Deep tendon hyporeflexia Somnolence Respiratory insufficiency, deep tendon areflexia Heart block, respiratory paralysis Cardiac arrest Rx D/C Mg, IV CaCl, diuretics, dialysis
Marfan syndrome: Page 140 of 217 AD, length of long bone A TMJ laxity dislocation with intubation B scoliosis, kyphoscoliosis, Pectus excavatum, restrictive lung defect spontaneous Pneumothorax careful with PPV C cystic media necrosis, aortic dissection, AR, MVP, MR, arrhythmia, aneurysm Avoid sudden in contractility, -blockers and volatiles are good, need endocarditis prophylaxis Other lens dislocation, retinal detachment Position careful Neuraxial potential difficult, may need a bigger dose and volume of LA Lab Echo, CT-chest and angio all for dissection, valve, tamponade, CXR pneumo, ABG, CBC, lytes, BUN, creat, PFT
Masseter Muscle Rigidity Page 141 of 217 most common in children and young adults. peak age incidence at 8–12 yrs of age. Characteristically, anesthesia is induced by inhalation with halothane or sevo, after sucx is given. Snapping of the jaw or rigidity on opening of the jaw is seen. this rigidity can be overcome with effort and usually abates within 2–3 minutes. A peripheral nerve stimulator usually reveals flaccid paralysis. However, increased tone of other muscles also may be noted. Repeat doses of succinylcholine do not relieve the problem. Tachycardia and dysrhythmias are not infrequent. (if the anesthetic is continued with a triggering agent), the initial signs of MH appear in 20 minutes or more. If the anesthetic is discontinued, the patient usually recovers uneventfully. However, within 4–12 hours, myoglobinuria occurs and CK elevation is detected. Muscle biopsy with caffeine–halothane contracture testing has shown that approx 50% of Pt who experience MMR are also susceptible to MH. DDx of MMR are: (1) myotonic syndrome, (2) TMJ dysfunction, (3) underdosing with Sux, (4) not allowing sufficient time for Sux to act before intubation, (5) increased resting tension after succinylcholine in the presence of fever or elevated plasma epinephrine.
Maxillofacial trauma Page 142 of 217 Lower 1/3 mandible (30% in the body of the mandible) Middle 1/3 maxilla, zygomatic, orbital, nasal LeForte I, II, III Upper 1/3 frontal and cranium ( CNS) Airway 100% O2, and clear the A/W from foreign bodies, blood, # teeth (count), if there is bleeding apply pressure, nasal packing, and consider a close reduction for a # In case of tongue injury laceration edema/swelling difficult intubation In case of mid and upper facial injury avoid nasal intubation Bleeding, and possible basal skull # Laryngeal injury S/S hoarseness, stridor, sub-Q emphysema with crepitus void blind technique After intubation with direct vision bypass the injury and make sure that the cuff is beyond the injury Trismus after facial injury due to muscle spasm relived by GA
Meconium Aspiration: Page 143 of 217 Risk of PPHTN. risk with post-term pregnancy The new recommendation it does not matter thin or thick meconium If there is meconium suction the hypopharynx Apply NALS If not vigorous (HR < 100, resp depression) ETT suction, 100% O2 If vigorous no need for ETT or tracheal suctioning
MH acute crisis Page 144 of 217 Manifestations : Hypercarbia, Tachycardia, Tachypnea, Temp (1°C–2°C increase every 5 minutes), HTN, Cardiac dysrhythmias, Acidosis, Arterial hypoxemia, Hyperkalemia, Skeletal muscle activity, Myoglobinuria DDx: pheo, thyroid storm, carcinoid Management: Call for help Discontinue inhaled anesthetics and succinylcholine Hyperventilate the lungs with 100% O2 Administer dantrolene (2.5 mg/kg iv) with repeated doses (up to a maximum of 10 mg/kg iv) based on Paco2, heart rate, and body temperature (each ampule of 20 mg is mixed with 50 ml of distilled water) If Dantrolene is not available, give procainamide IV 1mg/kg up to 15mg/kg Treat persistent acidosis with sodium bicarbonate (1–2 mEq/kg iv) Control body temperature (gastric lavage, external ice packs until 38°C) Replace anesthetic circuit and canister Monitor with capnography and arterial blood gases Be prepared to treat hyperkalemia and cardiac dysrhythmias
Mineralocorticoid Physiology Page 145 of 217 Aldosterone is a major regulator of extracellular volume and K homeostasis through the resorption of Na and the secretion of K. Renal perfusion pressure+ sympathetic stimulation+ Na, and hypovolemia renin from juxtaglomerular Renin splits angiotensinogen to angiotensin I ACE in the lung Angiotensin II aldosterone. Other stimuli that aldosterone includeK and, to a limited degree, Na, PGE, and ACTH. So aldosterone K and Na and HTN, while is the opposite Mineralocorticoid Insufficiency: Common in CRF, and DM, Pt usually on fludrocortisone 0.05-0.1 mg/d C hypovolemia, heart block due to K, M K, Na, and metabolic acidosis (hyperchloremic) D Avoid Sux, and NSAID PGE Renin exacerbation
Mitral Regurgitation Page 146 of 217 Chronic regurgitation caused by abnormal leaflet anatomy can be due to congenital or rheumatic disease, myxomatous degeneration(MVP), CTD, infective endocarditis and LV hypertrophy. CTD associated with MR include SLE, rh arthritis, ank spondylitis, and scleroderma. Valvular involvement in CTD is variable; about 50% of patients with SLE have detectable MR, and approximately 25% have significant regurgitation. Acute severe MR is caused by infective endocarditis which result in chordae tendineae, acute MI with papillary muscle rupture or retraction usually from RCA, or prosthetic valve dysfunction. Almost always associated with MS. Pathogenesis Long latent period 30-40 yrs. LA volume overload LV volume overload with foreword LV SV, Eccentric hypertrophy of the LV, Regurgitation fraction > 0.6 associated with severe MR, PAWP giant V wave, In acute MR there is sudden in LAP pul edema. History Patients with chronic MR remain asymptomatic for an extended period. Later, patients develop symptoms of fatigue and exertional dyspnea, followed by more overt symptoms of CHF, including orthopnea and paroxysmal dyspnea. When CHF develops rapid deterioration with 5 yrs mortality rate 50% Physical Findings
Mitral Stenosis Page 147 of 217 normal MVA 4.0 to 6.0 cm2, Symp(exercise or tachycardia) 2.0 to 2.5 cm2; rest < 1.5 cm2. 2 mild gradient < 5 mm Hg and VA >1.5 cm . Severe gradient > 10 mmHg, and valve area < 1 cm2. MS in adults is predominantly of rheumatic origin. F>M. The MV is the most common site of rheumatic valve disease. Long latent period > 20 yrs. Pathogenesis Obstruction to LV inflow LA dilation and HTN and resultant pul venous HTN interstitial edema work of breathing dysponea, and predispose to supraventricular tachyarrythemia. Pul arteriolar and capillary vasoconstriction protect against pul edema, although PVR exacerbates pul arterial and RV HTN and causes RVH. Pul HTN can be severe late in the course of MS, with eventual RV systolic dysfunction. Acute decompensation occur due to stress e.g. sepsis, pregnancy, A fib, PE which can lead to pul edema Stasis of the blood in the LA thrombi A fib systemic emboli. History Early fatigue or dyspnea precipitated by events with associated tachycardia, including strenuous physical exercise, emotional stress, fever, pregnancy, or surgery.
MR Page 148 of 217 Well tolerated in pregnancy risk of A.fib with systemic embolization due to hypercoaglable state in pregnancy hemodynamic Goals: o preload maintain, LUD, avoid overload o R/R slightly maintain sinus, aggressively treat arrhythmia o Cont maintain, avoid cardiodepressant o Afterlaod o PVR avoid pain, hypoxia, PCO2 If mild no need for aggressive monitoring, but if severe then art-line, CVP/PAC MVP manage as MR
MS Page 149 of 217 Not well tolerated, with risk of pul edema. Arrhythmias are not tolerated at all, and needs to treated very aggressively with -blockers, Digoxin, over even cardioversion, then lasix mortality during labor/post-partum Mild is usually tolerated ok But mod/severe pregnancy worsen NYHA by 1-2 classes Need invasive hemodynamic monitoring art-line, PAC, O2 all the time In the 2nd stage avoid explosive effort valsalva VR pul edema Avoid overzealous hydration pul edema Tachycardia -blockers hemodynamic Goals: o preload maintain, LUD, avoid overhydration o R/R slow and sinus o Cont maintain, avoid cardiodepressant o Afterlaod maintain, avoid sudden in SVR o PVR avoid by pain, hypoxia, PCO2 Neo is the best choice in case of hypotension
Mucopolysaccharoidosis: I H Hurler I H/S Hurler/Scheie I S Scheie II Hunter III Sanfilippo IV Morquio
Page 150 of 217
A Coarse facial features, macrogolssia, short neck difficult A/W B Restrictive defect C CAD, VHD, AR, Cardiomyopathy GI hepatosplenomegaly MSK joint stiffness, AO instability, odontoid hypoplasia, kyphoscoliosis, Dwarfism Routine lab + Echo, CXR
Multiple Sclerosis Page 151 of 217 demyelination in the brain and spinal cord, F>M symptoms depend on the sites: visual disturbances, nystagmus, limb weakness and paresthesias, The legs are affected more than the arms. Bowel retention and urinary incontinence are frequent complaints. Involvement of the brain stem can produce diplopia, trigeminal neuralgia, cardiac dysrhythmias, and autonomic dysfunction, while alterations in ventilation can lead to hypoxemia, apnea, and respiratory failure. As is typical in many immune disorders, pregnancy is associated with an improvement in symptoms, but relapse frequently occurs in the first three postpartum months. treatment Corticosteroids, immunosuppressants (azathioprine, methotrexate, cyclophosphamide, and cyclosporine) Symptoms exacerbation with stress (emotional, surgical) temp, infections Management of Anesthesia Possible exacerbation post-op Document neurological symptoms pre-op, re-exam post-op the patient should be advised that surgery and anesthesia could produce a relapse despite a well managed anesthetic
Murmurs Page 152 of 217 Innocent murmurs: soft, systolic and not radiated, may vary with position, not characteristic of any lesions Noninnocent murmurs: all diastolic murmurs, all pansystolic, continues, late systolic and transmitted murmurs For innocent murmurs no need for surgical delay, and no need for prophylaxis Not noninnocent one’s if heard in the pre-op delay, and further investigation
Midsystolic Page 153 of 217 flow across aortic or pulmonic valve (e.g., secondary to AR or ASD) Aortic valve leaflet sclerosis (e.g., in elderly patients) Aortic or pulmonic outflow obstruction (valvular, subvalvular, supravalvular) Dilatation of aortic root or proximal pulmonary artery Papillary muscle dysfunction Holosystolic MR, TR, VSD Late Systolic MVP, Papillary muscle dysfunction Early Diastolic Aortic or pulmonic valve insufficiency Mid-Diastolic MS, TS flow across nonstenotic AV valve (e.g., secondary to MR or ASD) Presystolic MS (with sinus rhythm) Continuous Murmurs PDA
Muscular dystrophy
Page 154 of 217
7 main types with progressive and variable rate in losing of muscle function.
Duchenne’s muscular dystrophy
The most common, and the most severe form. Due to lack of protein Dystrophin. Painless degeneration of the skeletal muscle. X-linked trait (boys) S/S 2-5 yrs old. In the wheelchair by age of 12. The affected muscle may become enlarged, due to fatty infiltration. Death by 15-25. Secondary to CHF and pneumonia. Serum CK reflect the progression of the disease, with 30-300 folds above normal, later with complete degeneration the level well . Smooth muscle involvement GI hypomotility and gastroparesis. CVS o myocardial degeneration loss of R-wave in the lateral leads o contractility dilated cardiomyopathy, and arrhythmias
MVP: Page 155 of 217 More common in young female than in male May associated with other disease e.g. marfan syndrome, connective tissue disease. Risk of endocarditis, stroke, arrhythmias, sudden death If associated with MR or CHF, Pt could be on ACEI, -blockers, Diuretics, antiarrhythmics, anticoagulants P/E late systolic click, if MR late systolic murmur A N/A unless associated with other disease B if CHF plu edema, ? scoliosis restrictive lung defect C CHF, Arrhythmias, Endocarditis prophylaxis D avoid histamine releasing drugs, and ketamine CNS Stroke, anxious Pt may benefit from pre-op meds Hemodynamic goals Preload maintain Contractility avoid R & R sinus, little fast Afterload avoid , better
Myasthenia Gravis Page 156 of 217 Osserman and Genkins classification: • Class I—ocular symptoms only • Class IA—ocular S’s with EMG evidence of peripheral muscle involvement • Class IIA—mild generalized symptoms • Class IIB—more severe and rapidly progressive symptoms • Class III—acute, presenting in weeks to months with severe bulbar symptoms • Class IV—late in the course of the disease with severe bulbar symptoms and marked generalized weakness autoimmune disease with anti-acetylcholine receptor antibodies, F>M Abnormal thymus glands 75% of pts(85% show hyperplasia; 15% thymoma). 75% of pts either go into remission or are improved post-op Medical ttt: anticholinesterase, steroids, other immunosuppressant (azathioprine, cyclophosphamide, cyclosporine)and plasmapheresis. underdosage ―myasthenic crisis‖ whereas overdosage will produce a ―cholinergic crisis.‖ Excessive doses of cholinesterase inhibitors produce abdominal cramping, vomiting, diarrhea, salivation, bradycardia, and skeletal muscle weakness that mimics the weakness of myasthenia , to differentiate
Myasthenic Syndrome (Lambert-Eaton Syndrome) Page 157 of 217 Associated with small cell ca of the lung IgG antibodies against Ca channel in the presynaptic membrane Ach release in response to nerve stimulator M>F, age 50-70 Mainly proximal muscle weakness A B rarely respiratory failure C autonomic dysfunction orthostatic hypotension D sensitive to both Sux and NDMR, Pt could be on diaminopyridine Sz Keep high index of suspicion in a Pt with Lung Ca Consider Art-line
Page 158 of 217
NALS Page 159 of 217 Exam table goes trend for drainage and reverse trend to PO2 Avoid hypothermia VO2 metabolic acidosis Assess for choanal atersia usually cyanotic and resp depression at rest, pink when crying If Apgar score < 8 with not resp depression give O2 by ―blow by‖ So If not breathing or cyanotic suction the A/W, warmth, dry, tactile stimulation by rubbing the back, flicking the soles of the foot, give O2 not breathing or HR < 100 PPV with initial P 30-40 cmH2O for 4-5 sec to open the alveoli, the vent @ rate 40-60 min if HR > 100, and Pink ongoing care, if HR < 60 PPV and start Chest compression for 30 sec if still HR < 60 five Epi ….. Bicarb……….. For vent I:E = 1:1, @ 40-60 min, after the 1st breath the P 20-30 cm H2O For chest compression to vent 3:1 1,5:0.5 sec 90:30 pre minute Chest compression using two thumbs just below a line drown between two nipples to compress the AP diameter by 1/3 to ½ Intubation can be considered at any time If Vent without ETT for > 2-3 min decompress the stomach
Necrotizing fasciitis Page 160 of 217 Emergency and life threatening with high mortality rate Possible underlying disease: DM, alcoholism, malnutrition, renal and CV diseases Septic shock, possible under resuscitated A full stomach RSI B ARDS, respiratory failure, pul edema C septic shock with SVR, CO M lactic acidosis, lytes abnormalities R ARF CNS LOC Lab and Mx as septic shock Post-op ICU
Neonatal Considerations: Page 161 of 217 In addition to the pediatrics considerations Metabolic risk of hypoglycemia S/S: apnea, convulsion Glucose infusion @ 4-8 mg/kg/min hyperglycemia cerebral hemorrhage, glucosuria H2O and lytes depletion Physiological jaundice alter drugs pharmacokinetics, and free bili kernicterus, which by hypoxia, acidosis, hypothermia Renal Na loss, immature renal function CNS fragile cerebral vessels risk of IVH by hypoxia, hypercarbia, Na, fluctuation in BP, low Hb, rapid administration od NHCO3 Eye ROP maintain O2 sat 90-95% or PO2 50-70
Peri-op nerve injury: Page 162 of 217 History: Symptoms: pain, paresthesia, motor weakness, where, when did it start Presence of risk factors or conditions that may have neuropathy as a symptoms: DM, Obesity, R Arthritis, PVD, smoking, alcohol, Drugs that may cause neuropathies chemo, anti-virals Review anesthetic records, OR note for documentation of padding, position A block done or not if yes any symptom at the time of the block pain or paresthesias with injection If the surgical procedure done in the same side ? surgical complication or prolonged use of a tourniquet, also BP cuff may cause injury Exam: V/S, complete neurological exam, and mainly examining the affected side sensory, motor, reflex, and looking for any pressure demarcation Also assess for nerve or dermatomal distribution Obtain a Neurology consult for further evaluation and need for nerve conduction study, and possible MRI Sensory only F/U in 2wks, motor further evaluation
Neuraxial Anesthesia and anticoagulation Page 163 of 217 IV heparin e.g. vascular Sx delay IV heparin 1hr post catheter placement, and catheter removal 2-4 hr after the last dose or one hr before the next dose S.C heparin also delay catheter placement 2-4 hrs, or delay the heparin 1 hr post catheter placement LMWH: needle placement 10-12hrs after the last dose of LMWH, if Pt receiving a higher dose 1mg/kg delay 24hr Post-op 1st dose of LMWH delay 24 hr, and may keep the catheter until next AM, give LMWH 2hrs later Anti-PLT: plavix ?? no data, but better at least 10 days before needle placement, NSAID are OK Pt on oral med (Warfarin) stop 5 days per-op INR= 1.4 is OK
Neurofibromatosis Page 164 of 217 AD, café-au-lait spots >6, with > 1.5 in diameter, with CNS vascular and skin involvement, and short stature Could be a part of MEN IIB A difficult intubation, due to laryngeal or tracheal compression B restrictive lung defect, interstitial lung disease, possible mediastinal mass C HTN due to renovascular, Pheo, coarctation, Wilm’s tumor CNS Astrocytoma, meningioma (ICP), spinal cord tumor, Sz disorder M diffuse endocrine disorder as well as carcinoid tumor MSK Kyphoscoliosis Regional Anesthesia could be difficult, Avoid if there is spinal cord tumor Lab CBC, Lytes, BUN, creat, ECG, Echo, CXR, PFT with F/V loop
Neuroleptic Malignant Syndrome (NMS) Page 165 of 217 S/S include fever, rhabdomyolysis, tachycardia, hypertension, agitation, muscle rigidity, and acidosis, mental changes, and stupor, hypoxia, acidosis, CK, and myoglobinuria The mortality rate is unknown, but may be as high as 20%. Dantrolene is an effective therapeutic modality in many cases of NMS. there are significant differences between the two. MH is acute, whereas NMS often occurs after longer term drug exposure. Phenothiazines and haloperidol or any of the newer potent antipsychotic agents alone or in combination are usually triggering agents for NMS Sudden withdrawal of drugs used for Parkinson's disease may also trigger NMS (ECT) with Sux does not appear to trigger the syndrome. does not seem to be inherited, . possible due to dopamine depletion in the CNS by psychoactive agents. bromocriptine, a dopamine agonist, is often useful in treatment of NMS with dehydration, rapid titration of triggering drugs, and psychomotor agitation Other DDx: CNS diseases meningitis, tumor,
Non-obstetrical surgery during pregnancy Page 166 of 217 Obstetric consideration Risk of abortion and premature labor Minimize the amount of drugs as much as possible Use only the drugs that are known to be safe(STP, Sux, NDMR, Opioids, Ketamine, Etomidate) If urgent Sx consider delay to the 2nd trimester Have an obstetric consultation For GA < 16 wks have FHM pre, and post op, for >16 wks have it intra-op for abdominal procedure consider a transvagainal monitor FHR variability present @25-27 wks Maintain normal maternal BP, Oxygenation, acid-base status, avoid aortocaval compression For pelvic and lower limb and upper limb consider regional technique For laparoscopic procedures max peritoneal inflation pressure 8-12 mm Hg For spinal or epidural give a fluid bolus before Always give reflux prophylaxis, and do RSI, with maintaining LUD
Obesity Page 167 of 217 A difficult intubation B OSA, pickwickian syndrome, restrictive defect, with FRC and Pul HTN C HTN, CAD, pul HTN with cor-pulmonale, RV and LV dysfunction GI GERD, gastric acidity, fatty liver with liver dysfunction M DM D calculate the drug dosage according to the lean body mass H/P evidence of OSA, and RV/LV dysfunction snoring, orhtopnea, PND, EXAM RV/LV failure LAB CBC-D, Lytes, BUN, Creat, ABG, PFT, ECG,LFT, and consider Echo Difficult IV access, and regional anesthesia
Obstetric considerations: Page 168 of 217 Physiological and anatomical changes A difficult A/W, Full stomach, ,RSI B easy desat FRC, VO2 C hyperdynamic state, Aortocaval compression BP, UP blood flow D MAC, cholinesterase, albumin Free F of drugs, placental drug transfer GI/Hepatic full stomach, gastric empting, liver enzyme
Omphalocele and Gastroschisis Page 169 of 217 o Impaired blood supply to the herniated organs, and intestinal obstruction o Major intravascular fluid shift and dehydration full-strength balanced salt solution o Hypothermia and hypoglycemia A possible difficult airway Beckwith-Wiedemann syndrome consists of mental retardation, hypoglycemia, congenital heart disease, a large tongue, and an omphalocele. B respiratory failure C CHD in 20% of infants with omphalocele. Induction: NG aspirate gastric content then RSI , need large IV , possible central, and arterial line Post-op keep intubated M intravascular volume, with lytes abnormality
Organophosphate poisoning Bind to acetylcholinestrase enzyme S/S: Nicotinic: muscle weakness, fasciculation Muscarinic: DUMBELS syndrome D diaphoresis, diarrhea U urination M miosis B bradycardia, bronchorrhea, bronchospasm E Emisis L lacremation S salivation A salivation, aspiration B Respiratory failure, , bronchorrhea, bronchospasm C hypotension, bradycardia, shock, arrhythmias, QT(poor prognosis) D Avoid aminoglycosids ABx M lytes abnormalities, acidosis, dehydration GI N&V, diarrhea
Page 170 of 217
Osteogenesis Imperfecta: A connective tissue disorder with 4 subtypes Multiple #, short stature, blue sclera A deformity of the base of the skull, vertebral # Awake FOI B kyphoscoliosis restrictive lung defect C Cor-pulmonale Heme impaired PLT function
Page 171 of 217
Other hemolytic anemia’s: Page 172 of 217 Spherocytosis: Membrane defect abnormal shape RBC hemolysis May have a hemolytic crisis which can triggered by infection and folate deficiency May come for splenectomy G6PD Deficiency: RBC enzyme defect Can have a hemolytic crisis if exposed to some food and drugs: Fava beans, PNC, Tyhlenol, antimalarial drugs, methylene blue, ASA in large dose Usually happened 2-5 day after ingestion May have DIC
Oxygen Delivery and Oxygen Consumption Page 173 of 217 Oxygen Delivery. Oxygen delivery is a function of arterial oxygen content (Cao2) and cardiac output. Cao2 is expressed as the number of milliliters of oxygen contained in 100 ml of blood and is calculated as follows: Cao2 = (Hgb × 1.34 × Sao2) + (0.003 × Pao2) DO2 = CO × Cao2 Oxygen Consumption. O2 consumption = CO x (CaO2-CvO2) Oxygen extraction Ratio ER= O2 consumption / O2 delivery ER= [ CO x (CaO2-CvO2)] / CO x CaO2 = CaO2 – CvO2/CaO2
Pancreatitis:( acute, chronic) Page 174 of 217 Associated with: chronic alcohol abuse, blunt abdominal trauma, gallstone, perforated PUD Lab amylase DDx cholecystitis , MI, Pneumonia Chronic mainly with alcoholism, CF, old blunt trauma A RSI, for GI ileus B ARDS C hypovolemia, hypotension D narcotic tolerant, malnourished albumin free fraction of drugs careful titration M Ca, acidosis, DM, acute alcohol withdrawal Renal ARF due to dehydration CNS encephalopathy Heme anemia, DIC Consider art-line , CVP Post-op ICU, pain management
Parkinson's Disease Page 175 of 217 degenerative disease of the CNS caused by loss of dopaminergic fibers in the basal ganglia of the brain.(substantia nigra) clinical features are resting tremor, cogwheel rigidity of the extremities, bradykinesia, shuffling gait, stooped posture, and facial immobility. A laryngospasm, muscle rigidity before giving MR difficult vent consider RSI B frequent aspiration, VC, COPD C arrhythmias due to L-dopa, autonomic dysfunction, intravascular volume D L-dopa(sinemet) Levodopa+ a peripheral dopamine decarboxylase inhibitor carbidopa to systemic side effect give in AM t1/2 6-12, avoid Maxran, Demerol, alfenta, droperidol, sux may use for RSI, K one case report Post-op: In the postoperative period, patients with Parkinson's disease are more susceptible to the development of mental confusion and even hallucinations.
PDPH Page 176 of 217 In a supine position very mild, sitting severe fronto-occipital headache May associated with cranial N symptoms: diplopia, tinnitus, N&V DDx: meningitis, migraine Action: Review anesthetic Record for Neuraxial procedure, type and size of needle for spinal, and wet tab documentation, and any other complications Review past-medical Hx neurological Hx (headache) Headache: character, severity, aggravating and relieving factors (position), associated symptoms, and the location of the headache Exam: V/S include Temp, meningeal signs (meningismus, photophobia, fever), Neuro Exam looking for any sensory or motor deficit Rx: bed rest, hydration, caffeine 300mg PO q8-12hrs, Tylenol, and NSAID’s if not working or severe headache Epidural blood patch Peri-tonsilar abscess Emergency and potential life threatening A airway obstruction, with trismus , possible full stomach, do a gas induction with no muscle relaxant , gentle intubation avoid rupture the abscess
Pheochromocytoma Page 177 of 217 In normal medulla, norepinephrine account for only 20% of the secretion, where it is greater in a Pt with pheochromocytoma. halothane and histamine-releasing drugs, can exacerbate the life-threatening cardiovascular effects of the catecholamines secreted by these tumors. Most (85–90%) are solitary tumors localized to a single adrenal gland, usually the right, 10% of adults and 25% of children have bilateral tumors. extra-adrenal sites (10%) along the paravertebral sympathetic chain. 95% in the abdomen, a small % located in thorax, urinary bladder, or neck. Malignant spread of highly vascular tumors in approximately 10% of cases. In about 5% of cases, this tumor is inherited as a familial AD trait. It may be part of the polyglandular syndrome as MEN Type IIA or IIB. Type IIA includes: medullary carcinoma of the thyroid, parathyroid hyperplasia, pheochromocytoma; Type IIB consists of: medullary carcinoma of the thyroid, pheochromocytoma, neuromas of the oral mucosa. may also arise in association with von Recklinghausen's neurofibromatosis or von Hippel-Lindau disease (retinal and cerebellar angiomatosis).
Phosphate Page 178 of 217 distributed in similar concentrations throughout intracellular and extracellular fluid.90% in bone, 10% is intracellular, and <1%, in the ECF. free ion (55%), complexed ion (33%), and in a protein-bound form (12%). Control of phos concentration by altered renal excretion and redistribution within the body compartments. Absorption occurs in the duodenum and jejunum and is largely unregulated. Phos reabsorption in the kidney is primarily regulated by PTH, dietary intake, and insulin-like growth factor. Phos provide the primary energy bond in ATP and creatine phosphate. Therefore, severe phosphate depletion results in cellular energy depletion. Phos is an essential element of second-messenger systems, including cAMP and phosphoinositides, and a major component of nucleic acids, phospholipids, and cell membranes. As part of 2,3-DPG, phos is important for off-loading oxygen from the hemoglobin molecule.
Physiological changes in pregnancy: Page 179 of 217 A venous engorgement, edema, by PIH, URTI and fluid overload, easy nasal bleed B FRC, TLC, ERV, IRV, TV, minute vent, and O2 consumption, shunt from 5% to 14 %, shift of O2-Hgb curve to the Rt with P50 30mmHg C CO, Normal BP due SVR, plasma volume Pierre Robin Syndrome: A difficult A/W due to micrognathia, glossoptosis, cleft palate B obstruction pul edema, Aspiration C CHF, pul HTN, cor pulmonale, associated CHD CNS Sz due to hypoxic brain injury Do awake FOI, have ENT surgeon in the room for possible trach A/W obstruction improve with age Extubate awake only
PIH and HELLP Page 180 of 217 In addition to the changes in pregnancy A airway edema, difficult intubation difficult A/W cart in the room B pul edema, more after delivery C CHF, BP, volume, oncotic pressure D Mg, other meds, could be on ASA M Mg, albumin Heme anemia, hemolysis, thrombocytopenia , fibrinogen CNS LOC, headache, blurred vision, seizure, bleeding , edema Renal GFR, oliguria, ARF GI/Hepatic RUQ pain, liver rupture Rx start Mg bolus 4g then infusion @ 1-3 g/h, consider other anti-HTN meds e.g. labetolol, SNP, NTG, hydralazine, (ACEI are C/I due to fetal effect) Monitor Mg level avoid Mg toxicity, consider early epidural help BP, improve UP blood flow (if PLT are OK) Monitors: art line, fetal monitoring, CVP/PAC Before giving any fluid bolus look for evidence of CHF Lab: CBC-D, Lytes, BUN, Creat, Mg, PT, PTT, fibrinogen, LFT, BT
Pituitary Tumors, and transsphenoidal approach Page 181 of 217 Ant regulated by the hypothalamus secret 7 hormones Post ADH, Oxytocin Tumors could be non-functioning, or hyper secreting The non-functional mass effect headache impaired vision, N&V, CN palsy, and ICP, or pan-hypopitutarism hyper secreting could be a MEN I, usually small, the most common is adenoma secreting prolactin , then GH, then ACTH, other effect hyperthyroid, DM pituitary apoplexy due to sudden hemorrhage neuro deficit and pituitary function Mx steroids and surgical decompression May not develop DI until after starting steroids therapy Monitors routine with art-line for acromegaly, CVP if head-op position Lab CBC, lytes, ABG, CXR, ECG, lateral neck XR Critical structures internal carotid artery, cavernous sinuses, CN III, IV, V, VI A possible difficult intubation B OSA C HTN, Cardiomegaly, cardiomyopathy D hormone replacement, stress dose steroid,
Placenta previa Page 182 of 217 Risks: previous C/S, previa Painless vaginal bleeding in the 2nd-3rd trimester Risk of abruption and IUGR Avoid vaginal exam and tocolytic therapy A and B obst C hypovolemia, shock D avoid tocolytic Heme DIC rare, most are dilutional thrombocytopenia Mx: lab as in abruption shock as in abruption GA Vs spinal/epidural depend wither if the placenta is anterior or >1 C/S with risk of accreta GA, if posterior may consider spinal/epidural if the Pt is stable
Porphyrias Page 183 of 217 A group of inborn error of metabolism, with defect in heme synthesis Complete deficiency of enzymes is incompatible with life Deficiency of one enzyme will lead to accumulation of one or more intermediates molecules which will give the clinical manifestation of Porphyria. The rate-limiting step in heme synthesis is the conjugation of succinyl-CoA with glycine to form D-aminolevulinic acid ALA (the enzyme is aminolevulinic acid synthetase). generally manifest after puberty. Inheritance is an AD pattern, but congenital erythropoietic porphyria is inherited as an AR pattern. A functional classification for the anesthesiologist is based on a division of the porphyrias into: o Inducible: acute symptoms are precipitated on drug exposure, which are: Acute intermittent Porphyria variegate Porphyria ( 80% photosensitive) hereditary coproporphyria o noninducible forms.
Post-op Stridor: Page 184 of 217 Emergency, and life threatening Proceed immediately to the PARR Review the V/S, and quick AMPLE history , 100% O2, and Call for help, do jaw thrust, apply oral A/W, apply CPAP, suction the A/W DDx: 1-Laryngeospasm, 2-laryngeal edema due to volume overload or Trendelenburg position intra-op,3- VC paralysis due to neck or thoracic Sx, or residual NM blockade, 4- A/W foreign body (secretion, blood, vomit
Post-op Altered LOC/Agitation: Page 185 of 217 With LOC could be life threatening, agitation potential harm to him self and nurses Proceed immediately to the PARR ABC, restrain the Pt if needed, 100% O2. obtain new V/S Review anesthetic chart/ talk to the anesthetist who did the case, review the old chart DDx: o Psychological response to emergence o Co-existing mental/psychological problem (post-traumatic stress) o Intra-op re-call o Residual anesthetics, NMB Agents, Ketamine. o Drugs/alcohol withdrawal o Withdrawal of anti-psychotic, seizure, Parkinson meds o Surgical pain, bladder distention o A/W obstruction with hypoxia and hypercarbia o Other metabolic abnormalities Na, Ca, hypoglycemia o CNS: hypoperfusion, CVA, Sz, postictal
Post-op hepatic dysfunction Page 186 of 217 Classify as pre, intra and post hepatic The main S/S is jaundice Need repeat measurement of bili, AST/ALT, and ALP Most likely multifactorial One of the main factors could be intra-op hepatic hypoxemia Steps: 1) Review all meds given to the Pt without any exclusion peri-op, includes intra-op use of vasopressors splanchnic vasoconstriction B flow 2) Look for source of infection 3) Blood Tx bili load in Pt with co-existing liver dysfunction 4) Look for hematoma hyperbilirubinemia 5) Role out hemolysis Hb, retics 6) Review anesthetic and PARR records for any evidence of hypoxemia, hypotension, hypovent, hypovolemia 7) Look for extra-hepatic source of liver dysfunction CHF, resp failure, PE, RF 8) Could be benign post-op intrahepatic cholestasis
Post-tonsillectomy bleeding Page 187 of 217 Emergency and potential life threatening Go immediately to see the Pt OR emerg meds , airway equipment double setup X2 suction , X2 scops A full stomach, possible difficult airway use ketamine for induction, RSI B hypoxia C hemorrhagic shock, resuscitate the Pt H possible bleeding disorder. Lab CBC, lytes, PT, PTT, X-match
Pre-op Cardiac evaluation: Page 188 of 217 See other card for clinical predictors See other card for stratification for noncardiac surgical procedure See the algorithm Recent MI wait 4-6 wks for elective surgery Lab evaluation o Resting LV function is not a predictor for ischemic event o 12 leads ECG o Exercise or pharma stress test for Pt with intermediate risk, or when Pt is unreliable o Angio for Pt suspected or known CAD Pre-op therapy o CABG for high risk Pt, with possibility to improve outcome o PCA: no controlled trial for PCA vs medical therapy, If Pt had PCA, with balloon dilation only, wait only for one week for elective procedure, if stent 4-6 wks with minimum 2 wks, for anti-PLT therapy o Medical: -blokers Anesthetic consideration o No technique is superior
Preterm labor Page 189 of 217 Between 20-37 wks fetal M&M Pt may given tocolytic therapy if there is no C/I -agonist: Ritodrine and terbutaline o For short term only to allow time for lung maturity after steroids o The effect persist to 60-90 min after D/C, need at least 10 min D/C before giving anesthetic o S/E: hyperglycemia, tachycardia, with possible arrhythmia, pul edema, myocardial ischemia, hypotension, cerebral vasospasm, fetal tachycardia, rebound hypoglycemia o Avoid overzealous hydration which may risk of pul edema, and hyperventilation K o Lidocaine IV may prevent arrhythmia MgSO4 o See PIH for S/E, less severe than -agonist o Risk of hypotension with spinal/epidural o sensitivity to NDMR
Prone position Page 190 of 217 Difficult access to the A/W Difficult resuscitation Difficult to add invasive monitoring art-line, CVP, TEE Pressure injury to eyes, nose, iliac crest, knees, toes, breast, genitalia Brachial plexus injury CI, SV, Venus return due to pressure on the abdomen vena caval pressure epidural vein engorgement
Protein C and Protein S Deficiency Page 191 of 217 Congenital AD, or Acquired due to hepatic dysfunction, vit K deficiency, and DIC, post-op, hemodialysis, postpartum risk of thrombo-embolic phenomena post-op A N/A B PE, with possible Pul HTN, C IHD (MI, angina), Peripheral vascular disease D on coumadin stop pre-op and start heparin G bowel ischemia R renal vein and artery thrombosis. CNS sagital sinus thrombosis stroke, TIA’s for neuraxial anesthesia look in the ASRA guidelines may give FFP to protein C level. Antithrombin III deficiency risk of thrombo-embolic phenomena Resistance to heparin, may give Antithrombin III concentrate, or FFP
Pul HTN Page 192 of 217 The pulmonary vessels are more reactive compared to Eisenmenger High mortality rate Hemodynamic Goals: o preload maintain, LUD o R/R maintain normal and sinus o Cont maintain, avoid cardiodepressant o Afterlaod maintain, avoid sudden in SVR o PVR Avoid any thing that PVR pain, hypoxia, acidosis, PCO2 O2 all the time, Art-line, Consider: NO, prostacycline, CCB, NTG to PVR PAC risk/benefit No spinal, epidural slowly titrate GA same problem as in Eisenmenger Post-op ICU
Pulmonary embolism Page 193 of 217 Associated with hyper-coagulation state (protein C and S deficiency ), trauma, prolonged bed rest High M&M Pathophysiology: o Pulmonary arteries obstruction dead space ventilation hypoxemia , hypercarbia o PVR, Bronchospasm o RV dysfunction and arrhythmias Pt may present to the OR for emergency surgery, insertion of IVC filter or surgical embolectomy Also Pt may present with previous history of PE, and now anticoagulated have a hematology consult (Q: risk/benefit of holding meds pre-op) also discuss with the surgeon regarding continuing the anticoagulation med periop Have PT, PTT, and PLT count (HIT) Better to avoid Neuraxial technique in those Pt If diagnosis is in doubt Spiral CT, V/Q scan, Echo
Pulmonary HTN Page 194 of 217 @ rest mean of 25, with exercise > 30 Primary (idiopathic) F:M 3:1, age 20-40 Secondary: o pul disease: asthma, COPD, restrictive lung disease, cystic fibrosis, o heart disease: MS, AS, ASD, VSD o collagen vascular disease o thromboembolic disease: PE, sickle cell S/S SOBOE, easy fatigue wheezing, graham steel murmur Lab: CXR, ECG(RVH, RAD, Rt atrial enlargement), Echo, ABG, PFT, NO test to if responsive or not (Viagra) Cardiology consult and ICU Monitors: CAS, 5 leads EGC, art-line, CVP, PAC???, TEE, ECG look for acute strain pattern in leads II, III and aVF Options RA Vs GA, better RA Have NO ready, and inotropic support (milrinon, dobutamine) SNP, NTG Keep 100 O2 all time Avoid things PVR ( hypoxia, acidosis, hypothermia, PCO2)
Pyloric stenosis Page 195 of 217 M>F Not a surgical emergency, S/S appear 2-6wks With the consideration of neonate A full stomach RSI B compensated resp acidosis hypoventilation C hypovolemia shock M hypochloremic metabolic alkalosis, dehydration Pre op assess the level hydration skin turgor, anterior fontanel, moist tongue, urine OP, V/S Check lytes Na >132, Cl>88, K > 3.2, Give K, if + urine OP Induction give atropine, insert NGT, or OGT to empty the stomach (no guaranteed) and pre-oxygenate RSI with cricoid pressure Maintenance need to be paralyzed if not risk of mucosal perforation Infiltrate Marcaine with epi, give Tylenol 15mg/kg PR for pain control
Restrictive Cardiomyopathy Page 196 of 217 Causes: o Toxic :Methysergide, Anorectic agents, Radiation o Infectious: viral myocarditis o Infiltration: endomyocardial fibrosis o Genetic o Idiopathic o Infiltration Sarcoid, Hemochromatosis, Amyloidosis ,Glycogen storage disease Impaired diastolic filling Have the same clinical picture of constrictive pericarditis Except that the LV is more affected than RV Management of anesthesia: o As Tamponade
Restrictive lung disease Page 197 of 217 The main feature is lung compliance with TLC, normal FEV1/FVC, and VC N 70ml/kg, as low as 15ml/kg, and possible hyperventilation with PCO2 Could be acute Vs chronic, where the acute component could be reversible Causes: o intrinsic lung disease ( edema, pneumonia, aspiration, ARDS, fibrosis due to drugs, or idiopathic, and plural diseases) o Neuromuscular diseases: spinal cord transection, Guillian barre, muscular dystrophy, myasthenia, and myasthenic syndrome o MSK scoliosis, sternal deformity o Extrinsic: obesity, pregnancy, ascites S/S SOBOE, exercise tolerance, cough, breathing pattern Vt, RR With severe disease Pt may have pul HTN, with S/S of Rt heart failure Pre-op: determine the severity by H/P and Lab, and treat the possible acute reversible component A VC < 15ml/kg with PCO2 high risk Lab: CBC-D, lytes, BUN, creat, CXR, ABG, PFT, ECG, Echo
Rheumatoid arthritis Page 198 of 217 F> M, Age 30-50 The hands and wrists are involved first, particularly the metacarpophalangeal and proximal interphalangeal joints. A:C-spine: atlantoaxial subluxation, The degree of cord compression does not correlate well with the patient's symptoms, and asymptomatic patients may have a high degree of spinal canal stenosis., TMJ involvement, Cricoarytenoid arthritis which may cause pain, horseness, dyspnea, stridor and airway edema. So be caution with intubation and consider Fiberoptic intubation, and risk of postextubation stridor. B: pleural effusions, pulmonary nodules, interstitial lung disease, obstructive lung disease, restrictive lung disease. more common due to costochondral involvement Several of the antirheumatic drugs cause pulmonary dysfunction as well V/Q mismatch and hypoxia Consider PFT and possible post-op ICU bed C: Pericarditis in 30%, chronic constrictive pericarditis or pericardial tamponade myocarditis, coronary arteritis dysrhythmias secondary to development of rheumatoid nodules in the cardiac conduction system aortitis, producing aortic root dilation and aortic insufficiency, Valve fibrosis
Risk of RBC Tx Page 199 of 217 Citrate Intoxication o CPDA citrateionized calcium. o Signs hypotension, narrow pulse pressure, VEDP, and CVP o ECG changes: prolonged Q-T interval, widened QRS, and flattened T waves. o The hypocalcemia is directly related to the rate and volume of blood Tx. o Citrate is metabolized efficiently by the liver, Impaired liver function or perfusion will lower the rate threshold for developing citrate intoxication. o Treatment: CaCl Acid–Base Changes ? metabolic acidosis 2,3-DPG left shift of the O2–Hgb dissociation curve Hyperkalemia with rapid Tx by acidosis, hypovolemia, and hypothermia o ECG peaked T waves, a prolonged PR interval, and a widened QRS. o If ECG changes are observed the transfusion should be stopped and intravenous calcium should be administered. Bicarbonate, dextrose, and insulin may also be appropriate according to the severity of the episode Volume Overload Hypothermia CO, left shift of O2-Hgb, acidosis, coags Microaggregate Delivery
Sarcoidosis: Page 200 of 217 More common in African-American, F:M 2:1 A distorted anatomy with possible A/W obstruction difficult A/W FOI B restrictive lung disease with pulmonary fibrosis C Arrhythmias, heart block, CHF D on Steroid and immunosuppressant (stress dose) GI liver involvement CNS SOL, neuropathy, Sz Lab/DI CBC-D, Lytes, BUN, creat, ABG, CXR, PFT, ECG, LFT Consider ICU backup if bad PFT
SARS: Page 201 of 217 Not contagious until Pt become symptomatic with in 4-6 days(2-10) Transmission by close contact, and in a contact with resp secretion S/S and Lab: Fever, chills, headache, myalgia (nonspecific) Nonproductive cough, with SOB, other N&V, diarrhea Radiological evidence of pneumonia within 7-10 days of symptoms onset Lab: lymphopenia, PLT, PTT and Liver enzymes and CK SARS serum Antibodies positive SARS CoV isolation in cell culture PCR positive for SARS CoV RNA Action: Suspected Pt should be in resp isolation room ASAP if history contact with Pt with SARS or been in an epidemic area During Pt transfer have a surgical mask over the Pt Do CXR, pulse oxi, blood C/S, CBC-D, sputum for gram stain and C/S Test for other respiratory pathogens inf A, B, RSV, pneumococcal
Scleroderma Page 202 of 217 Progressive systemic sclerosis:Inflammation, Vascular sclerosis, Fibrosis of skin and viscera Tissue edema Some Pts have CREST syndrome, C: calcinosis, R: Raynaud’s phenomenon, E: esophageal hypomotality, S: scleroderma, T: Telengectesia F>M, Age 20-40 Pregnancy the progression of the disease in 50% of the Pt. A: flexion contracture difficult airway due to limited mouth opening, motility, LOS tone GERD need RSI B: A major cause of M&M, Chronic aspiration, Diffuse lung fibrosis restrictive lung disease, diffusion capacity C: risk of IHD, fibrosis of the conductive system arrhythmia, cardiomyopathy CHF, systemic and pulmonary HTN, pericarditis effusion tamponade, with systemic HTN intravascular volume hypotension , Raynaud’s phenomenon in 70% risk of ischemia with art-line CNS: peripheral and cranial nerve neuropathy o Eye: conjunctivitis and corneal abrasion
Scoliosis Sx Page 203 of 217 Need two stage Sx, 1st anterior approach to release the anterior spinal artery, and diskectomy, the 2nd stage to posterior instrumentation The scoliosis could be secondary to muscular disease ( muscular dystrophy) A Reflux RSI B Restrictive lung disease, risk of PPC (pneumonia, atelectasis) C myopathy, arrhythmias D avoid Sux Heme consider autologus blood donation pre-op Consult (ICU, Heme), talk to the Pt regarding awake test Lab:CBC-D, Lytes, BUN, creat, X-match, CXR, PFT, ABG, ECG, Echo if needed OR: blood in the OR, bear hugger, Art-line, IV wormer Position: prone check all pressure points, and frequent checking May consider deliberate hypotension if there is no C/I, with that HR will , so consider -blockers SSEP: if latency by 10% or amp by 60% BP, ask the surgeon to stop Volatiles have the least effect on SSEP See SSEP card Post-op: pain, PPC, ICU
SEP Any injury will cause in latency & amplitude SSEP 50% in amp to surgical maneuver significant Cortical ( SSEP, VEP) are more vulnerable to anesthetic drug effect brain stem/subcortical (SSEP, BAEP) are more resistance key points: maintain a constant anesthetic level, and avoid any sudden changes or a bolus doses of any drugs maintain and control other factors that may affect the SEP like temp, BP, PaO2 and PaCO2 Effect of inhalational agents: SSEP all lat/amp, except enf /, N2O 0/ VEP all lat/ amp BAEP alt/0 amp Effect of IV drugs: All drugs lat/ amp except ketamine and etomidate /, with 0/ effect on the VEP and no effect on BAEP at regular doses
Page 204 of 217
Septic shock: Page 205 of 217 A LOC, full stomach B resp failure, ARDS, pul edema C low or high output failure, SVR, D Abx, APC, steroids, inotrops, vasopressors Met lactic acidosis, base deficit, K, lytes disturbance, adrenal insufficiency Renal ATN, ARF Heme thrombocytopenia, DIC Management: ABC ECG, Sat, Art-line, CVP/PAC, frequent ABG, Lab: CXR, ABG, ECG, CBC-D, Blood C/S, sputum, and urine, lytes, BUN, creat, LFT, PT, PTT, Fibrinogen, D-dimer, ACTH stim test, if suspecting a source of infection do further investigation e.g. TEE or TTE for ? edocarditis, abdominal CT….. Early goal directed therapy( CVP 8-12, MAP >65, Urine>0.5ml/kg/hr, SvO2>70%) Broad spectrum ABx
Class I
Class II
Class III
Class IVPage 206 of 217
Blood loss (ml)
750
750–1500
1500–2000
2000
Blood loss (%)
15
15–30
30–40
40
HR (per min)
<100
>100
>120
140
Blood pressure
Normal
Normal
Pulse pressure
Normal or
RR
14–20
20–30
30–40
<35
30
20–30
5–15
Negligible
Mildly anxious
Anxious and confused
Confused, lethargic
Crystalloid
Crystalloid + blood
Crystalloid + blood
Urine ml/hr Mental status
Slightly anxious
Fluid (3:1 rule)‡ Crystalloid
Shoulder Sx: Page 207 of 217 Arthroplasy, and arthroscopy, and rotator cuff repair Use of a beach chair position VAE risk Limited access to the airway tighten the connection, reinforce with tap Possible eye and ears injury Avoid excessive head rotation brachial plexus injury Options GA, interscalene or combined Assess the arm before doing the block for any neurological deficit Risk of post-op neurological deficit the level of the injury is at the level of the trunk (same as interscalene) difficult to determine the cause (surgical Vs block) Neurapraxia 90% resolve within 3-4 months
Inappropriate Secretion of Antidiuretic Hormone (SIADH) Page 208 of 217 Causes: head injuries,intracranial tumors, pulmonary infections, small cell carcinoma of the lung and hypothyroidism. Clinical manifestations occur as a result of a dilutional hyponatremia, serum osmolality, and a reduced urine output with a high osmolality. Weight gain, skeletal muscle weakness, and mental confusion or convulsions are presenting symptoms. Peripheral edema and hypertension are rare. The diagnosis of the (SIADH) is one of exclusion, and other causes of hyponatremia must first be ruled out. The prognosis is related to the underlying cause of the syndrome. Treatment: Pt with mild/mod H2O intoxication is restriction of fluid intake to 800 ml·day– 1 . Pt with severe water intoxication associated with hyponatremia and mental confusion may require more aggressive therapy, with the iv administration of a hypertonic saline solution. This may be administered in conjunction with lasix Caution must be observed in patients with poor LV function. Isotonic saline is substituted for hypertonic solutions once the serum Na is in a safe range.
Sickle cell anemia Page 209 of 217 The defect in -chain, position 6 glutamic acid substituted by valine 3 types of crisis o hemolytic further anemia o sickling pain & vaso-occlusive o Aplastic may cause death. Ethnic background: Mediterranean and African-American. In infancy Hb F is protective. % of Hb S o trait (mild) o < 50% is Hb S o sickling do not occur under normal physiological conditions o may happen under extreme conditions e.g severe hypoxemia. o Disease (severe) o Hb S > 75% may up to 95% o Could be associated with other abnormal Hb e.g Hb C o Pt with Hb SC have a normal Hb level, but at a greater risk of sickling. Pre-op you need to knew what is the result of the Hb electrophoresis. mortality with in the number of the painful crisis in adult per-year.
Status asthmaticus Page 210 of 217 Emergency and life threatening Result in respiratory failure with hypoxia, hypercarbia, and respiratory/metabolic acidosis Management: o ABC, 100% O2 o Intubate deep/ also may consider BiPAP o Ventoline, ipratrupium bromide, steroids, thiophylline, leukotrine inhibitor, ABx if suspect infection o Other consider Ventoline IV, Isoprel/pei gtt, Ketamine, BNZ o Last volatile agent, and paralyze o Ventilation: volume control Vt 6-10ml/kg, PEEP 5-10, target normal PO2, pH, and PCO2, keep the platue pressure < 30cmH2O o If need switch to pressure control o Also may consider Heliox o Be aware of AutoPEEP disconnect the bag, if on vent reverse ratio ventilation
Stroke & TIA: Page 211 of 217 Hemorrhagic or ischemic Etiology: Atherosclerosis, embolic MI, A.fib, VHD, post-op CEA, trauma, severe HTN A LOC, loss of A/W reflux (RSI) B hypoventilation C HTN, CAD, VHD, A.fib, arrhythmias ECG, Echo D anti-PLT, ASA, coumadin, Avoid Sux, N. stimulator resistance N LOC, neuro deficit Peri-op Avoid swinging in BP, and hyperglycemia With chronic HTN the cerebral autoregulation curve shifted to the Rt
Supratentorial Intracranial Tumors Page 212 of 217 Review Pt overall medical condition Focus on Neuro-evaluation: LOC, S/S of ICP: headache, N&V, papilledema, unilateral pupil dilation, and the presence and extent of focal neurological deficit May have fluid and lytes abnormality Review CT/MRI head Lab: CBC, lytes, BUN, creat, ECG The main effect of Supratentorial masses is intracranial HTN The main anesthetic goal is to maximize the therapeutic modality to ICP, and to avoid any factor that may ICP ICP control SEE ICP card Monitoring: Standard + Art line, CVP, Foley cath, for the art-line have the transducer at the level of external auditory meatus ( level of circle of Willis) Induction: may need RSI, if CN involvement or LOC, give Lidocaine IV, with other standard induction drugs, Avoid Sux Maintenance: Isoflurane, No N2O Emergence: give Lidocaine IV 90 sec before extubation, and consider using antihypertensive Meds(labetolol), assess for any neurological deficit
Systemic Lupus Erythematosus Page 213 of 217 A cricoarytenoid arthritis hoarseness, stridor, or airway obstruction (awake intubation), post-extubation edema B effusion, pneumonitis, pul HTN, and alveolar hemorrhage. high correlation of pul HTN with Raynaud's phenomenon in patients with SLE.(CXR, PFT) C pericardial effusion, tamponade, Cardiomyopathy, cardiac conduction abnormalities, ventricular function, and coronary arteritis, noninfectious endocarditis (Libman-Sacks endocarditis) mitral insufficiency (ECG, ECHO) D immunosuppressants (corticosteroids) or cytotoxic drugs (cyclophosphamide, azathioprine, cyclosporine),avoid Drug-induced lupus quinidine, hydralazine, methyldopa, captopril, enalapril, clonidine, isoniazid, Hanti-phospholipid antibodies thromboembolic complications, anemia R common cause of M&M in patients with SLE, CRF CNS seizures, stroke, dementia, psychosis, and peripheral neuropathy GI peritonitis, pancreatitis, bowel ischemia, protein-losing enteropathy, and lupoid hepatitis
Tamponade: Page 214 of 217 Emergency and life threatening In acute as little as 200 ml cause S/S In chronic up to 1000 ml cause S/S Causes: o Infection: bacterial, viral, fungal, TB o Inflammatory disease with vasculitis: R.Arthritis, SLE, scleroderma o Metabolic: RF, myxedema o Radiation, malignancy, trauma, post-heart Pathophysiology: VEDV, SV, CO, SBP, CVP, Rt=Lt pressure Dx by keeping in mind a high index of suspicion with clinical S/S and lab Beck’s triad: hypotension, distended neck veins, muffled heart sound S/S: tachypnea, BP, narrow pulse pressure, HR, pulses paradoxus Signs of systemic hypoprefusion: oliguria, lactic acidosis, cool extr DDx: tension Pneumo, RV infarction, Pul HTN, cardiac herniation ECG: diffuse ST-changes, low voltage Lab: ECG, Echo, CXR, CT
TCA overdose: Page 215 of 217 Gives anticholinergic syndrome, So no Atropine Cardiac toxicity is the major cause of death No correlation between serum level and symptom A LOC RSI B depression, ARDS C toxicity, QT, wide QRS, sinus tach, heart block, hypotension due contractility, and vasodilation by -blockade, arrest CNS hallucination, coma, seizure M metabolic acidosis Management: o ABC o Gastric lavage o Activated charcoal 1g/kg with 60 ml sorbitol o Bicarb is the Key in the management 2 mEq/kg bolus then infusion 150mEq in 850 D5W to maintain pH 7.45-7.50 o For Vent arrhythmia give Lidocaine, Class 1A,1C are C/I o Hypotension Norepi gtt o Bradycardia Isoprel or pacing No Atropine
TEF Page 216 of 217 30% premature, associated CHD, and VATER, VACTREL syndromes Depend on the infant stability if stable complete repair, if not stage repair, with insertion of G-tube under LA, the ligation of the fistula, and reanastomosis of the esophagus A subglottic stenosis B resp distress, RDS, pneumonia C CHD, decompensation and CHF M dehydration, metabolic acidosis Worm up the room, big IV, standard CAS monitors, Art-line Lab CBC-D, lytes, ABG, Cap gas or VBG, CXR, Echo, X-match with 2U peds in the room Give atropine, not muscle relaxant until chest open, Inhalation induction bronch, then intubate after further mask ventilation to deepen the Pt, have different size ETT, after intubation with the bevel directed posteriorly, listen to the chest and initially intubate the Rt main bronchus, with listening to the chest withdraw the tube slowly till you here bilateral breath sound. Consider caudal epidural for post-op pain Run maintenance fluids with glucose maintenance as well
Page 217 of 217
