soap 2004 poster case reports: you did what? the … 2004 poster case reports: you did what? the...

72
SOAP 2004 Poster Case Reports: You did what? The Best Case Reports of the Year Presenter/Moderator: Peter H. Pan, MD Ft. Myers, Florida Sunday May 16, 2004 8:30-9:30 am Learning Objectives: 1. To understanding the pathophysiology of the complex diseases presented in the cases 2 To understand the anesthetic implications of these diseases and problems. 3. To be able to evaluate these patients preoperatively and provide plan for anesthetic 4. To understand the medical and peri-operative management of these patients Total of 30 case reports: Divided into Five Groups: A. Hemorrhagic/Hematological Challenges B. Neuraxial Complications C. Airway Challenges D. Cardiovascular Challenges E. Misc Problems A. Hemorrhagic/Hematological Challenges Abstracts # A111, 137, 121, 138, 119 What are the blood supplies to gravid uterus? What are the indications of embolotherapy? What is the success rate in controlling peripartum hemorrhage? What are the potential complications after uterine embolotherapy? What is possibility for future fertility after embolotherapy? Are parturients with von Willebrand (vWD) disease safe to have neuraxial analgesia? How would you evaluate a patient with vWD for neuraxial analgesia? What is vWD and what are the functions/mechanism of vWF ? How many types of vWD’s are there and how to differentiate one another? What are the diagnostic test and lab work for vWD’s? What do they mean? What are treatments for vWD’s if needed for surgery? What are the effects of pregnancy on vWD’s? Does it matter which type? What are the indications for using r FVIIa? What is the success rate?

Upload: vuthu

Post on 06-May-2018

214 views

Category:

Documents


1 download

TRANSCRIPT

SOAP 2004 Poster Case Reports: You did what? The Best Case Reports of the Year

Presenter/Moderator: Peter H. Pan, MD Ft. Myers, Florida Sunday May 16, 2004 8:30-9:30 am Learning Objectives: 1. To understanding the pathophysiology of the complex diseases presented in the cases 2 To understand the anesthetic implications of these diseases and problems. 3. To be able to evaluate these patients preoperatively and provide plan for anesthetic 4. To understand the medical and peri-operative management of these patients Total of 30 case reports: Divided into Five Groups: A. Hemorrhagic/Hematological Challenges B. Neuraxial Complications C. Airway Challenges D. Cardiovascular Challenges E. Misc Problems

A. Hemorrhagic/Hematological Challenges Abstracts # A111, 137, 121, 138, 119 What are the blood supplies to gravid uterus? What are the indications of embolotherapy? What is the success rate in controlling peripartum hemorrhage? What are the potential complications after uterine embolotherapy? What is possibility for future fertility after embolotherapy?

Are parturients with von Willebrand (vWD) disease safe to have neuraxial analgesia?

How would you evaluate a patient with vWD for neuraxial analgesia? What is vWD and what are the functions/mechanism of vWF ? How many types of vWD’s are there and how to differentiate one another? What are the diagnostic test and lab work for vWD’s? What do they mean? What are treatments for vWD’s if needed for surgery? What are the effects of pregnancy on vWD’s? Does it matter which type? What are the indications for using r FVIIa? What is the success rate?

B. Neuraxial Complications Abstracts # A115, 132, 122, 117, 140, 123, 130, 139 What are the initial manifestations and clinical stages of spinal/epidural abscess(SEA)? What are some prognostic indicators ? What are the risk factors in having SEA ? What diagnostic technique is most appropriate ? What are the importance of preoperative evaluation? How would one isolate anesthetic-related neuraxial complications? Are continuous spinal catheter safe to use? What are the indication for continuous spinal catheter? What drug /baricity should be use in such case? C. Airway Challenges Abstract # A114, 120, 116, 135 How would you choose between RA or GA for C/S for someone with difficult airway and abnormal back, such as with Harrington rods ? What are the anatomical abnormality and anesthetic implications of Klippel-Feil syndrome and Kugelberg-Welander syndrome? Should ENT be called/present for all difficult airway cases?Any selected pt? When is LMA indicated in parturient undergoing C/S? What are the relative risk comparing face mask (FM) ventilation vs. LMA ? Does cricoid pressure affect placement, position, ventilation from LMA and the subsequent blind intubation from classic LMA, Proseal or Intubating LMA? D. Cardiovascular Challenges Abstracts # A136, 118, 124, 125, 126, 131, 127, A134 What are the anesthetic and analgesic implications in parturients with POT syndrome? What are the effects of spinal anesthetic on parturients with complete heart block? How would you manage the anesthetic of such a patient for C/S? What is the anesthetic choice for C/S in parturients with IHSS, AS, or MS ? Are RA contraindicated in parturients with IHSS, AS, or MS ? What are some independent predictors of adverse cardiac complications in parturients with cardiac dz? How does pregnancy affect AS, MS, and IHSS ?

E. Misc Problems Abstracts # A113, 133, 112, 129, 128

Are epidural or spinal anesthetic contraindicated in patients with spinal cord stimulator (SCS)?

Does local anesthetic affect the function of spinal cord stimulator or vice versa?

Is it okay to do an epidural blood patch after a wet tap in patients with spinal cord stimulator (SCS)?

Does EBP affect the function of SCS or vice versa? What are your differential diagnosis when your laboring parturient present with spastic quadraparesis? How would you manage such a patient? How bad can one get by taking 10 TUM's/ day for dyspepsia with MVI?

Is ondansetron free of extrapyramidal side effects? If not, what would be the treatment?

SOAP 2004Poster Case Reports: You did what?The Best Case Reports of the Year

Ft. Myers, FloridaSunday May 16, 2004

8:30-9:30 am

Peter H. Pan, MDWake Forest University

Winston-Salem, NC

Introduction

• Total 30 case reports - divided into 5 gps:–Hematologic/Hemorrhagic Challenges–Neuraxial Complications–Difficult Airway Challenges–Cardiac and Hemodynamic Challenges–Misc. Problems

A111. A case report of bilat Uter. artery embolization for high flow uterine AV fistula in a term pt. (Brummel et al. Stanford Univ, CA)

31 y/o G2P1, now 36wk IUP for elective C/SPMHx: abnormal U/S lead to AVF Dx @ 8 wk, monthly monitor

Plan: LEA, 14-G IVs, A-lineIR placed bilat femoral arterial balloonPelvic arteriography Post baby delivery -> Brisk BleedingGelfoam embolized bilateral Uter. Arteries AVF obliterated -> Hemostasis, stable, no transfuse 2L EBL, Hct-26, Uneventful6wk pp U/S-> no AVF

A137. Planned C/S in a pt. with placenta accreta in the IR suite.(O’Rourke et al. Brigham & Women’s Hosp,MA)

36 y/o G3P2, Hx previa & myomectomyNow with accreta for C/S#3/hysterectomyBut pt wants to preserve uterus

Plan: C/S in IR suiteLEA for C/S, IV , A-lineIR placed Bilat Uterine A balloonsPost delivery->Balloon/Gelfoam embolize Uter. A X 2Bleeding Controlled, 1L EBL Hct 34->241 unit PRBC + fluid + hetastarchUneventful Recovery

Questions on Embolotherapy.(Brummel et al. O’Rourke et al)(B) Is U/S the diagnostic tool of choice for uterine AVF?sensitive?

How do you select candidates for embolotherapy?

What is the success rate in controlling PPH?

Is uterine ischemia a problem with Bilateral Ut. A embolized?

(o) Is embolization permanent ?

What are the potential side effects ?

What are the chances of future pregnancy?

What are the potential anesthetic implications of this?

• What arteries supply the gravid uterus? • Uterine A and Ovarian Artery (pregnant)• Abd Aorta->Common Iliac->Internal Iliac (Hypogastric A) ->

Uterine A->Ascend & Descending Trunk• Uterine A. Ascending Trunk->Fundus/Body• Uterine A Descending Trunk->Cervix/Vagina/Bladder• Other U A Br-> Ovarian branch anastamose with Ovarian A

branched from Abd Aorta to supply Ovary and Uterus• Are the gel foam embolization permanent? • Plenty Collaterals and recannulation possible if needed(3wk)

• (Pelage et al. Radiology 1999; 212:385-9) • (Obstetrics - Gabbe. Chapter 1- Anatomy)

• Gravid uterus blood supply? Embolize? Problems?(Pelage et al. Radiology 1999; 212:385-9) (Obstetrics - Gabbe. Chapter 1- Anatomy)

• Abd Aorta->Common Iliac->Internal Iliac (Hypogastric A) -> Uter. A->Asc & Desc Trunk->Uterus,cervix,vagina,bladder

• Other Uter. A Br-> Ovar. branch anastamose with Ovar. A branched from Abd Aorta to supply Ovary AND Uterus

• What is the success rate of embolotherapy? (Badawy 01)

• First by Brown(‘79), review 138 cases of embolotherapy for PPH, success 95% vs internal iliac A ligation <50% success. (0.5 million worldwide die of childbirth complications, 1/4 due to PPH)

• What are the potential complications? (minor 9%)• Gluteal Paresthesia, urin freq, fever, foot ischemia, bladder

ureter/rectal wall necrosis, nerve injury, muscle pain, late rebleed

• Can patient get pregnant again? (Ornan et al. 2003)• Fertility is usually preserved but rare reports of IUGR. ?ischemic

late complications. Nl menses in all in a series of 14/14.

• What are the anesthetic implications?• Multidisciplinary,A/V access,blood,Infusor, CSE/Epid

• (Ornan, Pollak, Tal. Obstet and Gyn. 2003; 102:904-10.) (Badawy et al. Clin Imaaging2001; 25:288-95.), (Brown et al. Obstet Gynecol 1979;54:361-5)

Von Willebrand’s Disease A138. vWD & preg not contraindicate to regional A/A.(James, Campbell. University of Saskatchewan, SK, Canada.)

• 3 pts with type I vWD• showed FVIII, vWF:Ag, vWF Ristocetin Co all

elevated >> normal since 8 wk GA to term.• Recommend: Evaluate Early, prenatal care, labs • Conclude RA not contraindicated in vWD type I ?

Case #1 (28-36 weeks) Coagulation Factor >50% = normal

0%

50%

100%

150%

200%

250%

300%

350%

400%

28 weeks 31 weeks 34 weeks 36 weeks

Factor 8 vW Ag vWF Rictocetin

Case #2 (8-36 weeks)Coagulation factor > 50% = Normal

0%

25%

50%

75%

100%

125%

150%

175%

200%

8wks 24wks 26wks 28wks 30wks 32wks 34 weeks 36 weeks

Gestation

Factor 8 vWF Ristocetin vW Ag

Case #3 (18 - 21 weeks)Coagulation factors >50% = normal

0%

25%

50%

75%

100%

125%

150%

18 weeks 21 weeks

Factor 8vW Ag124% 117% 141%

Von Willebrand’s Disease A121. Severe thrombocytopenia c/o vWD Type 2B (Hepner,

Tsen. Brigham and Women’s, MA.)

• 35y/o G2P1, Hx Type 2B vWD 36wk breech for C/S• PMHX: 2yrs ago, vag del, plt 20K, rcvd Humate P &

Amicar, No neuraxial analgesia

• This Preg: 2wks ago, plt-46K; Now-36K• Plan -> Give Humate P+Plt, then ?RA, but GA used• Plt 30K ->more Plt ->Plt 10K (intraop)->ok hemostasis

Postop- Humate P, plt 20K,31K,42K->53K POD#4

Questions on vWD (James et al. Hepner et al)

• Hepner et al What was the plt ct at induction/incision Why start surg with lower Plt count after tx?Why did her preop PLT decr with transfusion?Why Humate P & not FVIII concentrate?What is the function of Amicar?Any treatment to use if pt developed alloAb to vWF from multiple tx Hx?

• James et al. How would you assess a pt with Hx of vWD without previous lab values?Should epid cath be used for post C/S pain mgt?

• vWF - synth in endothel. cells & megakaryocytes; circulate as multimer & complexed with FVIII

• vWF Functions:1) binds to plt GPIb for plt adhere to vas subendoth 2) binds to F8 NH2 term. to prevent F8 degradation

• vWD->mutate vWF locus->quantit/qualitative defect• Defect->Incr BT,decr PLT;Incr F8clearance->Incr PTT(Intrinsic)

• Different phenotypes,vary penetrance & symptoms • Prevalence 1%(most common blood dz) ; 1:100-1:2

million varying forms; ADomin; similar in gender, race. • (Federici et al. Haemophilia 2002;8:607-21. Bardett, Robert. Clin Obstet &

Gynecol 1999;42:390-405. Batlle et al. Haemophilia 2002;8:301-7)

Three Types and 8 subtypes of vWD• 1. Partial quantitative deficient vWF (3 subtypes

on plt vWF content - nl, low,discordant)- (90%)• 3. Extreme/complete quantitative deficient vWF• Type 2 - Qualitative Deficiency of vWF• 2A. Decr plt-dep vWF func, lack HMWM• 2B. Incr abnormal plt-dep vWF func, lack HMWM• 2M. Decr plt-dep vWF func, no lack of HMWM• 2N. Marked Decr vWF affinity to FVIII • vWF: synth from endothelial and megakarocytes: 1) binds to plt GPIb for plt adhere to

vas subendoth 2) binds to F8 NH2 term. to prevent F8 degradation

Diagnostic Tests for vWD Types• Plasma vWF:Ag - Quantity• Ristocetin Cofactor (vWF:RCo) - Activity• vWF:RCo/vWF:Ag ratio - Activity relative to amt• Ristocetin Induced Plt Agglutination(RIPA) • HMWM analysis - multimers analysis• FVIII:C - Intrinsic PW factor• FVIII:C/vWF:Ag ratio• Clinical Tests: PLT, PTT, BT

Diagnostic Tests for vWD TypesTests Type I 2B 2A 2M 2N Type 3

vWF:Ag NL/Low Low or Normal Very Low

FVIII:C NL/Low Low or Normal Very LowvWF:RCo/vWF:Ag ratio

Proportion 0.7- 1.2

Discrepant < 0.7

Discrepant < 0. 7

Discrepant < 0.7

Proportion 0.7–1 .2

RIPA Nl Incr (.2-.8) decr(>1.2) decr(<1.2) decr(<1.2)

HMWM Present Absent Absent Present Present

FVIII:C/vWF:Ag

Proportion->plt vWFsubtypes

Discrepant->FVIIIbinding ---- -> Low

vWD Treatment• DDAVP:(class B preg drug)–> Type I (?2N,?2A,?2M)• Incr plasma FVIII and vWF from incr storage release• Incr plasma F8 & vWF 3-5X above base in 30m & last 8hr• Tachyphylaxis with repeated Tx• Most effective for type I (esp subytype - plt nl)• Poor/short effect in type I(subtype plt low),2N,2M• Type 2A - FVIII incr but often BT not shorten• Type 2B - mostly contraindicated ->decr plt ( few cases

reported usefulness in 2B)• Type 3 - typically NO response

• (Federici et al. Haemophilia 2002;8:607-21)

vWD Treatment• Nontransfusional Adjunct therapies: (Type I)• Antifibrinolytics: epsilon amniocaproic acid ->

interfere/prevent lysis of new form clot• Estrogen - incr vWF level, response variable• Transfusion Tx: Type 3, 2B, (2M, 2A), 2N, I refractory)• Humate P- Viral inactivated FVIII/vWF conc• Cryoppt - q 12-24 hr, (5-10X F8 & vWF than FFP)• *(FFP(large vol limits use); F8 conc-NO due to low vWF) • Platelets in some cases for Platelet vWF• Recombinant F8 cont. IV infuse, short T1/2, Type3 pt

with alloantibodies to vWF in case of emergent surgery • (Federici et al. Haemophilia 2002;8:607-21)

Pregnancy and vWD• Estrogen/Preg stim. synth and incr plasma vWF• Chediak et al-8 preg serially->incr by 10wk GA• FVIII:C max @ 29-32wk, vWF:Ag peak @ 35 wk• Most Incr in Type I, some in 2A and minimal/none in III • BT improves Type I, not in other subtypes. • Type 2B- Worsen; Incr bad vWF->incr abn aggluten plt

GP Ib-IX-V-> consume PLT, incr abn F8 binding and clearance -> Incr PTT (incr F8 clearance)

• Type 3 or severe Type I: minimal change vWF• FVIII:C can fall rapidly postpartum even in type I • Prevalence PPH 13-29% (<24hr); 22-29%(>24hr)

– (Battle. Haemophilia 2002;8:301-7. Mathew. Haemophilia 2003;9:137-44.)

vWD Problems during Pregnancy• Type 2 B: Incr bad vWF->incr abn aggluten plt

GP Ib-IX-V-> consume PLT, incr abn F8 binding and clearance -> Incr PTT (incr F8 clearance)

• Type 3 or severe Type I: minimal change vWF• BT,vWF activity, FVIII:C at term inadequate data

to correlate PPH. FVIII:C probably best: >40-50U/dl good; <20U/dl bad

• FVIII:C can fall rapidly postpartum even in Type I. - (speed not well documented)

• Prevalence of PPH 13-29% (<24hr); 22-29%(>24hr)

vWD Management in Pregnancy• Prenatal counsel/eval, vWD subtype, labs, DDAVP

response Hx, del/anes/ob/hemo plan• Type I and asymptomatic - no prophylactic need• TypeI,2N,2A(symptomatic)->DDAVP,antifibrinolytic• Type 3, 2B, (2A,2M) symptomatic->Humate P,

(Plt,cryoppt,DDAVP as adjunct if refractory)• Labs: plt,PTT,BT and vWD labs if available• Monitor PPH postpartum wk, Hemo f/u if need• Most vWD I parturients - not contraindicate to

neuraxial block, but individualized based on subtype, history, symptoms, labs;(low conc,early Epid remove)

• (Battle. Haemophilia 2002;8:301-7. Cohen. Anaesthesia 2001; 56:397.)

• A119. Abdominal compartment syndrome following complete abruption of the placenta, fetal demise and consumptive coagulopathy with cardiopulmonary and renal complic. Zibaitis, Schumann. Tufts-New England Medical Center, Boston, MA.

PT 17, INR 1.5, APTT 60, Hgb 5.2, Plt 66K, D-dimer >4 , fibrinogen 41Plan:Plan: Correct coagulopathy; Induce Labor, Vag deliveryCVP 10->40, UOP stop, pul edema p transfuse, CardioPul deteriorateAdminister rFVIIa ; Emergent Decompressive C/S under GA, uneventful recover

What is ACS?How is the diagnosis made?Why recombinant FVIIa? Who are candidates? What applications? Success rate?

Recombinant Factor VIIa(NovoSeven)• Acts in Extrinsic PW/Tissue Factor PW (normalize PT)

• Bypass Intrinsic PW (FVIII, IX)• May bind Plt loosely and activate FX->Xa to incr

thrombin formation in presence of FVa to support adequate hemostasis though not total normal.

• FDA approve - pts with hemophilia & inhibitors• (tx 90-120ug/kg q 2 hr first 24 hr, some cases 150-300ug/kg; other 20-80ug/kg)

• Off label– liver transplant, refractory transfusion, nephrect/prostatect/hepatectomy prop prophylaxis decr blood loss, reverse vit K antagonist

• ? Effectiveness in Reverse LMWH– (Roberts et al. Anesthesiology 2004;100:722-30.)

Neuraxial Labor Analgesia Complications

A115. Epid abscess after CSE analgesia in a healthy parturientGreenberg, Sullivan, Wong. Northwestern Univ, Chicago, IL.

- 32 y/o G2P1, unremarkable CSE, sterile technique-Uterine Atony, massage, no transfusion, LEA 6+hrs-Started ppd#6, PPD# 11->ED->, R low back pain to ant thigh, R med thigh numb/weak, R ant-med thigh decr sensory, decr psoas strength- R paravert tender over L5-S1, WBC14K,fever,chills- UA +ve, on levofloxacin

MRI->L5-S1 HNP -> no lat calf/foot symptoms. Tx:R L5-S1decompress, purulent fluid at S1 root axilla,All Cultures Negative, 2wk postop Antibiotic, Recovered.

Diagnostic Imaging (MRI)

Case Report

“Disc extrusion at L5-S1 with enhanced granulation tissue at the right S1 nerve root. Moderate central canal stenosis.”

Epidural Abscess

Neuroradiology 1999 41: 904-909

Can this be epidural abscess?

• Approp time course but symptoms, location & culture not c/w epid abscess

• Can levofloxacin make culture negative ?

• Can it be HNP superimposed arachnoiditis?

• ?Adhesive Arachnoidits (BJA 2004;92:109-20.Acta Anaesth Scan 2003;47:775-6)

A132. Paraspinal muscle abscess p epid cath placement.Goodman, Bartal. Univ Hosp of Cleveland, OH.- 20 y/o twin vag del, L3-4 epid X 48 hr (uretheral lac)- PPD#2->D/C Epid, R lowback pain, Discharged PPD#3- PPD#5->T39C, WBC, HA, stiffneck,backache, no defecit - LP failed (a good thing), presume meningitis, Tx:ABC

- PPD #8- Epid skin site purulent drainage- PPD# 8-> MRI->? Paraspinal mus incr intensity, no

spinal/epid abscess; Continue intermit fever- PPD#10+->MRI :abscess in R psoas mus - Tx: meropenem X 2wk; Cx+ S Aureus

- PPD#15 MRI no change, but clinical recovery.

A132. Paraspinal muscle abscess p epid cath placement.Goodman, Bartal. Univ Hosp of Cleveland, OH.

- How well was the epid cath protected in the pp ward?Was there any epidural infusion in the pp ward?

- Any risk factors in this patient?

- What sterile technique was used in epidural placement?

- What level was LP attempted? Can the multiple failed LP attempts contribute to the paraspinal abscess?

Spinal/Epid Abscess(SEA) - ManifestationInitial: Back/Neck Pain-72%,Leukocytosis-64%,Fever-60%

Clinical Stages: 1:backpain,fever,local tenderness; 2. spinal irritation-bakpain to arm/leg, Kernig, Brudzinski, stiff neck; 3.neuro deficit-weak volunt. mus, incontinence; 4. paralysis.

Infect organism: S aureus(70%), S epidermidis(17%), other

Prognostic Indicators of poorer outcomes:Duration/presence of paresis, Cervicothoracic location, lower limb paresis, high WBC>14K, higher C-reactive protein. 38% complete recover, mild deficit 21%, paresis 27%; 14%death

(Soehle, Wallenfang. Neurosurgery. 2002;51:79-87. – 915 SEA meta-analysis)

Spinal-Epidural Abscess (SEA)Main problem is not TX, but early DX before major deficit .

Risk post epidural cath insertion:-est 1:13K-50K+ in OB,1:5K in non-OB VERSUS 1:10K hosp adm in US; Male:F-1:0.56-long catheter time (>24hr, >3d), immnunocompromised by complicating dz-anticoag (LMWH) use, DM, ETOH/drug abuse, skin abscess, furnuncle

Sterile technique-vary survey - no mask 14%, no gown-12%, no glove-1%, no skin antiseptic 0%

Early DX: Close F/U block recovery & Anesth F/U system after discharge homeEarly DX: Multidisciplinary,MRI gadolinium ctx w/u & Surgical decompress + Abc’s.

(Wang et al. Anesthesiology, 1999;91:1928-36. Sellors et al. Anaesthesia 2002;57:584-605.Reihsaus et al. Neurosurg Rev 2000;232:175-204 -915 SEA’s meta-analysis)

Neuraxial Labor Analgesia ComplicationsA117 SA Hemorrhage masquerading as PDPHRanasinghe et al. Miami, FL.31y/o 38wkGA with abnormal NST for urgent C/S Unremarkable PMHX Except new onset severe non-postural HA @ admission

Plan SAB: 27G SAB C/S->bloody tapX2Switch to GA, uneventful C/SPost op non-pos HA -> presume PDPH? , D/C Home analgesicNext day Readmit: Postop non-pos HA, photo/phono-phobia LP-93K RBC, CT-NL, MRI->SAH, MRA->3x2mm aneurysm->Dexamethasone, nimodipine -> Surg Clip -> recovery

QuestionsA117 SA Hemorrhage masquerading as PDPHRanasinghe et al. Miami, FL

Was pt seen by anesth for her HA prior to discharge? Why was non-pos HA presumed PDPH after 27G bloody

tap? (Hx of auto blood patch)Was the pt to be f/u at home by anesthesia (phone etc)?How red was the CSF X 2 ? What was the thinking at that time ?Would SAB still work in bloody CSF? Any major risks of

injecting the spinal drugs?What anesthetic choice for urgent C/S in same presentation

but knowing SAH being medically managed?(1-5/10K SAH, Incr bleed with gest age, 77%Berry aneurysm, 20+%AVM, 40% mortality)

Intracranial Hemorrhage in PregnancySAH:1-5 per 10K pregnancies

77% intracran saccular Berry aneurysm, 20+% AVMICerebH: often from HYTN,AVM; etiologies/incid less clear;

poor prognosis, often not amenable to surg correctionMortality similar to gen pop, bleed more with incr gest ageRisk of intrapartum rebleed greatest if initial bleed in 3rd trim.Risk of ICH incr with met choriocarcinoma(A140), cocaine

abuse, bleed diatheses.Combined C/S-neurosurgical procedure can be done.Both Epidural & GA for C/S or Epid for vag delivery reported

in medically managed intracranial aneurysm and AVM.

(Case Reports: Laidler et al. Anaesthesia 1989;44:490. Gupta et al. IJOA 1993;2:49. Hunt et al. Obstet Gynecol 1974;43:827. Hudspith et al. IJOA 1996;5:189.)

Neuraxial Labor Analgesia Complications

A117 (SAH) - preop HAA123 (LS trunk injury) - preop neuro symptoms

Importance of careful Preop Evaluation;Document pre-existing abnormal findings;

Correlate with postop complications/findings.

Neuraxial Labor Analgesia ComplicationsA130 (Intrathecal labetalol- paraben ok, ?labatelol, CAA!!!)(Balestrieri et al. U Va, Charlottesville, VA)

23y/o LEA->wet tap->spinal cath->SVD

12hr later->pp BTL -> labetalol injected via spinal cath

Uneventful Recovery -> Author Concluded labetalol non-toxic???

Meticulous ATTN to avoid drug errors; Luck may run out.Why keep spinal cath for ppBTL? Did pt go to pp ward?Was the spinal catheter/connector labeled clearly?What syringe was labatelol in ?Can one conclude labetalol is non-toxic with N=1?

Neuraxial Labor Analgesia ComplicationsA139 CSA for elec C/S in pt with pseudoxanthoma

elasticum(PXE) (Walton, Bullough.The Great Western Hosp,Swindon,UK)

PXE-degen and calcif of elastic tissue predispose to arterial bleed, MI.

No bleed Hx, NL CV, elec. C/S, 22G spinal needle, 28G spinal micro-cath-> 1.5 ml 0.5%hyperbaric bupiv,0.3mg diamorphine+.5ml bupiv T4->Uneventful Recovery

Questions:Why CSA for this pt? Any PDPH ?Why not SAB or Epid or CSE?Why hyperbaric bupiv?

Pay Attn to Details and Be Careful !

Liability !!

Airway !Airway !

Airway !

Difficult Airway – Would you do it any differently?

Difficult AirwayA114.Anesth mgt of Elective C/S for a pt with Klippel-Feil SyndromeDarwich et al. Univ of Pittsburgh, Magee-Womens Hosp, PA.

KFS -C2-3(typeII), all C+someT (typeI)fusion, short neck, limit motion,scapula displace,celft palate, kyphoscoliosis. Syncope episodes, clinical symptoms c/w compression of cerv cord, pons/medulla.

- 32y(4’9”,69Kg), 39wk GA, Breech C/S.- MHx: KFS II cleft, cerv fuse,MP II, scoliosis,

released tether cord, Arnold Chiari malf I, Sprengeldeformity, mild AS

- Plan GA->oral supine FOB failed->Reschedule->ENTpresent->

Sitting Nasal FOB success->Extub @ OR-> ICU recovery

Difficult AirwayA114.Anesth mgt of Elective C/S for a pt with Klippel-Feil SyndromeDarwich et al. Univ of Pittsburgh, Magee-Womens Hosp, PA.

A114.Anesth mgt of Elective C/S for a pt with Klippel-Feil SyndromeDarwich et al. Univ of Pittsburgh, Magee-Womens Hosp, PA.

• Comments on Xray? • Any Cervical fusion/cord compression• Any sedation for FOB? IF so, what?• Do you have to do neuro check after intub?• Why Post OP ICU ?• What would you do if second FOB failed?

Difficult AirwayA120. Anesth Mgt of a 26Kg pt with Kugelberg-Welander Syndrome. Younan et al. Albany Medical College, NY.

SMA III, degen periph motor neuron NOT upper, slow course, trunk/proximal limb.

- 24y/o (26Kg) 37wk GA for C/S.- MHx: KWS, spinal muscular atrophy type III, wheel-chair

bound, contracture, Harrington rods, limit neck/mouthRestrictive FEV1-13%predict. 2 trach for resp failure

-Plan GA->ENTpresent->Awake Nasal FOB 6.0ETT->Inhalation,narcotic, local, (no mus relaxant)-> -->Emerge/Extubate->Post OP Vent Assess??

How did you determine pt’s need for postop vent support?

Difficult AirwayA116. Dwarfism, Factor V Leiden Deficiency, anticoagulation, and Hx difficult AW:An OB anes challenge!(Fuller et al. Stanford, CA)

35y/o(45kg,101 cm) at 38wk for C/S with HYTN, dyspnea, wheezeMHx: dwarfism, multiple FOB intub for ortho procedures,

F V Leiden def, recent DVT, enoxaparin 60mg bidon labetolol , albuterol

PE: MP II AW,TMD 5cm, C1-2 fusion, mild wheeze; At 28wk, awake gradeII laryngoscopic view

Plan: off enoxaparin, on heparin 2 days, off Heparin 6 hr preop, Plan Epid->T4success->Epid Morphine post op analg->Early Epid removal--->Heparin, enoxaparin resume 6 and 24hr post op.

Difficult AirwayA116. Dwarfism, Factor V Leiden Deficiency, anticoagulation, and Hx difficult AW:An OB anes challenge!(Fuller et al. Stanford, CA)

What is the protocol for RA in pts on enoxaparin?

How would BID dose managed different from Q day?

Do pt on enoxaparin normally admitted 2 day preop for Heparin?

Do you check coag before RA after Heparin stopped?

Why Epidural and not SAB + IT morphine for this patient?

Would you do Epid anes if preop grade 3-4 laryngoscopic view?

Difficult AirwayA135. ILMA: life saving rescue device follow failed tracheal Intub during C/S. (Suresh, Key. Baylor Coll. Med, Houston,TX)

30y/o, 31wk GA, morbid obese, eclamptic szX3, Stat C/S with fetal brady/agonal rhythm.

ENT paged on way to ORClassIV AW, edematous,combative-->

RSI,intubX2 Fail-->SpO2-56% (23:00:00)-->-> ILMA4 ->SpO2 100% (23:00:30) -->-->100% in 30s.->deliver->ETT7.0->extub 36hr uneventful.

Suggest ILMA has many advantages over classic LMA.

ASAASA DIFFICULT AIRWAY ALGORITHMDIFFICULT AIRWAY ALGORITHM

AWAKE INTUBATION

Airway Approached byNon-Invasive Intubation

InvasiveAirway Access

Succeed FAIL

Consider FeasibilityOf Other Options

CancelCase

InvasiveAirway Access

INTUBATION ATTEMPTS AFTERINDUCTION OF GENERAL

ANESTHESIAInitial IntubationAttempts Successful

Initial IntubationAttempts UNSUCCESSFUL

FROM THIS POINTONWARDS CONSIDER:

1. Calling for Help2. Returning to Spontaneous

Ventilation3. Awakening the Patient

FACE-MASK VENTILATION NOT ADEQUATE

CONSIDER / ATTEMPT LMA

NON-EMERGENCY PATHWAYVentilation Adequate, Intubation

Unsuccessful

LMA ADEQUATE LMA NOT ADEQUATEOR NOT FEASIBLE

EMERGENCY PATHWAYVentilation Not Adequate,Intubation Unsuccessful

Call for Help

Emergency Non-Invasive Airway Ventilation *

IF BOTHFACE MASK

AND LMAVENTILATION

BECOMEINADEQUATE

Alternative ApproachesTo Intubation

Develop primary and alternative strategies:

FACE-MASK VENTILATION ADEQUATE

SuccessfulIntubation

FAIL AfterMultiple Attempts Successful Ventilation FAIL

EmergencyInvasive Airway

Access

InvasiveAirway Access

Consider Feasibilityof Other Options

AwakensPatient

*Options for emergency non-invasive airway ventilation include (but are not limited to) Combitube ventilation, rigid bronchoscope, or transtracheal jet ventilation.

Classic LMA Classic LMA –– FiberopticFiberoptic ViewViewDisadvantagesDisadvantages

• The respiratory tract is not isolated from the gastrointestinal tract, thus there is a risk of aspiration.

• The Classic LMA aperture, in relation to the glotticentrance, is variable.

Classic LMAClassic LMADisadvantagesDisadvantages

• Downfolding of the epiglottis can occur to obstruct the blind passage of the tracheal tube or a fiberoptic scope.

Intubating LMAIntubating LMAAdvantagesAdvantages

• Epiglottic elevating bar keeps epiglottis from obstructing airway when ILMA used as sole airway

• Protects and elevates epiglottis during ET passage

• “V” Shape Ramp Guides ET anteriorly, reduces the risk of arytenoid trauma

• Has tube centering effect and reduces risk of esophageal placement

Questions(Suresh, Key. Baylor Coll. Med, Houston,TX)

What enabled this MO pt to resaturate (SpO2) so fast in <<30s ?

Can this patient be ventilated by face mask?

Are there much study data available on CP effect on Proseal or ILMA in respect to position, ventilation and intubation?

If this pt can be FM ventilated, is LMA still indicated ?

Are ENT routinely paged for stat C/S in MO pt?

Why RSI and not FOB in known difficult AW?

LMA and ParturientsPart of ASA Emergency Difficult AW algorithm

When should LMA be used? Cricoid pressure(CP) effect?-Cannot Intubate/Cannot Ventilate (CV/CI)-FM vent less aspirate vs LMA methylene blue stain(0-25%),pH(22vs57%)

-CP can impede LMA position, vent and blind intub success. (Takenaka et al. CJA 1996;43:1035-40.)

-Proseal LMA eliminates reflux fluid, but effect of CP on Proseal or intubating LMA position, ventilation not clear

Is LMA safe with pregnant pt? LMA is acceptable as emergency alternative in parturient with

CV/CI, even though a series of 1067 selected healthy parturientshad no c/o with LMA for C/S. (Han, Brimacombe. CJA 2001;48:1117-21.)

(Barker BJA 1992;69:314-5. El Mikatti. BJA 68:529-530. Owens. A&A 1995;80:980-4.)

CRISIS Management

Support - call for helpResource - get what’s neededRoles - Know your role and othersCommunicate - ClearGlobal Assess - Don’t miss the big picture !!

(Parekh et al. SOAP 04)

Postural Orthostatic Tachycardia• A136. 18 y/o POT ‘s, labor epid analg. 1/8%

bupiv with fent, pain free, vacuum, stable vitals.POTs:

– a form of periph autonomic neuropathy– inability of periph vas. to constrict adequately in

response to orthostatics ->incr tachy and ctx • Diagnosis: (Kanjwal et al. Pace 2003;26:1747-57.)

1) HR incr >=30/m or >120/m in 10min p stand 2) orthostatic intol -> sympathetic hyperactivity 3) no other etiologies

(Hebbar et al. MUSC, Charleston, SC)

• POT syndrome Mechanism: (Kanjwal. Pace 2003;26:1747-57.)

– Impair effer. cardio/vagal func,hyper beta-adrenergic – excess venous pool, sinus node or brainstem dysfunc.

• Treatment:– vol, incr LEtone, compressive hose, alpha agonist– attenuate tachycardia, Incr Na/H2O, mineralcorticoid

• Anesthetic Implications: (Mchaourab et al. Anesthesiology 2000;93)

– Labile BP, Hydrate, Avoid Histamine agents– Pain control, avoid valsalva, vacuum delivery– LUD, compressive hose, slow movement – Orthostatic HA(not PDPH)(Mokri, Low. Neurology 2003;61:980-2)

– ? Response to RA (sympath block )

Complete Heart Block• A118. Pt. 36wkGA, asymptomatic CHB, 40bpm,. temp pacer,

SAB C/S, BP112->90,HR 48-53->73 tx ephedrine • (Raikhelkar. Tufts-NEMC,Boston, MA)

• (Dalvi et al. Ob Gynec 1992;79:802-4. - 3 case rpt)

• 4 deaths in 42 pregnant CHB without pacer• Sudden death: prolong QT , LAE• Recommend Pacer for Symptomatic/at risk pt• Avoid Valsalva -> brady, syncope

• What’s your recommendation for asympt pt with CHB for pacer?

• Are CHB pt more likely to have hypotension, brady with SAB/Epid?

IHSS, AS/MS, CM, Fotan

• A125. s/p AV/MV repair, severely worsen AS/MS + preeclampsia ->emergent C/S (Waters et al. Cleveland Clinic, OH)

• A131. s/p Fotan for C/S (Shih et al. Kansas UMC, KS)

• A124. IHSS,SSS,s/pCVA,plavix for elective C/S(Mehta)

• A126. CM Labor RA monitor in ICU(Ross et al. WFU, NC)

A125. s/p AVreplace/MVrepair, worsen AS/MS + preeclampsia ->emergent C/S (Waters et al. Cleveland Clinic, OH)

• peak/mean AS 80/45, MS 28/14, EF55%, PTT 70• Pt deteriorates, Awake Sit Nasal FOB -> GA -> C/S• Uneventful intraOp course, APGAR 8/9• Authors: 16% become preg with prosthetic valves ,

acute physiologic worsening can occur with preg + preeclampsia.

• Why AwakeFOB ? Why Nasal? • Would RA be an option if not anticoagulated?• (Afrangui, Malinow. RAPM.1998;23:204-9. - LEA in pt with severe preeclampsia+MS)

A131. 22y/o G2P1 (99kg,56”,MP3) (s/p BT shunt, Fotan) now for C/S under LEA (Shih et al. Kansas UMC, KS)

• No ventricle in pulmonary circulation – RA to PA– Circulation dependent

adeq systemic venous return and low PVR

– All passive flow

• Implications:

• Fontan Circulation negatively impacted by – Single Functioning Ventricle– Ventricular dysfunction (Sensitive to Inhalation, PPV)– Mitral regurgitation – Pulmonary hypertension (Intub,hypoxia,hypercarbia)– Volume depletion

IHSS , CM

• A124. IHSS,SSS,s/pCVA,plavix for elective C/S(Mehta)

• A126. CM Labor RA monitor in ICU(Ross et al. WFU, NC)

• A124,126. With early Prenatal Evalu, Multidisciplinary Mgt/Optimize/planning , and with meticulous attn to volume, hemodynamics and clinical signs/symptoms: Regional anesthesia/analgesia can often be done safely in pt with severe complicating cardiac dz. (IHSS 80mmHg gradient, CM-EF 25-30%)

Valvular Heart Dz in Pregnancy• Reinold SC, Rutherford JD. NEJM 2003;349:52-59• Among pt with congen/acquired HD, adverse mat. cardiac events (pul

edema, arrythmias, cva,arrest, death) occurred in 13% completed preg.

• MS being most common valvular dz • Prognostic indicators/Risk Factors:

– Decr LV sys func(EF<40%), – L heart obstruction(AS, area <1.5 or MS area <cm2)– Previous CV events( heart failure, TIA/CVA, >=NYHA II

• Adverse cardiac events occur in:– 4% pt with 0 risk factors– 27% pt with 1 risk factos– 62% pt with 2 or more risk factors

A113. Epid analg for VD in pt with SCS (Nelson,Crew).A133 Labor epid in pt with a SCS(Hanson, Goodman)

• 2 cases of successful labor epidural in pts with a cervical and a lumbar thoracic SCS respectively for complex regional pain syndrome (CRPS.)

• Multidisciplinary Planning, Know location SCS components• Straight sterile technique

• Questions:• Does epid drugs affect SCS function or vice versa?• If PDPH after wet tap, should EBP be done?• ?Effect of EBP on SCS functions?• Should SAB be done for C/S on these pts?

A113. Epid analg for VD in pt with SCS (Nelson,Crew).A133 Labor epid in pt with a SCS(Hanson, Goodman)

• Epidural injection may temporarily change pt’s response to SCS stimulation, but should have no long term effect.

• Ideally DPuncture should be avoided. If happen, EBP can be done under straight sterile technique, with smaller volume (10-15 not 15-20ml, slower injection to reduce effect on leads.

• EBP could change response char. of SCS temporarily, or long term by scarring. It can be overcome by changing stimulator output or lead selection.

• Avoid Infection, damage lead, meticulous technique to avoid dural puncture are keys.

Thank You !

Drive Safely !!Have a Nice Trip Back Home !

Thank You !

Have a Nice Trip Back Home !