Eclampsia Anesthetic Management Anesthetic Management by tkv74755

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									Anesthetic Management of the
  Patient with Preeclampsia




           Dmitry Portnoy, MD
       Anesthesiology Department
MATERNAL MORTALITY IN PREGNANCY IN THE UNITED
              STATES, 1980-1985


                        CAUSE                                 RATE (%)

          Embolism                                               17.0

          Indirect causes                                        15.6

          Hypertension in pregnancy                              12.3
          Ectopic pregnancy complications                        10.0

          Hemorrhage                                              9.1

          Stroke                                                  8.4

          Anesthesia                                              7.0

          Complications of termination                            5.2

          Cardiomyopathy                                          4.2

          Infection                                               3.5

          Other                                                   7.7


    Adapted from the US Maternal mortality Surveillance, 1980-1985. MMWR CDC Surveillance Summary, 1988.
Classification of Hypertensive Disease in Pregnancy
(Australian Society for the Study of Hypertension in Pregnancy, 1999)




                                       Hypertension in Pregnancy

      Preeclampsia            Chronic HTN with               Chronic HTN            Gestational HTN
                          superimposed preeclampsia

   Mild         Severe                                Essential HTN Secondary HTN   Transient HTN

           HELLP     Eclampsia
  Risk Factors and Mechanisms of Preeclampsia

 Risk of preeclampsia – up to 8% of all pregnancies
 Factors implicated in increased risk of developing preeclampsia
      Genetic determination, familial history
      Chronic HTN, DM, chronic renal disease, LSE, sickle cell
      Twin gestation, nulliparity, maternal age over 40, adolescents
 Pathogenesis of preeclampsia is poorly understood
      multisystem abnormalities - only in the presence of placental tissue
      generalized endothelial cell disorder
      excessive immunologic reaction
 Triad of physiological derangements
      Intense vasospasm    disruption     endothelium, platelets, trophoblasts
      Local or disseminated intravascular coagulation
      Plasma volume contraction
FACTORS THAT DIFFERENTIATE MILD FROM SEVERE
               PREECLAMPSIA

                                            Mild               Severe
Systolic arterial pressure              <160mm Hg           160 mm Hg
Diastolic arterial pressure             110 mm Hg           110 mm Hg
Urinary protein                          <5 g/24 hr          5 g/24 hrs
                                      Dipstick + or 2 +   Dipstick 3+ or 4+
Urine output                           >500 mL24 hr        ≤500 mL/24 hr
Headache                                     no                 yes
Visual disturbances                          no                 yes
Epigastric pain                              no                 yes
Right upper quadrant abdominal pain          no                 yes
Pulmonary edema                              no                 yes
Cyanosis                                     no                 yes
HELLP                                        no                 yes
Platelet count                         >100,000/mm3        <100,000/mm3
       Severe Preeclampsia: Diagnostic Criteria
                  Two or more of the following signs:
  Systolic blood pressure of 160 mmHg or diastolic pressure of 110
   mmHg recorded six hours apart with the patient at bed rest
  Proteinuria, 5g/24 hours or 3+ to 4+ protein on dipstick
  Oliguria, urine output less than 400 mL/24 hours, or less than 30
   mL/hour for two consecutive hours
  Cerebral or visual disturbances, including eye changes
  Pulmonary edema
  Epigastric pain
  Evidence of hemolysis, abnormal results from liver function tests,
   and/or thrombocytopenia
  Generalized convulsions and no history of seizure disorder


Adapted from: Stone JL, et al. Risk factors for severe preeclampsia. Obstet Gynecol
1994;83:357-361
    Organ System Derangements in Eclampsia

Cardio-        Renal          Hepatic       Hema-             CNS
vascular                                    tologic

Generalized   Decreased     Periportal   Decreased        Cerebral
vasospasm      GFR            necrosis      plasma volume     edema
Increased     Decreased     Hepatocell   Increased        Cerebral
SVR            renal plasma   ular damage   blood viscosity   hemorrhage
Increased     flow           Subcapsul    Hemo-
LV stroke      Decreased     ar hematoma   concentration
Decreased     uric acid                    Coagulopathy
CVP            clearance
Decreased
PCWP
Principles of Treatment of Preeclampsia




 1.   Delivery - definitive treatment (except for atypical)
 2.   Antihypertensive drug therapy
 3.   Bed rest, non-stimulating environment
 4.   Aspirin, Calcium supplementation, volume expansion
     DRUGS FOR TREATMENT OF SEVERE HYPERTENSION IN PREGNANCY


      Drug                Dose              Onset     Dura-           Adverse Effects
                                                       tion

Hydralazine     5–10 mg IV q 20 min       10–20 min   3–6 h     Tachycardia, headache,
                                                                flushing, aggravation of
                                                                angina
Labetalol       20–40 mg IV q 10 min 1
                mg/kg as needed
                                          10–20 min   3–6 h     Scalp tingling, vomiting, heart
                                                                block

Nifedipine      10–20 mg PO q 20–30 min   10–15 min   4–5 h     Headache, tachycardia,
                                                                synergistic interaction with
                                                                magnesium sulfate
Nicardipine     5–15 mg/h IV               5–10 min   1–4 h     Tachycardia, headache,
                                                                phlebitis

Sodium          0.25–5 μg/kg/min IV       Immediate   1–2 min   Nausea, vomiting, muscle
nitroprusside                                                   twitching, thiocyanate and
                                                                cyanide intoxication
Nitroglycerin   5–100 μg/min IV            2–5 min    3–5 min   Headache,
                                                                methemoglobinemia,
                                                                tachyphylaxis
           Magnesium Sulfate Therapy
 Potentiation of neuromuscular
                                             Magnesium Toxicity
  blockade (for all relaxants)
 Weakness
                                  Loss of patellar reflex   8–12 mg/dl
 Respiratory depression
                                  Warmth, flushing          9–12 mg/dl
 Cardiovascular effects
                                  Somnolence                10–12 mg/dl
     ECG changes
                                  Slurred speech            10–12 mg/dl
     Cardiac arrest
                                  Muscular paralysis        15–17 mg/dl
     Hypotension
                                  Respiratory difficulty    15–17 mg/dl
 Decreased uterine tone
                                  Cardiac arrest            30–35 mg/dl
 Excessive blood loss
 Neonatal effects                Theraputic range           4-8 mg/dl
       INDICATIONS FOR DELIVERY OF THE FETUS IN SEVERE
                                        PREECLAMPSIA
                   ABSOLUTE                                                RELATIVE
MATERNAL
Convulsion                                                           Severe hypertension
Cerebral irritability                                              Right upper quadrant
Heart failure                                                          Abdominal pain
Oliguria with urine output<20mL/hr                                    Heavy proteinuria
Uncontrollable hypertension
Rising serum creatinine (>50%)
Thrombocytopenia
Disseminated intravascular
coagulation
Clinical placental abruption
FETAL
Fetal distress                                               Intrauterine growth retardation

Modified from Gallery EDM: Hypertension in pregnancy. Practical management recommendations. Drugs 1995;49:4:561.
              Pre-anesthetic Evaluation
 Assessment of target organ-system involvement
      CV: HTN control, LV function, intravascular depletion
      Renal: degree of oliguria, creatinine level
      Liver: LFTs, signs of liver capsule streching
      Coagulation profile: platelet count, PT, PTT
      Airway examination: degree of laryngeal edema
 Anesthetic risk factors
      Poorly controlled hypertension
      >2+ urinary protein, elevated serum uric acid
      Thrombocytopenia less than 75,000
      Central vascular volume depletion
      Association with chronic HTN and IDDM
                    Invasive Monitoring

 Arterial catheter
      Sustained diastolic blood pressure greater than 90 mm Hg
      Use of parenteral vasodilaters (NTP, NTG)
      Induction of anesthesia with potential rapid BP fluctuations
      Inability to obtain accurate BP by cuff
      Need for frequent sampling
 Pulmonary artery catheter
      Severe HTN unresponsive to conventional treatment
      Severe pulmonary edema
      Persistent oliguria unresponsive to fluid challenge
 Regional Anesthesia for Preeclamptic Patient


 Advantages of epidural anesthesia
      Blunts hormonal and hemodynamic responses
      Provides better hemodynamic stability
      Increases renal and uteroplacental blood flow
      Decrease potential for seizures
 Spinal anesthesia
      Growing evidence of safety in preeclampsia
      Less hemodynamic stability (?)
      Less potential for hematoma
 Combined spinal-epidural
       Thrombocytopenia and Epidural Block

 Safe lower limit for platelet count before epidural –            ?
 Retrospective analysis of 2929 parturients (Rasmus, 1989)
      14 with platelet count 18,000 – 90,000 received neuraxial block
      None had sequelae of spinal hematoma
      No spinal/epidural hematomas in parturients reported
 Low-dose aspirin and neuraxial block – apparently safe
 Bleeding time – questionable indicator of risk of RA
 Recommendations
      Patient history, signs of bleeding, test tube clot formation, ACT
      Modification of technique that decreased the risk of bleeding
General Anesthesia for Preeclamptic Patient


 Airway edema
      Attention to hoarseness, high pitched or stridorous voice
      Small ETT (5-6 mm)
 Hypertensive response
      Induction, intubation and extubation
      HTN and tachycardia can lead to increased ICP
 Interaction of anesthetic agents with magnesium sulfate
                  HELLP Syndrome

H emolisis
Eelevated
Liver
Low
P latelets
 Occurs in 4-12% of severe PIH patients
 Reported perinatal mortality: 7.7- 60%
 Maternal mortality 3.5- 24.2%.
                           Eclampsia

 From Gr., a fancied perception of flashes of light
 Occurrence of a seizure that is not attributable to other
  causes in a preeclamptic patient
 Steps in managing an eclamptic convulsion:
      Maintain adequate oxygenation
      Prevent maternal injury during the convulsion
      Minimize the risk of aspiration
      Give adequate magnesium sulfate to control the convulsions
      Maternal acidemia should be corrected
      Do not attempt to shorten or abolish the initial convulsion
      Avoid polypharmacy
                           Conclusion


 Preeclampsia is fairly common multisystem disorder
 Associated with high maternal and perinatal M&M.
  (Mortality in obstetric patient can be 200%!)
 Important steps in anesthesia management
      Close communication with obstetrical colleagues
      Early and detailed preoperative assessment and plan
      Meticulous monitoring, including invasive monitors if indicated
      Utilization of advantages of RA when appropriate
      Close postoperative follow-up

								
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