ICU ADMISSION IN THE OBSTETRIC PATIENT

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ICU ADMISSION IN THE
OBSTETRIC PATIENT
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Respiratory Physiology

• Lung Volumes
• change second half of pregnancy.
• ? diaphragm
• ? ERV RV
• ? 10-25 ? FRC by term
• ? IC,
• ? VC, TLC
• Airway Function
• Spirometry normal

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Respiratory Physiology 2

• Ventilation and Pulmonary Gas Exchange
• ? Vt, Vd, Ve (50), Va/Ve , Ve/Vo2
• Ve reponse to CO2, hypoxia
• ABG respiratory alkalosis (pco2 28-30), pH
  (7.4-7.47), HCO3 18-21.

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Respiratory Physiology 3

• Oxygen Transport
• MOTHER
• CO increases by 30-50
• maximum by the end of 1/3
• supine (3/3) fall (decreased venous return)
• VO2 increases 20-33
• Red cell volume increases by 20-30
• Plasma volume increases by 50
• Blood volume increases by 25-50 (79 ml/kg)
• Hemodilution..anemia and decrease in COP maximum
  during 2/3hemoglobin to 11-12 g/dL
• PREDISPOSED TO
• O2 desaturation
• PULMONARY EDEMA

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Respiratory Physiology 4

• Oxygen Transport
• BABY
• placental O2 transport 
• Qplacenta 10 Qmother
• fetal factors
• Pao2 (20-30)
• Hb (155g/L)
• increased O2 affinity of Hbf (Os dissn curve
  shifted to the left)
• increased Cao2 (CNS damage with gt 75
  reduction)
• increased CO
• fetus vulnerable to decreases in DO2
• startegies to
• increase CO, Cao2 (maternal Pao2)

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Physiologic Changes
FRC Ve CO Blood Vol GFR
- 20 40 40 40 50
16 40 0 1 2 WEEKS
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MECHANICAL VENTILATION

• Airway  difficult
• Failure to intubate accounts for 47 of all
  anesthesia-related mortality
• 8 X incidence in general surgical population
• factors 
• hyperemic  oral route
• low FRC/O2 reservoir
• risk of aspiration (GER/LES, increased Pabd)
• Gas Exchange Pao2 high Pco2 Nal 30 keep lt60
• Mechanics Pplateau higher
• PEEP for FRC, but keep up preload
• NIPPV  avoid (see upper airway)

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Acute Respiratory Distress in the Obstetric
Patient Differential Diagnosis

• VTED
• AFES
• PET/HTN
• Tocolytics
• Aspiration
• PP Cardiomyop
• Air Embolism
• Pneumothorax/mediastinum
• Other  can lead to ARDS
• ARDS
• Asthma sepsis (esp pyelonephritis, PROM,
  Pneumonia antepartum infection), hemorrhagic
  shock, etc.
• Cardiac disease

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ALI/ARDS in the Obstetric Patient

• uncommon event, but the most common cause of
  respiratory failure in the peripartum period.
• incidence 0.2-.3
• mortality 43 (Smith West J Med 1990), 10.5
  (Karetsky Med 1998)
• risk factors 
• cesarian section
• placental abruption
• fetal distress
• dead fetus syndrome

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ALI/ARDS in the Obstetric Patient 2

• Following Tocolytic Therapy
• Low incidence 0-.4
• Low mortality (lt5)
• onset of dyspnea associated with tachycardia and
  tachypnea shortly after tocolytic therapy is
  terminated
• Bilateral pulmonary infiltrates and significant
  hypoxemia are common findings.
• Resolution within 12-24 hrs of discontinuation.
  Otherwise, look for other diagnosis
• The etiology of this syndrome is unknown
• had at least 1 other coexisting potential
  pathogenic mechanism
• accompanying risk factor (maternal or fetal
  infection,).

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ALI/ARDS in the Obstetric Patient 3

• Pregnancy-induced hypertension
• Pulmonary edema rare (2.9)
• mortality of 10
• usually accompanied by signs of multisystem organ
  dysfunction
• pulmonary edema occurred both pre- and postpartum
• proneness to edemasensitive to fluids
• For boththe role of
• Associated risk factors
• Cardiogenic factors
• remains controversial

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Amniotic Fluid Embolism (AFE)

• classic triad of hypotension, hypoxia,
• and coagulopathy.
• recognized since 1926
• Rare
• unique to pregnancy
• incidence 1/8,000- 1/80,000 deliveries
• "it is impossible to state the true incidence of
  this condition at the present time because the
  sublethal and even subclinical forms which
  undoubtedly exist have not been recognized."
• undiagnosed nonfatal cases outnumber the fatal
  cases
• acute cardiopulmonary collapse is not an
  invariable accompanying finding.
• Signs and symptoms may be delayed for many hours
  postpartum, and most patients survive even if
  undiagnosed

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Amniotic Fluid Embolism (AFE)

• mortality
• 86
• 25-50 of the patients die within the first hour
• the most common cause of peripartum mortality
• 5-7 of all maternal deaths
• Fetal death is common, but this may be a
  consequence of the cardiovascular collapse
  occurring in the mother

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Amniotic Fluid Embolism (AFE)RISK FACTORS

• age
• multiparity
• uterine stimulants
• uterine rupture
• tumultuousness of labor
• closed abdominal injury
• IUD present at full term
• Amniocentesis
• caesarian section
• placenta accreta
• retained placenta
• meconium-stained amniotic fluid
• complication of amnio-infusion for either a
  therapeutic instillationor to induce abortion

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Amniotic Fluid Embolism (AFE)

• AF in maternal circulation during pregnancy
  physiologic or abnormal ?
• AF how does it cause for AFES ?

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Amniotic Fluid Embolism (AFE)Clinical
Presentation

• May be dramatic, with the abrupt onset of
  dyspnoea cyanosis, hypotension, coma,and
  hypotension with rapid progression to
  cardiopulmonary arrest
• Pulmonary edema (ALIARDS) frequent (24-70 of
  cases), may predominate.
• coagulopathy mild in almost every case
• followed by some degree of consumptive
  coagulopathy
• Evidence of CNS hypoxia is present, with
  alterations in mental status progressing to coma.
  In 10-20 of cases, the patient my present with
  seizure activity.
• Abruptio
• fetal demise
• HEMODYNAMIC PROFILE

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Amniotic Fluid Embolism (AFE)Diagnosis/Treatment

• clinical
• Squames from PAC
• exclude other causes of respiratory distress and
  hypotension
• septic shock, aspiration pneumonia, uterine
  rupture, placental abruption, pulmonary
  thromboembolism, venous air embolism
• Treatment
• Supportive, maintaining DO2, correcting
  coagulopathy

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Why Mothers die

• The death rate from amniotic fluid embolism could
  be reduced by avoiding uterine over-stimulation
  and by prompt diagnosis of obstructed labour
• Rates of obstetric intervention in the form of
  amniocentesis and induction and augmentation of
  labour should be kept as low as possible, and
  research into the condition is still necessary.

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VTED in the OB patient 1

• 2-5/1000 deliveries
• 12 of maternal deaths
• marked increased in the incidence of
• DVT and PE in the first postpartum month.
• Pregnancy acquired thrombophilia
• alterations in clotting and fibrinolytic factors
• reduction in venous tone and venous flow from the
  lower limb
• Other OB factors that enhance the risks for
  thromboembolism
• Other non-OB risk factors

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VTED in the OB patient 2

• Diagnosis similar to the
• nonpregnant state
• false-positive test result by both
• IPG and duplex ultrasonography.
• Treatment
• Prophylaxis
• Despite the lack of confirmatory data, the trend
  has been to treat with subcutaneous heparin all
  pregnant women at risk for deep venous thrombosis
  because of a prior history of deep venous
  thrombosis, antiphospholipid antibody syndrome,
  or coagulation inhibitor syndrome.

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