CRITICAL ILLNESS IN

1

• CRITICAL ILLNESS IN
• OBSTETRICS,
• OBSTETRICIANS ROLE.
• DR MEENA MUTHIAH
• CONSULTANT OBGYN
• MANIPAL HOSPITAL
• MALATHI MANIPAL HOSPITAL

2
CRITICAL ILLNESS IN OBSTETRICS.

• ANTEPARTUM HAEMORRHAGE
• PLACENTA PREVIA
• ABRUPTIO PLACENTA
• POSTPARTUM HEMORRHAGE
• SHOCK IN OBSTETRICS
• PRE ECLAMPSIA AND ECLAMPSIA
• TRAUMA IN PREGNANCY
• BURNS IN PREGNANCY

3
ANTEPARTUM HAEMORRHAGE

• Bleeding from genital tract gt 24 weeks of
  gestation Causes before and after 24 weeks are
  the same.
• Massive obstetric haemorrhage - blood loss gt1
  litre from genital tract
• Significant cause of MMR in India, 3rd common.
• Incidence 5 of all haemorrhage.
• gt50 due to placenta previa abruption
• The rest is due to unclassified causes.

4
CAUSES OF APH

• Placenta - 2/3 due to previa or abruption
• Uterus- Before or after onset of labour
• Scarred uterus- Classical Caesarean section /
  Myomectomy/ Inverted T shaped incision.
• Unscarred uterus- Grand multipara when oxytocin
  is used for augmentation /Obstructed labour /
  Rotational forceps deliveries.

5
CAUSES OF APH

• Cervix - cervical erosion or polyps ,due to
  increased vascularity (after sex or infection)
• CA cervix / after cervical conisation or LLETZ.
• Vagina - uncommon , secondary to candida or HPV.
• Vulva due to varices.
• Consider pre existing clotting disorders VWF
  deficiency, decreased factor VIII activity along
  with defect in platelets

6
ANTEPARTUM HAEMORRHAGE (contd)

• Recurrence depends on the cause.
• In Previa there is 8-10 fold increase in risk.,
  LSCS increases the risk further and it is
  relevant as CS rates are on the rise.
• In abruption the risk is 10 and in gt50 cases
  recurrent episode is severe than the original
  one.

7
ANTEPARTUM HAEMORRHAGE (contd)

• Management
• Management is essentially the same whatever the
  cause of APH.
• Each unit should have a agreed protocol and it
  should be readily available.
• All staff should be familiar of this protocol and
  regular practice of firedrills held.

8
SIGNS AND SYMPTOMS - HAEMORRHAGE

• Depends on the degree of blood loss.
• Mild shock- lt20 of blood volume - decreased
  perfusion to non vital organs and tissues like
  skin, face, skeletal muscle and bone.
• Moderate shock- 20-40 of blood volume- decreased
  perfusion to vital organs like liver, GIT and
  kidneys. (decreased BP, oliguria, mottling of
  skin).
• Severe shock- gt40 of blood volume- decreased
  perfusion to heart and brain causing
  restlessness, agitation, coma, ECG, EEG changes
  causing possible cardiac arrest.

9
MANAGEMENT - APH

• Resuscitation
•  
• Best way to resuscitate the fetus is to
  resuscitate the mother.
•  
• Conversely the delivery of fetus (whatever the
  gestational age) may help to resuscitate the
  mother removing the fetoplacental unit and
  increasing the maternal venous return.
•  

10
MANAGEMENT - APH

• General principles
•  1) Call for HELP
•  Team of senior obstetricians , anaesthetists and
  peadiatricians should be called for.
•  
• To reserve and arrange cross matched blood
•  
• Operation theatre should be kept ready for
  immediate delivery if fetus is viable.
•  

11
MANAGEMENT - APH

• 2) ABC should be followed
•  Airway to assess and maintain.
•   High flow oxygen and reservoir
  bag 15 l/min
•   Monitor SPO2 and RR.
•  
• Breathing- Assess and protect airway
• Ventilate if adequate.
•  

12
MANAGEMENT - APH

• Circulation- External cardiac massage if required
• 15 degree lateral tilt no
  supine position
• To assess the volume of blood
  loss
•   To check peripheral perfusion
•   HR / BP/ output every half
  hourly
• Important always the blood loss is usually
  underestimated.
• 3 ) Replace the blood loss.
• Two large wide bore cannula (16G)
• Blood to be sent for CBC, coagulation screen,
  Kleihauer test, urea and electrolytes.
• Cross match 4-6 units of blood.

13
MANAGEMENT APH (contd)

• Initial management up to 2L of NS followed by
  synthetic colloid (Haemaccel).
• To transfuse blood.
• O negative blood can be used in case emergency
  (decreased risk of sensitization to antigen)
• Otherwise group specific crossmatched blood to be
  transfused.
• Consider warming of fluids and infusion with
  pressure bag.

14
MANAGEMENT APH (contd)

• Fresh whole blood does not allow time for full
  infection screen.
• gt 48 hours, platelet and clotting factors
  function is decreased.
• Stored whole blood is rarely available.
• PRBCs each pint contains 220ml of RBCs 80ml
  of SAGM solution (Saline, adenine,glucose,
  mannitol) it has shelf life of 35 days.
• Group specific blood following antibody screen -
  lt0.1 risk of haemolysis, risk increases to 1 if
  used without
  
  antibody screening.

15
MANAGEMENT APH (contd)

• If planning for caesarean section senior
  obstetrician / anesthetist.
• If fetus is dead induction of labour. In case
  of delay in delivery then consider Caesarean
  section as there is risk of DIC.
• PPH should be expected and need for caesarean
  hysterectomy should be discussed.
• Aggressively treat coagulopathies.

16
PLACENTA PREVIA

• Grading of placenta previa is important.
• Age gt35 years, parity, previous LSCS, repeat
  curettage for abortions increases risk by 2
  fold
• Multiple pregnancies, cocaine use - increases
  risk by 2-4 fold
• Smoking- increases risk by 3-6 fold
• Diagnosis routine USG
• TVS gold standard, no increased risk of
  bleeding.

17
PLACENTA PREVIA

• Complications
• Fetal major malformations
• Increased risk of RDS
• Fetal prematurity
• Anaemia

18
PLACENTA PREVIA

• Maternal related to bleeding
• 30 no bleeding
• 10 fold increased risk of
  antepartum bleeding.
• 2.5 fold increased risk of
  intrapartum bleeding.
• 1.9 fold increased risk of
  postpartum bleeding.
• Increased risk of abruption
  13.8 likelihood ratio.
• Peripartum hysterectomy x 33 fold.
• PPH is increased due to poor contractility of
  placental bed.
• Air embolism from low pressure venous sinuses.

19
MANAGEMENT PLACENTA PREVIA

• Caesarean section except grade I
• Aggressive approach to blood transfusion.
• Tocolysis if threatened preterm labour to
  prolong the pregnancy ?.
• Elective cervical circlage only clinical
  studies.
• Risk of fetal malpresentation transverse lie or
  oblique lie- caesarean section
• Caesarean section technique- posterior or
  anterior, transplacental approach with rupture of
  the amniotic sac.
• Should be done under GA, under regional
  anaesthesia hypotension

20
ANTEPARTUM HAEMORRHAGE (contd)

• Adherent placenta
• Uterine artery ligation / embolisation or
  systemic methotrexate.
• Vasa previa
• Fetoplacental vessels over the internal os rather
  than the placenta.
• Associated with succenturiate lobe, multilobed
  composition.

21
ABRUPTIO PLACENTA

• Incidence 15
• revealed 2/3
• concealed 1/3
• Classification
• I haemorrhage with pain and uterine
  irritability, no maternal or fetal compromise.
• II- No maternal compromise, but fetal
  distress is recognised.
• III- Uterine tetany, maternal compromise and
  fetal demise.
• It is clinical diagnosis.
• USG- sensitivity for abruption poor 24.

22
ABRUPTIO PLACENTA

• Risk factors
• Cigarette smoking.
• Hypertension disorders.
• Direct abdominal trauma- RTA, domestic violence,
  gt1 incidence risk of abruption increased by 4
  fold
• Acquired and inherited thrombophilias including
  APLA syndrome.
• Sudden uterine decompression polyhydramnios
  with rupture of membranes.
• Obstetric procedure- External cephalic version.

23
ABRUPTIO PLACENTA (contd)

• Management
• Depends on
• 1) Grade of presentation
• 2) Fetal gestational age.
• 3) Concomitant pathology.
• Conservative treatment in grade 0 only.
  (retroplacental clot)

24
POST PARTUM HAEMORRAHAGE

• Accounts for ¼ of all maternal deaths worldwide,
  where as 1/3rd of all maternal deaths in
  developing countries, including INDIA.
• Severe obstetric morbidity may be a more
  sensitive measure of pregnancy outcome than
  mortality alone as its highest for haemorrhage.
• Definition
• Estimated blood loss gt 500ml following vaginal
  delivery / gt 1litre following caesarean section.

25
POST PARTUM HAEMORRAHAGE (contd)

• Major haemorrhage loss gt 2.5L or requiring gt
  5units transfusion or treatment for coagulopathy.
  (FFP/ cryo/ platelets)
• Depends on her blood volume and underlying health
  factors , Not only on the amount but rate of
  blood loss.
• Primary - lt24 hours
• Secondary - gt24 hours.

26
POST PARTUM HAEMORRAHAGE (contd)

• Etiology
• Tone
• Tissue
• Trauma
• Thrombus

27
POST PARTUM HAEMORRAHAGE (contd)

• Common risk factors
• Overdistended uterus
• Primigravida
• Increased maternal age Assisted reproductive
  techniques , multiple pregnancies, increased
  LSCS, instrumental deliveries, complex medical
  disorder, previa.
• Chorioamnionitis, prolonged PROM
• Fibroid, previous LSCS
• APH, induction of labour, preeclampsia
• Prolonged labour, instrumental delivery
• Previous PPH
• Without risk factors still PPH can be there in
  60 of cases.

28
POST PARTUM HAEMORRAHAGE (contd)

• Pathophysiology
• Living ligatures.
• Active management of III stage of labour enhances
  the process.
• Prevention
• Anemia and other health issues are treated
  antenatally

29
POST PARTUM HAEMORRAHAGE (contd)

• Appropriate management of labour and delivery as
  follows
• Uterotonic agents.
• Controlled cord traction.
• Uterine massage after placental delivery.
• Early cord clamping vs. delayed cord clamping
  less fetal anemia, IVH late onset sepsis.

30
POST PARTUM HAEMORRAHAGE (contd)

• Drugs
• Oxytocin 5 units IV or 10 units IM, bolus
• Ergometrine maleate 500ug IM
• Misoprostal PGE1 analogue- oral or sublingual or
  rectal routes. (low resource setting)
• Carbetocin long acting oxytocin agonist.
• PGF2 alpha 250mcg IM stat

31
POST PARTUM HAEMORRHAGE (ctd)

• A recent Cocharane review neither im
• prostaglandins/ misoprostal preferable to
• conventional injectable uterotonics in low risk
• women.

32
POST PARTUM HAEMORRAHAGE (contd)

• The WHO held technical consultation on the
  prevention of PPH in 2006 recommended that
• Active management of III stage of labour should
  include uterotonic soon after birth of baby,
  delayed cord clamping and delivery of placenta by
  controlled cord traction.
• Risk of uterine inversion, therefore offered by
  skilled attendants.
• oxytocin is offered in preference to misoprostol.

33
TREATMENT - PPH

• General
• H- ask for help
• A- assess (vital, blood loss) and resuscitate
  golden hour the time at which resuscitation
  is initiated for best chance for survival.
• E- Establish the etiology, 4Ts
• Ecbolics (bolus syntocinon,
  ergometrine)
• M-massage uterus
• O- Oxytocin infusion, Prostaglandins
  (IV/rectal/im/ intramyometrial)

34
TREATMENT - PPH

• Specific surgical management
• S Shift to OT, bimanual compression.
• T- tissue, trauma excluded by exploration under
  GA proceed to tamponade balloon / uterine
  packing.
• A- Apply compression sutures.
• S- Systemic pelvic devascularisation (uterine,
  ovarian, quadruple, internal iliac).
• I - Interventional radiology uterine artery
  embolisation
• S - Subtotal or total abdominal hysterectomy.

35
SHOCK IN OBSTETRIC PATIENTS

• Shock- critical condition and life threatening
  medical emergency
• Results from acute generalized inadequate
  perfusion of the tissues below that needed to
  deliver oxygen and nutrients for normal cell
  function.
• Commonly due to haemorrhage or sepsis.
• Substandard care is still an issue in the
  management of shocked patient.
• Prompt recognition and management can improve
  maternal and fetal outcome in shock.

36
SHOCK IN OBSTETRIC PATIENTS (contd)

• Etiology -
• Hypovolemia due to haemorrhage, dehydration due
  to hyperemesis, DKA, burns.
• Sepsis endotoxemia.
• Cardiogenic- massive PEM, cardiomyopathies,
  obstructive structural lesions, dysrrhythmias,
  regurgitant lesions.
• Distributive shock (Neurogenic )
• anaphylaxis
• regional anaesthesia
• spinal injury.

37
PATHOPHYSIOLOGY- SHOCK

• Untreated shock progresses through 3 stages
  
• Compensated - no fluid required if underlying
  cause is treated.
• Decompensated decreased perfusion to heart,
  brain, kidneys.
• Irreversible- Acute tubular necrosis, severe
  acidosis with decreased myocardial contractility.

38
SHOCK IN OBSTETRIC PATIENTS (contd)

• Diagnosis
• No laboratory tests is required.
• A high index of suspicion and physical signs of
  inadequate perfusion are the basis of initiating
  treatment.
• It does not depend on the underlying cause.

39
INITIAL MANAGEMENT - SHOCK

• Successful management requires team work.
• Established protocols and practice fire drills.
• Management of the underlying cause is secondary.
• Delivery may be considered as a part of
  resuscitating the mother.
• ABC situation along with control of haemorrhage.
• Vasoactive drugs (inotropes and vasopressors) if
  cause of shock is due to myocardial depression.

40
SPECIFIC PROBLEMS

• Haemorrhage and hypovolemia
• Due to APH or PPH.
• Haemodynamic considerations in pregnancy
  increased cardiac output by 50 and blood volume
  by 45 reaching a peak at 28-34 weeks of
  gestation.
• Correspondingly greater fluid losses (gt30 of
  circulating volume) can occur before anything
  other than maternal tachycardia is seen.
• If Antenatal decreased fetal perfusion causes
  abnormal FHR pattern.

41
MANAGEMENT OF SHOCK (contd) Developments in
management of massive haemorrhage

• Cell salvage
• Blood from operative site -? heparin tubing ,
  filtered -? washing and centrifugation
• Widely used in cardiac, vascular, trauma and
  other major situations. Obstetric theatres are
  slow to introduce this technique because of the
  risk of amniotic fluid embolism and rhesus iso
  immunization.
• Autologous transfusion
• Pre-donation Isovolemic hemodilution
• economically viable
• only red cells with HCT 55-80
• Will not correct coagulopathy

42
MANAGEMENT OF SHOCK (contd)

• Recombinant factor VIIA key initiator in
  haemostasis
• Increases thrombin, factor V, VIII and
  platelet at the site of injury
• Activates factor IX and generates more factor
  Xa.
• Pelvic arterial embolisation.
• Balloon tamponade.

43
MANAGEMENT OF SHOCK (contd)

• SEPTIC SHOCK
• Uncommon in pregnancy in developed countries,
  still the second common cause of MMR in India.
• In obstetric patients mortality due to sepsis is
  3, upto 50 due to non obstetric cases.
• Strict aseptic precautions should be followed for
  any obstetric procedures especially in rural
  India.

44
MANAGEMENT OF SHOCK (contd)Spectrum of related
pathologies

• Systemic inflammatory response (SIRS) presence
  of two or more of following
• (i) temperature lt36 or gt38 degree F.
• (ii) HR gt90/min, RR gt30/min,
  (hyperventilation) or In ABG paCO2 lt 32mmHg.
• (iii) WBC gt12000 / cu mm or gt10 immature
  neutrophils.
• Sepsis SIRS evidence of infection (suspected
  or known)

45
MANAGEMENT OF SHOCK (contd)Spectrum of related
pathologies

• Septic shock at least 2 criteria to be met
• evidence of infection through a positive blood
  C/S
• Refractory hypotension despite adequate fluid
  replacement needs inotropes and vasopressors.
• Sepsis with multiorgan dysfunction
  Hypotension oliguria, decreased level of
  consciousness, metabolic acidosis /- lactic
  acid, thrombocytopenia.

46
MANAGEMENT OF SHOCK (contd)

• Predisposing factors for sepsis
• Prolonged rupture of membranes.
• Retained products.
• Post LSCS/ vaginal delivery endometritis.
• Cervical encerclage in RO Memb.
• Emergency LSCS, UTI, CAM.
• Water birth due to faecal contamination.

47
MANAGEMENT OF SHOCK (contd)

• Labs- Abnormal WBC
• Decreased platelets
• Coagulopathy
• Increased BUN and creatinine
• Deranged LFT, metabolic acidosis with
  
• increased lactate and increased CRP.

48
MANAGEMENT OF SHOCK (contd)

• General management of septic shock
• Basic shock treatment
• Special aspects
• Transfer to High dependency unit or ICU.
• Invasive monitoring with CVP and arterial line
• Blood C/S and C/S from other sites and IV
  antibiotics
• Removal of infected tissues
• Goal directed therapy.

49
MANAGEMENT OF SHOCK (contd)

• Advances in sepsis management
• Early goal directed therapy involves modifying
  the components of treatment to achieve specific
  end points.
• MAP gt/ 65mmHg
• Urine output gt0.5 ml/kg/hr
• CVP 8-12 mmHg
• Normal mixed venous arterial saturation in ABG.
• Insulin treatment, APC not contraindicated in
  pregnancy, steroids not known.

50
MANAGEMENT OF SHOCK (contd)

• III Cardiogenic shock
• Pre existing cardiac disease makes the parturient
  at risk.
• Anaphylaxis
• Due to drugs, food, latex and insect stings.
• Upto 5 of cases causative agent cannot be
  identified.
• Clinical features cutaneous / CVS/
  respiratory/ CNS/ GI

51
MANAGEMENT OF SHOCK (contd)

• Basic shock management , ABC and circulatory
  management.
• Special aspects
• Immediate Stop administration of
  suspected agent and call
  for help, Airway early intubation.
• Supine or
  trendelenburg position.
• Give epinephrine IM
  every 5-15min, titrated to pulse or BP
  until improvement occurs.
• In severe
  hypotension IV epinephrine.
• IV expansion and
  crystalloid.
• If cardiac arrest CPR and ALS protocols.

52
MANAGEMENT OF SHOCK (contd)

• Secondary
• If hypotension persists IV epinephrine infusion
  alternative pressor agents / Atropine - if
  bradycardia
• If bronchospasm salbutomol nebulisation,
  inhaled ipratropium if on B blockers,
• Antihistamines.
• Steroids IV but the effect is not immediate.
• All patients with severe anaphylaxis ? critical
  care.
• Investigations immediate - Serum tryptase may
  be elevated due to mast cell degranulation.
• Late- refer to immunologist for investigations.

53
MANAGEMENT OF SHOCK (contd)

• AF embolus
• Rare but devastating.
• Characterized by abrupt CV collapse and
  Coagulopathy.
• During labour or in the immediate post partum
  period.
• Pathophysiology- mechanism of AFE is poorly
  understood.
• The term anaphylactoid syndrome should be
  considered.

54
MANAGEMENT OF SHOCK (contd)

• Clinical features
• Late stage of labour- acute dyspnoea,
  hypotension, seizures, and cardiac arrest may
  quickly follow. Most of them die with in one hour
  of arrest.
• Left ventricular failure and massive DIC
  associated hemorrhage occurs in survivors of
  initial event.

55
MANAGEMENT OF SHOCK (contd)

• Management
• Basic CPR followed by ICU admission.
• Circulatory support
• Perform LSCS in arrested mothers, who are
  unresponsive to resuscitation with in 5 minutes
  (Perimortem caesarean section) to aid CPR.

56
MANAGEMENT OF SHOCK (contd)

• IV DISTRIBUTIVE SHOCK
• No loss of intravascular volume or cardiac
  function.
• The primary defect is massive vasodilatation
  leading to hypovolemia, reduces perfusion
  pressure and therefore poor flow to tissues.
• A) Spinal injuries reduced sympathetic tone-
  profound vasodilatation.
• Special aspects Fluids / vasopressor/ atropine
  for unopposed vagal activity.

57
MANAGEMENT OF SHOCK (contd)

• B)Anaesthesia (i)shock due to GA- anaphylaxis.
• (ii)Regional blocks- epidural / spinal.
• Factors include- use of standard non obstetric
  dose , excessive spread of intrathecal injection
  of appropriate dose, accidental intrathecal
  injection of the drug due to unrecognized dural
  puncture or migration of epidural catheter.
• Hypotension can be increased by incorrect
  positioning of the patient , eg absence of
  lateral tilt causing aorto caval compression.

58
MANAGEMENT OF SHOCK (contd)

• Clinical features
• All regional anaesthesia technique produce a
  level of sympathetic blockade (vasodilatation),
  motor blockade (weakness).
• Signs of high block
• Hypotension- feeling unwell / nausea.
• Bradycardia- (T1-T4)
• Upper limb neurological signs C5-T1
• Tingling of finger and weakness C6-C8
• Difficulty in breathing as block progress in
  cephalad direction, intercostal muscles and
  diaphragm may be involved (C3-C5)

59
MANAGEMENT OF SHOCK (contd)

• Management
• - Basic
• - Special aspect
• Support CVS- vasopressor drugs, inotropes
  to maintain blood pressure.
• Sedative agents can reduce the risk of
  awareness.
• (iii) Local anaesthetic toxicity (due to
  increased plasma concentration)
• Accidental IV injection, rapid absorption,
  absolute overdose
• It can cause seizures, dysrrhythmia, hypotension.

60
MANAGEMENT OF SHOCK (contd)

• Treatment
• Basic shock management.
• Seizure management.
• Deliver the baby
• Sedation.

61
SEVERE PREECLAMPSIA

• Stepwise system of management of Gestational
  hypertension
• Screening in pregnancy.
• Positive family history
• Past h/o or preexisting hypertension
• Signs and symptoms of impending eclampsia-
  headache / visual disturbances, abdominal pain,
  vomiting.

62
SEVERE PREECLAMPSIA (contd)

• Prior to delivery
• Regularly update management protocols.
• Stabilise with antihypertensive drugs if
  required.
• Prophylactic steroids if lt34 weeks.
• Consider the need for Magnesium sulphate.
• Continue monitoring for signs of disease
  progression and fetal monitoring.
• Delivery of baby in the best way / best day /
  best place.

63
SEVERE PREECLAMPSIA (contd)

• Antihypertensive regimen
• Labetolol, methyldopa, hydralazine, nifedipine
  are effective.
• Anticonvulsant im or iv in case of eclampsia-
  magnesium sulphate.
• To monitor respiratory rate, knee jerk, urine
  output during anticonvulsant therapy.
• For Magnesium sulphate toxicity Inj calcium
  gluconate I V.

64
SEVERE PREECLAMPSIA (contd)

• Maternal sequaelae of gestational hypertension
• CVA
• Convulsions
• Occipital lobe blindness
• HELLP syndrome
• Liver failure / rupture.
• DVT

65
SEVERE PREECLAMPSIA (contd)

• Maternal sequaelae of gestational hypertension
  (contd)
• Renal failure
• Pulmonary edema
• Aspiration syndrome
• PPH
• Status eclampticus.

66
SEVERE PREECLAMPSIA

• Risks of fetus in PIH
• Abruption
• IUGR
• Iatrogenic prematurity.

67
SEVERE PREECLAMPSIA (contd)

• CVP misleading in PIH , due to pulmonary edema.
• Not gt5cm H2O or 7cm of H2O.
• Oxygen saturation- pulse oximetry
• Fluid dry side 80ml/hr
• Overload occurs gt16hours when there is failure of
  post partum diuresis
• If pulmonary edema- 40mg frusemide followed by
  20g mannitol.

68
MANAGEMENT PROTOCOL

• Maternal management
• Keep blood crossmatched
• Control of blood pressure by antihypertensives
• Average 4 readings for BP monitoring
• Labs- uric acid, platelets, and LFT for enzymes
  twice weekly.
• Proteinuria /- quantification.

69
MANAGEMENT PROTOCOL

• Fetal management (main risks- placental
  insufficiency and prematurity)
• Prophylactic steroids if gestational age lt34
  weeks
• Initial USG for estimated fetal weight (serial
  growth is of no use every 2 weeks because maximum
  prolongation of pregnancy may be so much)
• Daily NST (change in the trace is important)
• Doppler USG of umbilical artery and AFI twice
  weekly.

70
ECLAMPSIA (contd)

• Indications for delivery in severe PIH
• Eclampsia all cases
• Severe PIH at 34 weeks
• If lt34 weeks with PROM, IUGR, abruption.
• Maternal disease BPgt160/110, oliguria, severe
  proteinuria gt75 g/dl, platelet lt1lakh, pulmonary
  edema.
• Fetal compromise (depends on NICU/ GA) abnormal
  KCC, NST, BPP, REDF.

71
MANAGEMENT PROTOCOL

• Care after delivery
• Continued closed monitoring of mother.
• Careful fluid balance and use of diuretics
  (colloids better than crystalloids as they pass
  quickly across the interstitial space).
• Gradual decrease of antihypertensives.
• Stop anticonvulsants gt48 hours if stable (if
  prophylaxis 24 hours)

72
SEVERE PREECLAMPSIA

• Follow up
• Long term to make sure that BP resolves.
• Discussion regarding what has gone on and the
  significance for future.
• If BP increases gt 6 weeks refer to physician
  for other investigations.

73
SEVERE PREECLAMPSIA (contd)

• Anaesthesia
• GA intubation and extubation increases BP.
• Epidural is better for labour analgesia as it
  keeps the patient awake.
• Adequate pain relief maintains normal BP.
• No need to cut short the II stage of labour if
  adequate pushing efforts are present.
• Post delivery inj methergine is contraindicated,
  inj syntocinon/ prostaglandin can be given.

74
ECLAMPSIA

• The progression of preeclampsia to eclampsia is
  1/200 - Prophylactic Magsulph decreases it.
• (MAGPIE TRIAL)

75
ECLAMPSIA (contd)

• Mild treatment
• Initial hospitalisation 1) 4th hourly Blood
  pressure
• 2) baseline
  BUN, Sr creatinine, platelets, uric acid,
  dopplers, BPP twice a week.
• DFMC
• Next visit OPD weight, BP, urine albumin, NST ?
  if abnormal ? admit
• Alphamethyl dopa, low dose aspirin, high dose
  calcium
• Encouraged till term 37-38 weeks if everything is
  normal.

76
TRAUMA IN PREGNANCY

• Key to effective management of traumatic pregnant
  lady is to resuscitate the mother aggressively
  and then to deliver the baby ? decrease in
  maternal morbidity but allows the best chance of
  fetal survival.
• Principles of resuscitation are the same only
  anatomical and physiological changes in
  pregnancy, requires to modify certain steps in
  resuscitation.

77
TRAUMA IN PREGNANCY (contd)

• Team of trauma care, obstetricians,
  peadiatricians, general surgeons should be
  involved in.
• Note the mechanism of injury
• deceleration injury
• direct impact (motor vehicle)
• penetrating injury (stab wound/ bullet or
  projectile)
• domestic violence
• To perform primary survey, ABC care, reevaluate
  simultaneously .

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TRAUMA IN PREGNANCY (contd)

• Assess fetal well being and viability, decide for
  delivery depends on gestational age- Perimortem
  caesarean section with in 5 minutes of
  unsuccessful CPR.
• Assess and treat the wound in the abdomen.
• The pregnant uterus is resilient organ and it can
  tolerate the severe pressure without rupturing.

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TRAUMA IN PREGNANCY (contd)

• Rupture of uterus may follow blunt trauma in
  association with seat belts, although they reduce
  overall mortality.
• The fetus and the placenta are vulnerable despite
  the buffering effect of amniotic fluid. The
  placenta is inelastic unlike the uterus and
  therefore liable to shearing. There is high
  chance of fetomaternal haemorrhage and risk of
  abruption.

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TRAUMA IN PREGNANCY (contd)

• With regard to examination
• Detection of intraperitoneal haemorrhage is even
  more difficult in pregnant women 800ml of blood
  needs to be present.
• Peritoneum has decreased sensitivity in
  pregnancy.
• The USG focused abdominal sonography in trauma
  (FAST) may be useful.
• The indications for diagnostic peritoneal lavage
  are same as non pregnant.

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TRAUMA IN PREGNANCY (contd)Penetrating wounds
(Stab/ gunshot)

• Above uterine fundus extensive GI or vascular
  damage.
• Uterine injury at any stage of pregnancy.
• Meticulous examination of abdominal contents is
  essential.
• Uterus should be opened when
• If a bullet is entered the uterus and the fetus
  is alive and considered viable, the fetus should
  be delivered by caesarean section.

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TRAUMA IN PREGNANCY (contd)Penetrating wounds
(Stab/ gunshot)

• To assess for fetomaternal haemorrhage (Kleihauer
  test)
• To perform secondary survey and start definitive
  treatments.
• To transfer the patient, if appropriate to higher
  centre.
• Keep a record chart of vitals, document injuries,
  findings and treatment.

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BURNS IN PREGNANT WOMEN

• ABC situation
• Consider early intubation if smoke inhalation or
  gt70 burns according to rule of nine.
• ABG, fluid replacement with crystalloids.
• Assess for other injuries.
• Pregnancy does not affect maternal outcome of
  burns

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BURNS IN PREGNANT WOMEN

• Fetal prognosis relates to the extent of burns.
• Spontaneous abortions if gt33 burns, during II
  trimester.
• Fetal loss during III trimester can be expected
  unless delivery occurs within 5-7 days.
• Remove all clothes and keep warm.
• Need for eschcerotomies.
• To document and consider transfer.

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