This document discusses complications of hypertensive disorders of pregnancy (HDP). It begins by providing background on HDP, noting that it complicates 5-8% of pregnancies worldwide and is a leading cause of maternal death. The document then discusses various maternal complications that can occur, including central nervous system issues like eclampsia and posterior reversible encephalopathy syndrome, respiratory failure, HELLP syndrome, acute kidney injury, hepatic complications, and hematological complications. It also outlines fetal complications such as preterm delivery, stillbirth, and intrauterine growth restriction. The objectives are to understand, predict, prevent, identify, and manage these complications through problem-based learning.

1. Dr. Shashwat Jani.
M. S. ( Obs – Gyn )
Diploma in Advance Laparoscopy.
Consultant Assistant Professor,
Smt. N.H.L. Municipal Medical College.
Sheth V. S. General Hospital , Ahmedabad.
Mobile : 99099 44160.
E-mail : drshashwatjani@gmail.com

2. Introduction
 Giving birth should be a time for celebration,
but for more than half a million women each
year—one every minute—pregnancy and
childbirth end in death and mourning.
 Six percent (approx. 1 in 16) of preeclamptic
patients develop one or more major systemic
complications .
Many maternal and fetal deaths or “near-misses”
are associated with substandard care.
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3.  HDP complicates 5 to 8% of all
pregnancies.
 This represents 8.5 million cases a
year worldwide.
 This pathology remains one of the
three leading causes of maternal death.
 The majority of these maternal
deaths are related to cerebral
hemorrhage that is secondary to poorly
controlled hypertension.
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4. Objectives
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 Understanding the complications of HDP
 Predictions and prevention of these
complications
 Early identification and appropriate
management
 Problem based learning .
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5. Complications
Obstetric
Mother Fetus
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6. OVERVIEW
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7. Maternal
CNS
• Seizures
• Cerebral Edema
• Cerebral Hemorrhage
• Strokes (thrombosis)
Hepatic
• Hepatic Failure
• Hepatic Rupture
• Subcapsular Hemorrhage
Heamatological
• DIC
• HELLP
Renal
• Renal Failure
• Oliguria
• Proteinuria >> Hypoproteinemia (Glomerular
Injury)
Lungs
• Pulmonary Edema
Fetal
Preterm Delivery
Stillbirth (IUFD)
Intrapartum Fetal Distress
Placental Abruption
Uteroplacental Insufficency
•Hypoxic Neurological Injury
•IUGR
•Oligohydraminos
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8. Obstetric
 Increased risk for cesarean section
 Placenta abruption
 Premature labor
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9. COMPLICATIONS
Acute Future Pregnancy Late
Dynamics and incidence patterns of maternal complications in early-onset hypertension of pregnancy
Ganzevoort W et al PETRA investigators. Obstet Gynecol. 2000 Jun;95(6 Pt 2):1017-9
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10. Acute Complications of HDP
 CNS Complications including eclampsia
 Acute Respiratory Failure
 HELLP Syndrome
 Uteroplacental Complications
 CVS Complications
 Acute Kidney Injury
 Hematological Complications
 Hepatic Complications
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11. CNS
Complications
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12. • Eclampsia is the most common, easily
identifiable complication.
• Antepartum is the most common type (38-53%)
intrapartum (18-36%)
postpartum (11-44%)
• Atypical eclampsia
- < 20 weeks
- Convulsions despite adequate MgSo4 .
- 48 hours post partum (also called as late post
partum eclampsia)
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13. Intracranial hemorrhage
 Infarcts
 Cerebral edema
 PRES
 Blindness
SEIZURES
Focal
neurological
signs
Prolonged
coma
Atypical or
recurrent
convulsions
Seizures even
after delivery
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14. Posterior Reversible Encephalopathy
Syndrome (PRES)
• A clinical neuroradiologic syndrome
of heterogenous etiologies , that are
grouped together because of similar
findings on neuroimaging studies.
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15. Pathophysiology
• Likely due to vasogenic edema secondary to an
acute increase in arterial blood pressure, which
overwhelms the autoregulatory capacity of the
cerebral vasculature, causing arteriolar vasodilation
and endothelial dysfunction, leading to extravasation
of fluid (i.e preeclampsia) .
(Thackeray and Tielborg, 2007)
• OR an acute and significant episode of
hypertension that causes cerebral vasoconstriction
with subsequent ischemia and edema .
(Thackeray and Tielborg, 2007)
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16. Autoregulatory failure
 Normal autoregulation maintains
constant cerebral blood flow over a range of
systemic blood pressures .
 When the upper limit is exceeded, the
arterioles dilate, allowing breakdown of the
blood-brain barrier, thus allowing extravasation
of fluid and blood into the brain parenchyma.
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17. PRES :
Clinical manifestation and Etiopathogenesis
• Postulations
• Vasogenic cerebral oedema
• ischaemia of brain tissue
• Posterior circulation
– more susceptible
– less sympathetic innervation
of the vertebro-basilar
vasculature to protect the
parenchyma from rapid
increases in arterial blood
pressure
 Headache, nausea, vomiting
 Confusion, behavioral changes
 Changes of consciousness (from
somnolence to stupor)
 Vision disturbances (blurred vision,
hemianopia, cortical blindness)
 Epileptic manifestations (mostly
focal attacks with secondary
generalization)
 Mental functions are characterized
with decreased activity and
reactivity, confusion, loss of
concentration and mild type of
amnesia.
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18. Management
 Clinical symptoms and radiologic evidence
support the diagnosis .
 Should be recognized promptly so
treatment can be initiated
 In our patient population with
preeclampsia/eclampsia, this typically means
delivery and treatment of Convulsions &
Hypertension .
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19. The immediate issues in caring
for an eclamptic woman include …
• Maintenance of maternal vital
functions,
• Control of convulsions and blood
pressure,
• Prevention of recurrent seizures, and
evaluation for delivery.
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20. Prognosis
Most cases of PRES are reversible
in days to weeks with removal of the
inciting factor and treatment of the
blood pressure .
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21. ACUTE RESPIRATORY FAILURE
/ Pulmonary edema
 Pulmonary edema
refers to an excessive
accumulation of fluid in the
pulmonary interstitial and
alveolar spaces.
 It complicates around
0.05% of low-risk pregnancies
but may develop in up to 2.9%
of pregnancies complicated by
preeclampsia.
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22. Only 30 % Antepartum
• Mainly,
- Post Partum,
- Mulatiparity
- Advance Maternal Age
- Associated Medical Disorders
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23. Diagnosis
Dyspnea
Orthopnea
Tachypnea
Auditory crackles and rales
Hypoxemia
ABGA, CHEST X RAY , ECG , CT SCAN , VQ SCAN
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24. Pulmonary Edema ARDS Pleural Effusion
B/L Air bronchogram
Central bat wing pattern
Right side pleural effusion
Diffuse B/L Coalescent
opacities
Left hemithorax
Obliteration of right
costophrenic angle.
Mediastinal shift to
right
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25. Treatment
Oxygen
Propped up position
I v lasix
Fluid restriction
Input – output charting
I v antibiotics
In refractory cases,
Pulmonary artery catherisation and ventilation .
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26. HELLP Syndrome
• HELLP stands for:
 Hemolysis (abnormal smear),
 Elevated liver enzymes (serum SGOT >70 U/L
serum LDH >600 U/L,
 Low Platelets (< 100000)
 6 % - one abnormalities
 12 % - two abnormalities
 10 % - three abnormalities
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27.  Occurs in approximately 10% of
pregnant women with pre-eclampsia or
eclampsia.
 One third of all cases of HELLP
syndrome occur postpartum, and only
80% of such patients were diagnosed with
preeclampsia before delivery.
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28. CAUSE :
It is thought to arise
as a consequence of
endothelial and
microvascular injury,
increased vascular
tone and platelet
aggregation.
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29. Spectrum of presentation
 Severity ranges from a mild and self-limited
course to a fulminant process leading to multiple
organ failure.
 In rare cases, occurs in normotensive
pregnancy, only with epigastric pain and
tenderness on palpation at the right
hypochondrium as initial symptoms.
 In most cases, resolves spontaneously
within 48 hours of delivery.
Esan K, Moneim T, Page IJ. Postpartum HELLP syndrome after a normotensive pregnancy.
Br J Gen Pract 1997;47:441−2.9-Aug-16
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30. HELLP post partum
• Decreasing LDH and increasing PLT count
should be routinely observed on 4th
postpartum day.
• Women not showing significant recovery
should be suspected of TTP…
- Normal coagulogram
- Greatly elevated LDH 20,000 IU/L
- Neurological signs and symptoms
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31. Beware of Postpartum HELLP :
 30% cases occur postpartum
 Majority within 48 hrs
 Risk of renal failure and pulmonary edema
is significantly increased compared to
antenatal onset HELLP.
Clin Perinatol 2004,31:807-33
Am J Obstet Gynecol 1993,168
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33. Management
 Stabilization of pt.
 Rx of HTN
 Termination of pregnancy ( Depends on
Gest. Age & maternal condition )
 Role of steroids ?????
With or without corticosteroids, the vast
majority of women with HELLP syndrome
will recover within 96 hours of delivery.
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34. FUTURE PREGNANCIES
 The reported risk of Recurrent HELLP
syndrome in a subsequent pregnancy ranges from
3% to 27%.
 Future pregnancies are also at increased risk
of other adverse events, including other
manifestations of preeclampsia, preterm delivery,
fetal growth restriction, placental abruption, and
cesarean delivery.
 The overall risk of such complications is 19–43%.
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35. Acute Kidney Injury
 AKI may occur in the context of severe
preeclampsia.
 In preeclampsia , due to the underlying
endothelial dysfunction the predominant
abnormalities seen on renal histology are to the
endothelium and glomeruli.
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36. Diagnostic Criteria :
Creatinine clearance by measuring 24 hr
urine creatinine remains the gold standard
of GFR estimation in pregnancy.
Any Sustained Fall In Output < 0.5ml/Kg/Hr
OR
Rising Serum Creatinine Should Alert The
Clinician Of Likelihood Of AKI.
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37. Management
 Supportive therapy includes blood
pressure control, positioning patients so as to
improve renal blood flow, correcting fluid and
electrolyte imbalance, and maintaining
adequate nutrition.
 If dialysis is required in pregnancy,
hemodialysis is preferred over peritoneal
dialysis.
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38. CVS COMPLICATIONS
Low filling pressures and a hyperdynamic circulation
• Cardiomyopathy
Rare complication
Treatment similar to other types of CCF
HDP patient with pulmonary may wrongly labeled as a case of
peripartum cardiomyopathy. HTN CMP shows good recovery
and regain cardiac function on follow up.
Acute MI Enhanced vascular reactivity to angiotensin II &
norepinephrine
Endothelial dysfunction
Decreased uterine perfusion leading to renin release
Use of ergot alkaloids – Acute MI
• Malignant Ventricular Arrhythmias 38

39. HEPATIC COMPLICATIONS
 Transaminases frequently elevated
 Epigastric/Subcostal pain (distension of liver
capsule by edema or subcapsular bleeding)
 Coagulopathy (high INR)
 Acute fatty liver
 Deficiency of the long chain 3-hydroxyacyl
coenzyme A dehydrogenase
Serum bilirubin - Important factor in predicting Maternal mortality
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40. Jaundice
High colored Urine
Liver Hematoma
Hepatic complications
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41. Liver Rupture / Hematoma
• Mortality Is high.
• First stabilize hemodynamically.
• Then Exploratory Laparotomy with C.S.
• Simple suturing is rarely effective because the entire
liver is edematous and friable and the hepatic parenchyma does
not have the tensile strength to retain the sutures.
• Other surgical options include packing with gauze,
topical coagulant agents or collagen fleeces coated with fibrin
glue, incorporation of omental pedicles or surgical mesh into the
liver, ligation of the hepatic artery, radiologic embolization of the
hepatic artery, or hepatic lobectomy.
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42. Hematological Complications :
Hemolysis / Anemia
Bleeding as the incision is being closed
& Incision site bleeding
Target cells, schistocytes &
paucity of platelets
Associated with increased LDH
DIC
(In preeclampsia there is vasoconstriction which affects
blood flow to the liver. Liver releases coagulation factors.)
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43. DIC
• DIC is a hematologic disorder characterized
by a generalized increase in both fibrin formation
and fibrinolysis, leading to excessive consumption
of clotting factors, which presents clinically as a
bleeding diathesis.
• The most common causes of DIC in
pregnancy : are excessive blood loss with
inadequate blood component replacement,
placental abruption, amniotic fluid embolism,
and severe preeclampsia / HELLP syndrome.
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44. Management
 Evidence of DIC in the setting of severe
preeclampsia / HELLP syndrome should prompt
immediate delivery.
 The decision of whether to proceed with
induction of labor or cesarean delivery depends
on such factors as gestational age, parity,
cervical Bishop score, motivation of the patient,
and the severity of DIC .
 A rapidly falling platelet count may make
cesarean delivery a more appropriate choice.
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46. Ocular Manifestations
Ocular involvement includes :
 Conjunctival vascular anomalies,
 Hypertensive retinopathy,
 Exudative retinal detachment,
 Vitreous and pre-retinal haemorrhages,
 Ischemic optic neuropathy ,
 Hypertensive choroidopathy
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47. UTEROPLACENTAL COMPLICATIONS
PLACENTAL
ABRUPTION
BE ON
GUARD
IUGR/
OLIGOHYDRAMNIOS
PRETERM DELIVERY
(Iatrogenic)
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48. COMPLICATIONS DUE TO DRUGS
 Antihypertensive use : Maternal hypotension
& placental abruption
 Fluid overload and Betamimetics – pulmonary
edema
 Diuretics can cause pancreatitis especially in
patients with ARF
Marcovici et al,Am J Perinatol 2002
 Sublingual Nifedipine can lead to Sudden
Hypotension & myocardial infarction and hence
not to be used.
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49. Treatment :
• Management of maternal hemodynamics &
prevention of eclampsia are key to a favorable
outcome
• MgSO4 - Rx of choice for preeclampsia.
• Goals
• Control BP
• Prevent seizures
• Deliver the fetus
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50. TAKE HOME MESSAGE
 Look for complications at Primary evaluation of
the patient.
 Ongoing risk assessment, continued surveillance
and interventions must be offered through
comprehensive critical care.
 Avoid Iatrogenic complications- drugs, fluids
 Tertiary care management and Multidisciplinary
Team approach.
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