Eclampsia or Epilepsy Pre eclampsia Eclampsia and HELLP syndrome by mikeholy

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									Eclampsia or Epilepsy?
Dr. F. Moses
Is There A Difference?
• De Sauvages (1739) differentiated eclampsia from
  epilepsy in his Pathologia Methodica.

• He indicated that epilepsy is chronic and that the
  fits recur over long periods of time.

• All convulsions of acute causation De Sauvages
  called eclampsia.
A Safe Assumption
• Seizures in a pregnant patient beyond 20 weeks
  are generally assumed to be eclampsia until
  proven otherwise.

• Other possible causes include epilepsy.

• Amniotic fluid embolism is very rare but
  seizures can be a presenting symptom (with
  absence of proteinuria).
The History, The BP, The Urine
• History, physical examination (chiefly BP) and
  urinary protein determination are key.

• Patient may be known to have epilepsy or
  previous seizures.

• Diagnosis is based on history. Previous EEG may
  show characteristic pattern.

• Absence of proteinuria also suggests epilepsy.

 A disorder associated with pregnancy consisting
• Hypertension
• Proteinuria and
• New-onset dependent oedema
most commonly after 20 weeks of gestation

 Pre-eclampsia complicated with seizures.

• Hypertension
 ▫ Systolic > 140mmHg or 30mmHg above
   pre-pregnancy level
 ▫ diastolic > 90 mmHg or 15mmHg above
   pre-pregnancy level

• Two abnormal measurements, on two occasions,
  more than 6 hours apart
• Exact pathophysiology unknown
• It occurs only in the presence of a placenta and is
  resolved by its removal
• Possible causes:
 ▫ placental hypoperfusion
 ▫ increased sensitivity of the maternal vasculature to
   pressure agents leading to vasospasm and
   hypoperfusion of multiple organs
 ▫ an activation of the coagulation cascade leads to
   microthrombi formation and aggravates the
   perfusion problem
• Loss of plasma from the vascular tree with the
  resulting oedema additionally compromises the
• These events lead to signs and symptoms of
  toxaemia including hypertension, renal,
  pulmonary, and hepatic dysfunction, and - in
  eclampsia specifically - cerebral dysfunction.
• Preclinical markers of the disease process are
  signs of increased platelet and endothelial
Signs and symptoms

• Typically patients show signs of PIH and
  proteinuria prior to the eclamptic convulsion.

• Other cerebral signs may precede the convulsion
  such as
      Nausea
      Vomiting
      Headaches
      Cortical blindness.
Signs and symptoms
• With the advancement of the pathophysiological
  process, other organ symptoms may be present
      abdominal pain
      liver failure
      pulmonary oedema, and
      Oliguria
• The foetus may have been already compromised
  by IUGR, and may suffer foetal distress.
• Placental bleeding and placental abruption may
Risk Factors
•   Low socioeconomic class
•   Multiple foetuses, or hydatid
•   Maternal age <20 or >35yrs
•   Primip
•   Gestational or pre-gestational DM
•   Renal disease
•   Afro Caribbean- twice as likely
•   Family history- 4x the risk
The eclamptic seizure
• L. C. Chesley distinguishes these four stages of an
  eclamptic event:
  ▫ Stage of invasion: facial twitching can be observed around
    the mouth.
  ▫ Stage of contraction: tonic contractions render the body
    rigid; this stage may last about 15 to 20 seconds.
  ▫ Stage of convulsion: involuntary and forceful muscular
    movements occur, the tongue may be bitten, foam appears
    at the mouth. The patient stops breathing and becomes
    cyanotic; this stage lasts about one minute.
  ▫ Prolonged coma: the final stage. When the patient
    awakens, she is unlikely to remember the event. In some
    rare cases there are no convulsions and the patient falls
    directly into a coma. Some patients when they awake from
    the coma may have temporary blindness.
• During a seizure, the foetus may experience bradycardia
•   Hypertension
•   Urinalysis- proteinuria greater than 2+
•   Blood tests
•   CT head
•   Foetal USS
• Treatment of eclampsia requires prompt
  intervention and aims to prevent further
  convulsions, control the elevated blood pressure
  and deliver the foetus.

• Prevention of convulsions is by using
  magnesium sulphate.

• The serum Mg2+ therapeutic range for the
  prevention of the eclamptic uterine contractions
  is 4.0-7.0 mEq/L.
• Serum Mg2+ concentrations associated with
  maternal toxicity (also neonate depression or
  hypotonia and low Apgar scores) are:

 ▫ 7.0–10.0 mEq/L - loss of patellar reflex

 ▫ 10.0–13.0 mEq/L - respiratory depression

 ▫ 15.0–25.0 mEq/L - altered atrio-ventricular
   conduction and (further) complete heart block

 ▫ >25.0 mEq/L - cardiac arrest
 MgSO4 Regimen

As described by Pritchard & colleagues:
• Loading dose of 4 gm IV (20%solution) over 5 min
  minimum (preferably 10-15 min) followed
  immediately by 5gm in a 50% solution as a deep
  I/M injection into the upper outer quadrant of each

• Maintenance dose is a further 5 gm IM every 4 hrs,
  continued for 24 hours after the last fit.
• Permanent brain damage
• Renal insufficiency
• Abruption
• Death
• 25% of eclamptics will be so in future
• Increased risk of essential hypertension
• Epileptic seizures from brain damage
HELLP syndrome
• Undiagnosed pre-eclampsia progresses to cause-
          Elevated Liver enzymes
          Low Platelets

• May also occur de novo
• Incidence-    0.1-0.6% of pregnancies
                  4-12% of pre-eclampsia
• Similar to pre-eclampsia with
 ▫   RUQ/epigastric pain
 ▫   Jaundice
 ▫   Microangiopathic anaemia
 ▫   Deranged LFT’s
• Treatment- ABC, O&G, admit, deliver
HELLP syndrome
 • Microangiopathic hemolytic anemia, consumptive
   thrombocytopenia, liver dysfunction
 • 4-12% of patients with severe preeclampsia, 30% occur
 • DIC often secondary to placental abruption, sepsis or fetal
 • Platelet count indirectly proportional to severity of disease
 • Differential diagnoses: TTP, HUS, SLE, sepsis, acute fatty
   liver of pregnancy
 • Complications: ARF, ARDS, hemorrhage, placental
   abruption, rarely liver hematoma with rupture

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